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Infodump/FAQ on SARS-CoV-2

C0nt3mplat3
Jun 15th, 2020 (edited)
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  1. ****************************************************************
  2. ****************************************************************
  3. ******* Index *************************************************
  4. ****************************************************************
  5. ****************************************************************
  6.  
  7. ******* 1. Useful Links
  8. ******* 2. Immunity
  9. ******* 3. ADE
  10. ******* 4. Excess mortality, statistics and related news
  11. ******* 5. Eyes
  12. ******* 6. Virus' spread
  13. ******* 7. Transmission from mosquitoes - not possible
  14. ******* 8. Recovery and reinfection/reactivation
  15. ******* 9. Mentions of flu in SARS-CoV-2 studies
  16. ******* 10. SARS-CoV-2 and MIS-C (SARS2-induced Kawasaki-like disease)
  17. ******* 11. Lungs
  18. ******* 12. Brain and the nervous system
  19. ******* 13. Cardiovascular system
  20. ******* 14. Kidneys
  21. ******* 15. SARS-CoV-2 and Male/Female Sterility/Fertility/Hormonal system
  22. ******* 16. Studies on masks
  23. ******* 17. Info on testing for SARS-CoV-2 infection
  24. ******* 18. Pancreas
  25. ******* X. Other
  26.  
  27. ******* 1. Useful Links/Summaries ***************************************
  28.  
  29. From 'happy hypoxia' to purpuric rashes — here are all the perilous ways the coronavirus attacks the body
  30. https://archive.is/CWUrp
  31.  
  32. Brain deficits, nerve pain can torment Covid patients for months
  33. https://archive.is/TG1yH
  34.  
  35. /cVg/ Report #40 MSM (((Catches up))): SARS2: A Multisystem Disease
  36. >SARS2 damages not only the lungs, but the kidneys, liver, heart, brain and nervous system, skin and gastrointestinal tract, virtually every major system in the human body. It causes the blood to clot, the heart to lose healthy rhythm, the kidneys to shed blood and protein and the skin to erupt in rashes/swollen, purple "COVID" toes.
  37. >It causes headaches, dizziness, muscle aches, stomach pain and other symptoms along with classic respiratory symptoms like coughing and fever.
  38. >These clots can cause lethal strokes, cardiac arrest or can lodge in the lungs or legs. They clog the kidneys and interfere with dialysis treatments.
  39. >"There's a lot of news about clotting but it's also important to understand that a substantial proportion of these patients suffer kidney, heart, and brain damage, and physicians need to treat those conditions along with the respiratory disease."
  40. >The virus gains entry into the body though ACE2 receptors. Cells lining the blood vessels, in the kidneys, the liver ducts, the pancreas, in the intestinal tract and lining the respiratory tract all are covered with ACE2 receptors.
  41. >Damage to the pancreas can worsen diabetes
  42. >SARS2 infection also activates the immune system. This includes the production of inflammatory proteins called cytokines. This inflammation can damage cells and organs and the so-called cytokine storm is one of the causes of severe symptoms.
  43. >Blood clotting effects appear to be caused by several different mechanisms: direct damage of the cells lining the blood vessels and interference with the various clotting mechanisms in the blood itself. Low blood oxygen caused by pneumonia can make the blood more likely to clot.
  44. >In the immune system, SARS2 can also deplete the T-cells the body usually deploys to fight off viral infections.
  45. >Doctors need to treat all of these effects when coronavirus patients show up in the hospital.
  46. archive.is/3hKzk
  47.  
  48. Coronavirus symptoms fall into six different groupings, study finds
  49. >Cluster 1: Mainly upper respiratory tract symptoms, such as a persistent cough, with muscle pain also present. About 1.5% of patients in this group required respiratory support, with 16% making one or more trips to hospital. This was the most common cluster of symptoms, affecting 462 participants.
  50. >Cluster 2: Mainly upper respiratory tract symptoms, but also a greater frequency of skipped meals and fever. Of patients in this group 4.4% required respiratory support, with 17.5% making one or more trips to hospital.
  51. >Cluster 3: Gastrointestinal symptoms such as diarrhoea, but few other symptoms. While only 3.7% of patients in this group later needed respiratory support, almost 24% made at least one visit to hospital.
  52. >Cluster 4: Early signs of severe fatigue, continuous chest pain and cough. Of patients in this group 8.6% required respiratory support, with 23.6% making one or more trips to hospital.
  53. >Cluster 5: Confusion, skipped meals and severe fatigue. Of patients in this group 9.9% required respiratory support, with 24.6% making one or more trips to hospital.
  54. >Cluster 6: Marked respiratory distress including early onset of breathlessness and chest pain, as well as confusion, fatigue and gastrointestinal symptoms. Almost 20% of this group needed respiratory support and 45.5% made one or more visits to hospital. But this was the least common symptom cluster, affecting 167 participants.
  55. https://archive.is/Hrrst
  56.  
  57. 'Silent' neurological damage: May lead to future health problems
  58. >3 stages of neurological deficits caused by coronavirus.
  59. >Damage to the epithelial cells of the nose and mouth begins. 1st stage:Temporary loss of smell and taste.
  60. >2nd: Inflammation caused by a cytokine storm begins in lungs. Can spread to other organs and cause blood clots, leading to stroke
  61. >3rd: Inflammation damages a protective layer in the blood vessels of the brain, allowing blood content, and virus particles to invade the brain.
  62. >Doctors suggest MRI brain scans and follow ups with these patients
  63. >Patients with severe inflammation develop seizures, confusion, coma or encephalopathy which alters the function/structure of the brain. This increases risk of Parkinson's disease/Alzheimer's/Multiple sclerosis
  64. >Fotuhi says patients who COVID caused gave brain impairments in should be monitored for cognitive decline, attention deficit, brain fog or Alzheimer's disease
  65. >A French study found 84% of ICU patients with COVID had positive abnormalities on their neurological exams. 15% of patients who leave the ICU have residual neurological deficits, including poor attention and difficulties with decision-making and behavior control
  66. >Anywhere from 1/3 to 59% of hospitalized COVID-19 patients will experience confusion, dizziness, headaches, mini strokes and paralysis
  67. >Mini strokes may lead to a slowness in thinking
  68. Strokes in the young
  69. >"Patients in their 30s are having massive strokes more commonly seen in 80 year olds
  70. >2 unusual findings: Massive strokes in both hemispheres of the brain;also in both arteries and veins
  71. >Mortality rate of stroke patients with COVID: 42%-higher than the typical 10% rate
  72. >Coronavirus may enter cells by attaching to a protein abundant in cells that line the bodies blood vessels, heart/kidney/lungs.
  73. >Also, virus could be affecting cells' ability to control brain blood-flow. Also possibility: inflammation of blood vessels causes mini blood clots in the vessels.
  74. archive.is/PitHD
  75.  
  76. The four known ways in which SARS-CoV-2 affects human brain
  77. >When it comes to the brain and nerves, the virus appears to have four main sets of effects:
  78. >A confused state (known as delirium or encephalopathy), sometimes with psychosis and memory disturbance.
  79. >Inflammation of the brain (known as encephalitis). This includes a form showing inflammatory lesions – acute disseminated encephalomyelitis (ADEM) – together with the effects of low oxygen in the brain.
  80. >Blood clots, leading to stroke (including in younger patients).
  81. >Potential damage to the nerves in the body, causing pain and numbness (for example in the form of post-infectious Guillain-Barré syndrome, in which your body’s immune system attacks your nerves).
  82. http://archive.is/7Y538
  83.  
  84. The Possible Long-Term Health Impacts of Being Infected With the Coronavirus: A look at potential permanent damage in the the lungs, heart, brain, and the overall well-being after infection in some:
  85. archive.is/IuTa9
  86.  
  87. Coronavirus May Be a Blood Vessel Disease, Which Explains Everything
  88. archive.is/jwj8w
  89.  
  90. Non-respiratory manifestations of SARS-CoV-2
  91. http://archive.is/mOoiw
  92.  
  93. SARS-CoV-2 and Pathological Anatomy (in Russian)
  94. https://mosgorzdrav.ru/uploads/imperavi/ru-RU/patanatomiya_covid19_fullv2_compressed.pdf
  95.  
  96. Neurological complications of SARS2 (as of 29-05-2020)
  97. >Overall, the articles covered 630 individuals with confirmed SARS2 and nervous system compromise
  98. >Of those cases, 23 (3.6%) involved the CNS (encephalitis, encephalopathy, and myelitis); 564 (89.6%) involved the PNS (anosmia, Guillain Barré Syndrome, cranial nerve palsy and Miller Fisher Syndrome and muscle lesion) and 43 (6.8%) were neurovascular (stroke)
  99. http://archive.is/2DGpW
  100. http://archive.is/lIjGM
  101.  
  102. SARS2 is indicated to aggravate preexisting non-respiratory conditions based on a kidney study
  103. >renal tropism is a potential explanation of commonly reported new clinical signs of kidney injury in patients with Covid-19,5 even in patients with SARS-CoV-2 infection who are not critically ill.
  104. >Our results indicate that SARS-CoV-2 has an organotropism beyond the respiratory tract, including the kidneys, liver, heart, and brain, and we speculate that organotropism influences the course of Covid-19 disease and, possibly, aggravates preexisting conditions.
  105. http://archive.is/HLzvR
  106.  
  107. [reportanon's SARS-CoV-2 summary reports]
  108. https://pastebin.com/raw/csBRKKJH
  109.  
  110. [main pastebin]
  111. https://pastebin.com/fqdFu7Qi
  112.  
  113. ******* 2. Immunity **************************
  114.  
  115. Structure of SARS-CoV-2 ORF8, a rapidly evolving coronavirus protein implicated in immune evasion
  116. >ORF8 is a rapidly evolving accessory protein that has been proposed to interfere with immune responses.
  117. >The crystal structure of SARS-CoV-2 ORF8 was determined at 2.04 Angstrom resolution by x-ray crystallography.
  118. >The structure reveals a ~60 residue core similar to SARS-CoV ORF7a with the addition of two dimerization interfaces unique to SARS-CoV-2 ORF8.
  119. >A covalent disulfide-linked dimer is formed through an N-terminal sequence specific to SARS-CoV-2, while a separate non-covalent interface is formed by another SARS-CoV-2-specific sequence, 73YIDI76
  120. >SARS-CoV-2 ORF8 can form unique large-scale assemblies not possible for SARS-CoV, potentially mediating unique immune suppression and evasion activities
  121. https://www.biorxiv.org/content/10.1101/2020.08.27.270637v1
  122. https://www.biorxiv.org/content/10.1101/2020.08.27.270637v1.full.pdf
  123.  
  124. Monocytes, B & T lymphocytes, susceptible to SARS-CoV-2 active infection
  125. http://archive.is/HcTpX
  126.  
  127. Acute SARS-CoV-2 infection impairs dendritic cell and T cell responses
  128. https://www.cell.com/immunity/fulltext/S1074-7613(20)30333-2
  129.  
  130. US, Nevada: Genomic Evidence for a Case of Reinfection with SARS-CoV-2
  131. https://archive.is/YyIdG
  132.  
  133. SARS-CoV-2 re-infection by a distinct strain confirmed by whole genome sequencing
  134. https://archive.is/acmfj
  135.  
  136. Confirmed coronavirus re-infections in Belgium and Netherlands raise concerns about immunity
  137. >Belgian virologist Marc Van Ranst said the Belgian case was a woman who had contracted COVID-19 for the first time in March and then again with a different coronavirus strain in June. Further cases of re-infection were likely to surface, he said.
  138. >The National Institute for Public Health in the Netherlands said it had also observed 4 Dutch cases of re-infection with a different strain
  139. https://archive.is/Is5Wk
  140. https://archive.is/aIsu5
  141.  
  142. Pre-SARS2 humoral immunity to common coronaviruses does not confer cross-protection against SARS-CoV-2
  143. http://archive.is/QbUTH
  144. https://www.medrxiv.org/content/10.1101/2020.08.14.20173393v1.full.pdf
  145.  
  146. Platelets can contain SARS-CoV-2 RNA and are hyperactivated in COVID-19
  147. >Exhaustive assessment of cytokines in plasma and in platelets revealed the modulation of platelet-associated cytokine levels in COVID-19, pointing to a direct contribution of platelets to the plasmatic cytokine load. Moreover, we demonstrate that platelets release their alpha- and dense-granule contents and phosphatidylserine-exposing extracellular vesicles. Functionally, platelets were hyperactivated in COVID-19 subjects, with aggregation occurring at suboptimal thrombin concentrations. Furthermore, platelets adhered more efficiently onto collagen-coated surfaces under flow conditions. Conclusions: These data suggest that platelets could participate in the dissemination of SARS-CoV-2 and in the overwhelming thrombo-inflammation observed in COVID-19
  148. http://archive.is/SnsVS
  149. https://www.medrxiv.org/content/10.1101/2020.06.23.20137596v1.full.pdf
  150.  
  151. Broad phenotypic alterations and potential dysfunctions of lymphocytes in COVID-19 recovered individuals
  152. >The CR COVID-19 individuals still showed remarkable phenotypic alterations in lymphocytes after clinical recovery 4 to 11 weeks. This suggests SARS-CoV-2 infection imprints profoundly on lymphocytes and results in long-lasting potential dysfunctions.
  153. >The broad and long-term dysfunction of these lymphocytes subsets might profoundly impair the immune surveillance and protection executed by lymphocytes in the COVID-19 clinical recovered individuals, though broad and strong SARS-CoV-2 specific memory CD4+ T cells and CD8+ T cells could be detected in COVID-19 patients
  154. >A recent study on the SARS-CoV-2-specific humoral and cellular immunity in COVID-19 convalescent individuals highlighted that anti-viral T cells may not be maintained at high numbers in the PBMCs in the recovered patients.
  155. http://archive.is/R6QSt
  156. https://www.medrxiv.org/content/10.1101/2020.07.01.20144030v1.full.pdf
  157.  
  158. Multi-pronged human protein mimicry by SARS-CoV-2 reveals bifurcating potential for major histocompatibility complex detection and immune evasion
  159. >These findings highlight molecular mimicry as a shared strategy adopted by evolutionary titans -- the virus in its quest for escaping herd immune surveillance, and the host immune systems that are constantly learning the patterns of 'self' and 'non-self'
  160. >Here, we identify 33 distinct 8-mer/9-mer peptides that are identical between SARS-CoV-2 and human proteomes, including 20 novel peptides not observed in any previous human coronavirus (HCoV) strains.
  161. >The proteome is the entire set of proteins that is, or can be, expressed by a genome, cell, tissue, or organism at a certain time. It is the set of expressed proteins in a given type of cell or organism, at a given time, under defined conditions.
  162. >Given the high expression of ANXA7, PGD and PAM among cells of the respiratory tract, lungs, arteries, cardiovascular system, and pancreas, as well as in macrophages, their striking mimicry by SARS-CoV-2 raises the possibility of individuals with HLA-B*40 and HLA-B*35 alleles being predisposed to potential immune evasion or autoinflammation
  163. >Human ANXA7 mimicking peptide ESGLKTIL is only present in SARS-CoV-2, with the closest known evolutionary homologs being from BAT SARS like coronavirus (ESGLKTIL), pangolin coronavirus, and the NL63-related bat coronavirus strains.
  164. >This peptide has in-vitro evidence for positive MHC Class-I binding. Additionally, there are 4 human helicases (MCM8, DNA2, MOV10L1, ZNFX1), each containing peptides with established evidence of MHC Class-I binding that are also mimicked by SARS-CoV-2
  165. >Further, immunohistochemistry (IHC) data on 45 human tissues 14 shows that the PAM protein is detected at high levels in HEART MUSCLES, epididymis, and the adrenal gland
  166. http://archive.is/jijwu
  167. https://www.biorxiv.org/content/10.1101/2020.06.19.161620v1.full.pdf
  168.  
  169. Immunity to SARS-CoV-2 may wane just 2-3 months after infection, study suggests
  170. >When the researchers looked at antibody levels again eight weeks after each case was discharged from the hospital, they found that both groups had significant declines in antibodies. In the asymptomatic group, 40 percent had no detectable levels of one type of antibody—IgG—while 13 percent of symptomatic cases had no detectable levels. For comparison, in people who had been infected with SARS-CoV-2's relative, SARS-CoV (the coronavirus that causes SARS), researchers have seen sustained IgG levels for more than 2 years
  171. >But not all antibodies are equally effective at thwarting invading viruses, like SARS-CoV-2. The most effective are called neutralizing antibodies. The researchers of the new study specifically looked for these antibodies using an engineered pseudovirus designed to mimic SARS-CoV-2 as bait. The researchers found that 8 weeks after recovering, neutralizing antibody levels were still present—but they had declined in 81 percent of asymptomatic cases and 62 percent of symptomatic cases
  172. >The asymptomatic cases were identified by contact tracing from known cases, then isolated in a hospital for the entirety of their infection ... Though none developed noticeable symptoms, more than half had abnormalities in their chest scans during their infection.
  173. http://archive.is/fuGJB
  174.  
  175. Antibodies after coronavirus infection don't last for long
  176. >They are questions that have haunted scientists since the pandemic began: Does everyone infected with the virus produce antibodies? And if so, how long do they last?
  177. >Not very long, suggests a new study published Thursday in Nature Medicine. Antibodies — protective proteins made in response to an infection-may last only two to three months, especially in people who never showed symptoms while they were infected.
  178. >The conclusion does not necessarily mean that these people can be infected a second time, several experts cautioned. Even low levels of powerful neutralizing antibodies may still be protective, as are the immune system’s T cells and B cells.
  179. >But the results offer a strong note of caution against the idea of “immunity certificates” for people who have recovered from the illness
  180. >Antibodies to other coronaviruses, including SARS and MERS, are thought to last about a year. Scientists had hoped that antibodies to the new virus might last at least as long.
  181. >Several studies have now shown that most people who are visibly ill with COVID-19 develop antibodies to the virus, although it has been unclear how long those antibodies last. The new study is the first to characterize the immune response in asymptomatic people.
  182. >The researchers compared 37 asymptomatic people to an equal number who had symptoms in the Wanzhou District of China. The investigators found that asymptomatic people mount a weaker response to the virus than those who develop symptoms.
  183. >Antibody levels fell to undetectable levels in 40% of asymptomatic people, compared with just 13% of symptomatic people.
  184. >About 1/3 of the asymptomatic people had the “ground-glass opacities” characteristic of COVID-19 and abnormalities in the lungs and in cell types
  185. >“We cannot rely on natural infection to achieve herd immunity.”
  186. archive.is/1fmMp
  187.  
  188. SARS-CoV-2 Viral Load Predicts SARS2 Mortality
  189. http://archive.is/LOoke
  190.  
  191. Top researchers agree with Danish authorities' statements on immunity: "We will get sickness and death - and gain nothing"
  192. https://archive.vn/Yb8rX
  193.  
  194. Possible immunity evasion via SARS-CoV-2 ORF8 protein
  195. http://archive.is/t0IxV
  196. https://archive.is/3S2ck
  197.  
  198. Targeted Immunosuppression Distinguishes SARS2 from Influenza in Moderate and Severe Disease
  199. >The majority of SARS2 patients with acute respiratory failure do not have a cytokine storm phenotype but instead exhibit profound type I and type II IFN immunosuppression when compared to patients with acute influenza
  200. https://www.medrxiv.org/content/10.1101/2020.05.28.20115667v1
  201.  
  202. Reactivation/chronic illness from SARS-CoV2
  203. >A proportion of recovered patients still exhibit as the virus carriers and the case of CD8+ lymphocytes dysfunction was reported. These clinical characters of SARS2 suggest that SARS-CoV-2 could lead to adoptive immune disorder while remain active viral replication.
  204. >The discrepancy of ORF8 between SARS-CoV-2 and SARS-CoV could at least partially be responsible for specific SARS2 clinical and pathological characteristics, which somehow behaves as a chronic viral infection."
  205. http://archive.vn/YHRTD
  206.  
  207. SARS-CoV2 uses same strategy as HIV to dodge immune response, Chinese study finds
  208. http://archive.is/ifJPW
  209.  
  210. >Immune system
  211. Another consideration is how SARS-CoV-2 could impact a person’s risk for other infections. In a recent study, researchers found that 20% of people with Covid-19 were also infected with other viruses, including influenza, rhinovirus, and respiratory syncytial virus.
  212. >Typically, the presence of one virus decreases a person’s risk of another infection because the immune system is already activated. At the root of the issue is a type of protein called interferon that’s released with the first wave of the immune response and interferes with the virus’s ability to replicate.
  213. >“This protein is produced by the cell that’s attacked by the virus, and its job is to push back the virus. And what happens is that when the infected cell has produced the interferon, what we understand is that some of that interferon then seeps into noninfected cells that are adjacent and sits there waiting to become a protector of that cell,” explains Harvard professor of medicine Mandeep Mehra, MD. “So when a second virus, for instance, comes back in a certain period of time, there may actually be partial immunity to that second infection.”
  214. >One reason the novel coronavirus is so pernicious is that it appears to suppress these interferons, meaning that not only is the Covid-19 infection worse, but there may also be a heightened risk for future infections.
  215. >“This virus teaches the cells somehow to stop making interferon, and so it actually reduces your immunity to either second infections or potentially to even other viruses,” says Mehra. If this is the case, there is a real concern that people who recovered from Covid-19 could have an increased risk for influenza in the winter.
  216. >While the research on the novel coronavirus’s impact on interferons is preliminary, SARS and MERS had a similar effect on the immune system, and there are several cases of people infected with MERS also contracting influenza and tuberculosis.
  217. archive.is/IuTa9
  218.  
  219. >SARS-CoV-2 has a receptor binding domain specifically designed for the human angiotensin converting enzyme-2 receptor (ACE2) found in lungs, kidneys, intestines and blood vessels
  220. >SARS-CoV-2 has a furin polybasic cleavage site not found in any closely-related bat coronaviruses as well as other artificially inserted charged amino acids that enhance the virus’ ability to bind to and enter human cells by forming “salt bridges” between the virus and the cell surface
  221. >he SARS2 pandemic is revealing neurological, haematological and immunological pathogenicity, which cannot be explained by infectivity via the ACE2 receptor alone
  222. >SARS-CoV-2 binding to the bitter/sweet receptors in the upper respiratory tract provides a perfect location for transmission by coughing
  223. >oral and upper respiratory infection can lead to transmission to the lower respiratory tract, gastrointestinal effects and a cascade of inflammation-producing immunological responses
  224. http://archive.li/NUN4Y
  225. >These data reveal the biological structure of SARS-CoV-2 Spike and confirm that accumulated charge from inserts
  226. and salt bridges are in surface positions capable of binding with cell membrane components other than the ACE2
  227. receptor
  228. >Analysis of the Spike protein of SARS-CoV-2 shows 78.4% similarity with human-like (HL) epitopes
  229. >antibodies can only recognize 5-6 amino acids and therefore a 6 amino acid rolling window search for
  230. antibody epitopes was performed. A search so tailored to match against all human known proteins will give a 78.4%
  231. human similarity to the SARS-CoV-2 Spike protein, i.e if all epitopes on the 1255 amino acid long SARS-CoV-2 Spike
  232. protein can be used by antibodies then there will be 983 antibody binding sites which also could bind to epitopes on
  233. human proteins
  234. https://www.cambridge.org/core/services/aop-cambridge-core/content/view/DBBC0FA6E3763B0067CAAD8F3363E527/S2633289220000083a.pdf/biovacc19_a_candidate_vaccine_for_covid19_sarscov2_developed_from_analysis_of_its_general_method_of_action_for_infectivity.pdf
  235.  
  236.  
  237.  
  238.  
  239.  
  240. ******* 3. ADE **************************
  241.  
  242. IgG antibody seroconversion and the clinical progression of SARS2 pneumonia: A retrospective, cohort study
  243. >The respiratory failure due to SARS2 viral pneumonia observed in week 2 may be related to an antibody-related mechanism rather than uncontrolled viral replication. In the critical form of COVID-19, inflammation was sustained after IgG seroconversion.
  244. >In conclusion, the results of the present study suggest that severe COVID-19 pneumonia is related to antibody-dependent inflammation
  245. http://archive.is/Xyqbq
  246. https://www.medrxiv.org/content/10.1101/2020.07.16.20154088v1.full.pdf
  247.  
  248. A perspective on potential antibody-dependent enhancement of SARS-CoV-2
  249. >no clinical findings, immunologic assays or biomarkers are known to differentiate any severe viral infection from immune-enhanced disease, whether by antibodies, T cells or intrinsic host responses
  250. >In vitro systems and animal models do not predict the risk of ADE of disease, in part because protective and potentially detrimental antibody-mediated mechanisms are the same, and designing animal models depends on understanding how antiviral host responses may become harmful in people
  251. >The implications of our lack of knowledge are twofold:
  252. >First, comprehensive studies are urgently needed to define clinical correlates of protective immunity against SARS-CoV-2
  253. >Second, since we cannot predict ADE of disease reliably after either vaccination or treatment with antibodies, regardless of what virus is the causative agent, it will be essential to depend on careful analysis of safety in humans as immune interventions for COVID-19 disease move forward
  254. >More mechanism-focused studies are needed to determine whether small animal and NHP models of virus infection, including SARS-CoV-2, can predict the likely benefits or risks of vaccines or passive antibody interventions in humans
  255. http://archive.is/jAslK
  256. https://www.nature.com/articles/s41586-020-2538-8_reference.pdf
  257.  
  258. >Concerns persist that SARS-CoV-2 vaccines could cause antibody-dependent enhancement, which can potentiate viral entry into host cells and worsen disease.
  259. >the company, like others in this space, remains on alert for a dangerous phenomenon known as antibody-dependent enhancement (ADE). “It’s important to talk about it [ADE],” says Gregory Glenn, president of R&D at Novavax, which launched its SARS-CoV-2 vaccine trial in May. But “we can’t be overly cautious. People are dying. So we need to be aggressive here.”
  260. >There are mounting theoretical concerns that vaccines generating antibodies against SARS-CoV-2 may bind to the virus without neutralizing it. Should this happen, the non-neutralizing antibodies could enhance viral entry into cells and viral replication and end up worsening infection instead of offering protection, through the poorly understood phenomenon of ADE. ADE “is a genuine concern,” says virologist Kevin Gilligan, a senior consultant with Biologics Consulting, who advises thorough safety studies. “Because if the gun is jumped, and a vaccine is widely distributed that is disease enhancing, that would be worse than actually not doing any vaccination at all.”
  261. http://archive.is/MaXKX
  262.  
  263. Implications of antibody-dependent enhancement of infection for SARS-CoV-2 countermeasures
  264. >Here, we highlight clinical and experimental observations from earlier CoV outbreaks and suggest strategies that may reduce ADE in treating the SARS-CoV-2 pandemic. Whether SARS-CoV-2 can cause ADE effects remains an open question.
  265. >Epidemiological studies investigating ADE in individuals with multiple SARS-CoV-2 infections or cross-reactivity to common-cold-causing CoVs will likely take several years. However, given that ADE has been observed with the closely related SARS-CoV, we believe that the question of ADE effects in SARS-CoV-2 should be urgently resolved using experimental immunology.
  266. >As a cautionary note, no effort has yet been able to identify epitopes that can fully avoid the problem of ADE for any single viral pathogen associated with the phenomenon.
  267. http://archive.is/gVLtJ
  268.  
  269. >Dengue Fever, SARS‐CoV‐2, and Antibody‐Dependent Enhancement (ADE): A Perspective
  270. Here, we review the possible antibody‐dependent enhancement (ADE) occurrence, known for dengue infections, when there is a second infection with a different virus strain. Consequently, preexisting antibodies do not neutralize infection, but enhance it, possibly by triggering Fcγ receptor‐mediated virus uptake. No clinical data exist indicating such mechanism for SARS‐CoV‐2, but previous coronavirus infections or infection of SARS‐CoV‐2 convalescent with different SARS‐CoV‐2 strains could promote ADE, as experimentally shown for antibodies against the MERS‐CoV or SARS‐CoV spike S protein.
  271. http://archive.is/oeoyA
  272.  
  273. Coronavirus and the possibility of ADE
  274. http://archive.is/Ztpx7
  275.  
  276. Paradoxical dynamics of coronavirus by herd immunity and ADE
  277. http://archive.is/9Fjih
  278.  
  279. ADE might be real:
  280. >the advantage might be related to the fact that D614 is embedded in an immunodominant ADE epitope of SARS-CoV, and perhaps the G614 form can facilitate ADE
  281. https://www.biorxiv.org/content/10.1101/2020.04.29.069054v1.full.pdf
  282.  
  283. Coronavirus: Cross-reactive antibody responses
  284. http://archive.is/26p4J
  285.  
  286.  
  287. ******* 4. Excess mortality, statistics and related news **************************
  288.  
  289. >excess mortality, statistics and related news
  290.  
  291. Excess mortality from the Coronavirus pandemic
  292. https://ourworldindata.org/excess-mortality-covid
  293.  
  294. Missing Deaths: Tracking the True Toll of the Coronavirus Outbreak
  295. https://www.nytimes.com/interactive/2020/04/21/world/coronavirus-missing-deaths.html
  296. https://github.com/nytimes/covid-19-data/tree/master/excess-deaths
  297.  
  298. Coronavirus: What is the true death toll of the pandemic?
  299. https://www.bbc.com/news/world-53073046
  300.  
  301. CDC US States Total Deaths by Week
  302. https://imageshack.com/a/eZqd7
  303.  
  304. Excess Deaths Associated with SARS2
  305. https://www.cdc.gov/nchs/nvss/vsrr/covid19/excess_deaths.htm
  306.  
  307. Excess mortality
  308. https://archive.is/n0vHs
  309.  
  310. There Has Been an Increase in Other Causes of Deaths, Not Just Coronavirus
  311. http://archive.is/3ZS7i
  312.  
  313. Coronavirus Pandemic Led to Surge in Alzheimer’s Deaths
  314. http://archive.is/2ZCTD
  315.  
  316. Extra 10,000 dementia deaths in England and Wales in April
  317. http://archive.is/vMC5e
  318.  
  319. SARS-CoV-2 pandemic could lead to 500,000 fewer births in U.S., study suggests
  320. http://archive.is/COzKE
  321.  
  322. The COVID-19 pandemic in New York City led to a surge in out-of-hospital cardiac arrests
  323. >During the height of the pandemic in New York, there was a "dramatic increase in cardiopulmonary arrests, nearly all presented in non-shockable cardiac rhythms (>90% fatality rate) and vulnerable patient populations were most affected"
  324. >relatively few, if any, patients were tested to confirm the presence of COVID-19, making it impossible to distinguish between cardiac arrests
  325. >We also can't rule out the possibility that some people may have died from delays in seeking or receiving treatment for non–COVID-19-related conditions.
  326. Data for adults with OHCA who received EMS resuscitation from March 1, when the first case of COVID-19 was diagnosed in NYC, through April 25
  327. >Compared with the same period in 2019, the COVID-19 period had an excess of 2653 patients with OHCA who underwent EMS resuscitation attempts (3989 in 2020 vs 1336 in 2019, P < .001), an incidence rate triple that of 2019 (47.5 vs 15.9 per 100,000).
  328. >Compared with 2019, patients suffering OHCA during the pandemic period were older (mean age 72 vs 68 years), less likely to be white (20% white vs 33%) and more likely to have hypertension (54% vs 46%), diabetes (36% vs 26%), physical limitations (57% vs 48%) and cardiac rhythms that don't respond to defibrillator shocks (92% vs 81%)
  329. http://archive.is/VXXp2
  330. http://archive.is/Vcf0B
  331.  
  332. SARS2 news lessens with time regardless of case increases
  333. http://archive.is/mZY8s
  334.  
  335. USA's SARS-CoV-2 statistics has “unheard of level of chaos in the data, the protocols, the information.”
  336. >In at least a dozen states, health departments have inflated testing numbers or deflated death tallies by changing criteria for who counts as a coronavirus victim and what counts as a coronavirus test
  337. >About a third of the states aren’t even reporting hospital admission data
  338. >CDC blended diagnostic and antibody tests, boosting the nation's overall testing numbers
  339. http://archive.li/XTlHy
  340.  
  341. https://www.ft.com/content/6b4c784e-c259-4ca4-9a82-648ffde71bf0
  342. >The UK has registered 59,537 more deaths than usual since the week ending March 20, indicating that the virus has directly or indirectly killed 891 people per million.
  343.  
  344. Tokyo's excess deaths far higher than SARS-CoV-2 count, data shows
  345. http://archive.is/ds2sc
  346.  
  347. Sweden admits strategy was a mistake
  348. http://archive.is/W0uT8
  349.  
  350. >Actual Victim number in Peru may be of 18 thousand
  351. https://translate.google.com/translate?sl=es&tl=en&u=https%3A%2F%2Fperu21.pe%2Fpolitica%2Fcoronavirus-en-peru-cifra-real-de-victimas-del-covid-19-puede-alcanzar-los-18-mil-en-peru-noticia%2F
  352.  
  353. Brazil estimated to have over 6 million of infected:
  354. https://translate.google.com.ar/translate?hl=&sl=pt&tl=en&u=https%3A%2F%2Fg1.globo.com%2Frs%2Frio-grande-do-sul%2Fnoticia%2F2020%2F05%2F25%2Fbrasil-tem-sete-vezes-mais-contaminados-por-covid-19-do-que-mostram-as-estatisticas-oficiais-aponta-pesquisa-da-ufpel.ghtml
  355.  
  356. The United Kingdom’s COVID-19 death toll surpassed 50,000 on Wednesday, according to a Reuters tally of official data sources that highlighted the country’s place as one of the worst hit in the world.
  357. https://www.reuters.com/article/us-health-coronavirus-britain-casualties/uk-covid-19-death-toll-surpasses-50000-reuters-tally-idUSKBN23A1Q4
  358.  
  359. UK Excess Deaths Research
  360. >Results: There were 56,961 excess deaths and 8,986 were non-SARS2 excess deaths. England had the highest number of excess deaths per 100,000 population (85) and Northern Ireland the lowest (34).
  361. >Non-SARS2 mortality increased from 23rd March and returned to the 5-year average on 10th May.
  362. >In Scotland, where underlying cause mortality data besides SARS2-related deaths was available, the percentage excess over the 8-week period when SARS2-related mortality peaked was: dementia 49%, other causes 21%, circulatory diseases 10%, and cancer 5%
  363. http://archive.is/xkNxi
  364.  
  365.  
  366.  
  367.  
  368. ******* 5. Eyes **************************
  369. >eyes
  370. SARS-CoV-2: eyes are affected, can be an entry point
  371. http://archive.is/X5Jji
  372.  
  373. Acute vision loss in a patient with SARS2
  374. http://archive.is/HVlMU
  375.  
  376. Transient cortical blindness in SARS2
  377. https://www.jns-journal.com/article/S0022-510X(20)30194-5/pdf
  378.  
  379. >All patients showed hyper-reflective lesions at the level of ganglion cell and inner plexiform layers more prominently at the papillomacular bundle in both eyes. Ganglion cell and plexiform layer findings could be associated with CNS manifestations that have been described in animal studies and in COVID-19 neurological events
  380. http://archive.is/mz7gn
  381.  
  382. >The ocular implications of human CoV infections have not been widely studied. However, CoVs have been known to cause various ocular infections in animals. Clinical entities such as conjunctivitis, anterior uveitis, retinitis, and optic neuritis have been documented in feline and murine models
  383. http://archive.is/2sOYQ
  384.  
  385. >Across all eye specimens, immunohistochemical analysis revealed expression of ACE2 in the conjunctiva, limbus, and cornea, with especially prominent staining in the superficial conjunctival and corneal epithelial surface. Surgical conjunctival specimens also showed expression of ACE2 in the conjunctival epithelium, especially prominent in the superficial epithelium
  386. http://archive.is/rhgAq
  387.  
  388. >It cannot be excluded that SARS-CoV-2 could both infect the eye and the surrounding structures. SARS-CoV-2 may use ocular structure as an additional transmission route, as demonstrated by the COVID-19 patients’ conjunctival secretion and tears positivity to reverse transcriptase-PCR SARS-CoV-2-RNA assay.
  389. http://archive.is/wLxe9
  390.  
  391. >12 patients had ocular manifestations, such as epiphora, conjunctival congestion, or chemosis, and these commonly occurred in patients with more severe systemic manifestations...more significant changes in blood test values appeared in patients with ocular abnormalities
  392. http://archive.is/1q5Fn
  393.  
  394. >Fifteen (27%) had aggravated ocular symptoms, of which 6 (11%) had prodromal ocular symptoms before disease onset. Ocular symptoms are relatively common in COVID-19 disease and may appear just before the onset of respiratory symptoms
  395. http://archive.is/yXzA4
  396.  
  397.  
  398.  
  399.  
  400.  
  401.  
  402.  
  403. ******* 6. Virus' spread **************************
  404. >local spread and transmission
  405. Aerosol particles laden with SARS-CoV-2 can travel up to 100 meters
  406. http://archive.is/tv1JO
  407.  
  408. Persistence of Severe Acute Respiratory Syndrome Coronavirus 2 in Aerosol Suspensions
  409. >Although we performed experiment only once across several laboratories, our findings suggest retained infectivity and virion integrity for up to 16 hours in respirable-sized aerosols.
  410. https://wwwnc.cdc.gov/eid/article/26/9/20-1806_article
  411.  
  412. >SARS-CoV-2 remained viable in air (aerosols) throughout the duration of our experiment (3 hours), with a reduction in infectious titer from 103.5 to 102.7 TCID50 per liter of air
  413. http://archive.is/XPsm1
  414.  
  415. [26 March 2020]
  416. Pathogen-bearing droplets of all sizes can travel 23 to 27 feet (7-8 meters)
  417. http://archive.is/eINRi
  418.  
  419. [19 May 2020]
  420. Saliva droplets can travel up to 6 meters with a decrease in the concentration and liquid droplet size in the wind direction
  421. http://archive.is/fLg9R
  422.  
  423. Clinical Course and Molecular Viral Shedding Among Asymptomatic and Symptomatic Patients With SARS-CoV-2 Infection in a Community Treatment Center in the Republic of Korea
  424. >In this cohort study that included 303 patients with SARS-CoV-2 infection isolated in a community treatment center in the Republic of Korea, 110 (36.3%) were asymptomatic at the time of isolation and 21 of these (19.1%) developed symptoms during isolation. The cycle threshold values of reverse transcription–polymerase chain reaction for SARS-CoV-2 in asymptomatic patients were similar to those in symptomatic patients
  425. http://archive.is/iyrwq
  426.  
  427. Prevalence of Asymptomatic SARS-CoV-2 Infection
  428. >The likelihood that approximately 40% to 45% of those infected with SARS-CoV-2 will remain asymptomatic suggests that the virus might have greater potential than previously estimated to spread silently and deeply through human populations.
  429. >Asymptomatic persons can transmit SARS-CoV-2 to others for an extended period, perhaps longer than 14 days.
  430. http://archive.is/bKHmC
  431.  
  432. Viral shedding is prolonged for 30+ days after symptoms wane
  433. http://archive.is/l4jzl
  434.  
  435. SARS2 is viable on surfaces 7 days, urine 4 days, feces several hours
  436. http://archive.is/bkYn3
  437.  
  438. Coronavirus can live for four days on animal skin
  439. http://archive.is/oGj9q
  440.  
  441. The virus can remain stable within water for up to 25 days
  442. http://archive.is/fsSQH
  443.  
  444. No evidence for less transmission above T=26°C/80F*
  445. http://archive.is/tGvA6
  446.  
  447. Surface and air contamination of SARS2
  448. http://archive.is/pCYen
  449.  
  450. Fomite transmissions of SARS2
  451. http://archive.is/lexYG
  452.  
  453. Evaporated SARS2 droplets on surfaces
  454. http://archive.is/F5Mcy
  455.  
  456. City disinfection needed to slow spread
  457. http://archive.is/SASx3
  458.  
  459. Dried droplet residues viable up to 24 hrs
  460. http://archive.is/F5Mcy
  461.  
  462. Rapid transmission of coronavirus between cats confirmed. Concerns about pet-humans transmissions grow
  463. http://archive.is/ZHCqD
  464.  
  465. SARS2 droplets remain for up to 14 minutes indoors
  466. http://archive.is/mXEjB
  467.  
  468. SARS-CoV-2 incubation period
  469. >median was 5.6, ranges from 1.35 to 13.04 days
  470. http://archive.is/Vb6r3
  471.  
  472. >28-Mar: Median incubation period is 5-6 days, says Harvard
  473. https://archive.is/JNx03
  474.  
  475. In China, 20% discharged patients still exhaling SARS-CoV-2
  476. http://archive.is/0tZnp
  477.  
  478. [High humidity benefits the viability of the virus. This means that the virus can survive in the air 23 times longer than in drier air and travel longer distances. Dryer air, on the other hand, causes droplets of infection to evaporate faster and not travel the same distances, according to the study published in the journal Physics of Fluids]
  479. Calculations with their model reveal, among other things, an important and surprising effect of humid air. The results show high humidity can extend the airborne lifetime of medium-sized droplets by as much as 23 times.
  480. >Droplets exhaled in normal human breath come in a range of sizes, from about one-tenth of a micron to 1,000 microns. For comparison, a human hair has a diameter of about 70 microns, while a typical coronavirus particle is less than one-tenth of a micron. The most common exhaled droplets are about 50 to 100 microns in diameter.
  481. >The investigators used an improved description of air turbulence to account for natural fluctuations in air currents around the ejected droplet. They were able to compare their results to other modeling studies and to experimental data on particles similar in size to exhaled droplets. The model showed good agreement with data for corn pollen, which has a diameter of 87 microns, approximately the same size as most of the exhaled droplets.
  482. >Humidity affects the fate of exhaled droplets, since dry air can accelerate natural evaporation. In air with 100% relative humidity, the simulations show larger droplets that are 100 microns in diameter fall to the ground approximately 6 feet from the source of exhalation. Smaller droplets of 50 microns in diameter can travel further, as much as 5 meters, or about 16 feet, in very humid air.
  483. >Less humid air can slow the spread. At a relative humidity of 50%, none of the 50-micron droplets traveled beyond 3.5 meters.
  484. https://onlinelibrary.wiley.com/doi/full/10.1111/tbed.13766
  485. https://phys.org/news/2020-08-humid-air-lifetime-virus-laden-aerosol.html
  486. https://archive.is/pD37h
  487.  
  488. Cautious handling of urine from moderate to severe COVID-19 patients
  489. >In conclusion, our results suggest that SARS-CoV-2 RNA may be excreted in the urine depending on the severity of SARS2
  490. http://archive.is/r7iE1
  491.  
  492. Estimate of airborne transmission of SARS-CoV-2 using real time tracking of health care workers
  493. >Simulations demonstrated that risk of infection is substantially reduced with increased ventilation of rooms. Overall, our findings suggest that SARS-CoV-2 is not well transmitted via the airborne route in controlled conditions. We speculate that SARS-CoV-2 may be only opportunistically airborne, with most transmission occurring via droplet methods
  494. https://www.medrxiv.org/content/10.1101/2020.07.15.20154567v1
  495. https://www.medrxiv.org/content/10.1101/2020.07.15.20154567v1.full.pdf
  496.  
  497.  
  498.  
  499.  
  500. ******* 7. Transmission from mosquitoes - not possible **************************
  501.  
  502. [19-07-2020]
  503. SARS-CoV-2 failure to infect or replicate in mosquitoes
  504. >Three widely distributed species of mosquito; Aedes aegypti, Ae. albopictus and Culex quinquefasciatus, representing the two most significant genera of arbovirus vectors that infect people, were tested
  505. >We demonstrate that even under extreme conditions, SARS-CoV-2 virus is unable to replicate in these mosquitoes and therefore cannot be transmitted to people even in the unlikely event that a mosquito fed upon a viremic host
  506. >In this study, the susceptibility of three mosquito species, Ae. aegypti, Ae. albopictus and Cx. quinquefasciatus, were determined through the intrathoracic inoculation with SARS-CoV-2
  507. >Infectious viruses were recovered from 13/15 mosquitoes collected within two hours of inoculation. It is possible, that in the two negative mosquitoes, the inoculated virus lost infectivity during the holding period
  508. >No virus was detected in the 277 inoculated mosquitoes collected and titrated at time points beyond 24 h, suggesting a rapid loss of infectivity and the lack of replication after injection
  509. >From a total of 48 mosquitoes analyzed, infectious viruses were only recovered from one Ae. albopictus collected at 24 h post-inoculation
  510. >Based upon the lack of detectable infectious virus in any of the 277 samples collected at all time points beyond 24 h post-inoculation, we conclude that SARS-CoV-2 is unable to replicate in mosquitoes and that even if a mosquito fed on a person with virus in the blood, that the mosquito would not be a vector if feeding on a naïve host
  511. http://archive.is/DZtRJ
  512.  
  513. Pediatric SARS-CoV-2: children may be a potential source of contagion in the SARS-CoV-2 pandemic in spite of milder disease or lack of symptoms, and immune dysregulation is implicated in severe post-infectious MIS-C
  514. >A total of 192 children (mean age 10.2 +/- 7 years) were enrolled.
  515. >Forty-nine children (26%) were diagnosed with acute SARS-CoV-2 infection; an additional 18 children (9%) met criteria for MIS-C.
  516. >Only 25 (51%) of children with acute SARS-CoV-2 infection presented with fever
  517. >Nasopharyngeal viral load was highest in children in the first 2 days of symptoms, significantly higher than hospitalized adults with severe disease
  518. >Age did not impact viral load, but younger children had lower ACE2 expression
  519. >IgM and IgG to the receptor binding domain of the SARS-CoV-2 spike protein were increased in severe MIS-C, with dysregulated humoral responses observed
  520. https://www.jpeds.com/article/S0022-3476(20)31023-4/fulltext
  521.  
  522.  
  523.  
  524.  
  525.  
  526.  
  527. ******* 8. Mentions of flu in SARS-CoV-2 studies **************************
  528. >just a flu?
  529. >A respiratory virus infecting blood cells and circulating through the body is virtually unheard of.
  530. >Influenza viruses like H1N1 are not known to do this, and the original SARS virus, a sister coronavirus to the current infection, did not spread past the lung. Other types of viruses, such as Ebola or Dengue, can damage endothelial cells, but they are very different from viruses that typically infect the lungs.
  531. >Benhur Lee, MD, a professor of microbiology at the Icahn School of Medicine at Mount Sinai, says the difference between SARS and SARS-CoV-2 likely stems from an extra protein each of the viruses requires to activate and spread. Although both viruses dock onto cells through ACE2 receptors, another protein is needed to crack open the virus so its genetic material can get into the infected cell. The additional protein the original SARS virus requires is only present in lung tissue, but the protein for SARS-CoV-2 to activate is present in all cells, especially endothelial cells.
  532. archive.is/jwj8w
  533.  
  534. Targeted Immunosuppression Distinguishes COVID-19 from Influenza in Moderate and Severe Disease
  535. >The majority of COVID-19 patients with acute respiratory failure do not have a cytokine storm phenotype but instead exhibit profound type I and type II IFN immunosuppression when compared to patients with acute influenza
  536. https://www.medrxiv.org/content/10.1101/2020.05.28.20115667v1
  537.  
  538. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis from coronavirus
  539. >In lungs from patients with Covid-19, the amount of new vessel growth — predominantly through a mechanism of intussusceptive angiogenesis — was 2.7 times as high as that in the lungs from patients with influenza (P<0.001).
  540. CONCLUSIONS
  541. >In our small series, vascular angiogenesis distinguished the pulmonary pathobiology of Covid-19 from that of equally severe influenza virus infection. The universality and clinical implications of our observations require further research to define.
  542. https://www.nejm.org/doi/full/10.1056/NEJMoa2015432
  543.  
  544. Reminder that if the ESTIMATED flu death numbers are real, then there should be fewer excess deaths a few months after an outbreak (if there isn't a new one).
  545.  
  546.  
  547. ******* 9. Recovery and reinfection/reactivation **************************
  548. >recovery and reinfection/reactivation
  549.  
  550. US, Nevada: Genomic Evidence for a Case of Reinfection with SARS-CoV-2
  551. https://archive.is/YyIdG
  552.  
  553. SARS-CoV-2 re-infection by a distinct strain confirmed by whole genome sequencing
  554. https://archive.is/acmfj
  555.  
  556. Confirmed coronavirus re-infections in Belgium and Netherlands raise concerns about immunity
  557. >Belgian virologist Marc Van Ranst said the Belgian case was a woman who had contracted COVID-19 for the first time in March and then again with a different coronavirus strain in June. Further cases of re-infection were likely to surface, he said.
  558. >The National Institute for Public Health in the Netherlands said it had also observed 4 Dutch cases of re-infection with a different strain
  559. https://archive.is/Is5Wk
  560. https://archive.is/aIsu5
  561.  
  562. >Doctors "don't understand" why some formerly healthy people can have coronavirus symptoms that linger for many weeks or even months, emergency care physician Dr. Ron Elfenbein tells CBS News. While most people with mild cases of COVID-19 recover in about two weeks, according to the World Health Organization, some who refer to themselves as "long-haulers" suffer debilitating symptoms for much longer, even after initially improving.
  563. >"We really don't understand the science behind this and we don't really understand the pathophysiology why this is continuing to go on," Elfenbein said. "Could it be that it's your immune response that's causing that? Or could it be that you have some late reactivation of the virus still inside your body, meaning that it's still in there and reactivating from time to time to cause these symptoms?"
  564. >Elfenbein said doctors don't know the answers to those questions yet and "the big problem" is they don't know how to treat the ongoing symptoms.
  565. archive.is/Tw1Aq
  566.  
  567. Death from complications 2 weeks after official (CDC-approved) recovery in SARS-CoV-2 case
  568. http://archive.is/4zhU6
  569.  
  570. SARS2-infected sick for months, receive little support
  571. http://archive.is/2bQHB
  572.  
  573. An online survey of 151 medical professionals who fell ill in March found 68 are still unable to work. A further 26 went back, only to stop again when symptoms returned.
  574. >It appears coronavirus may be a chronic condition. How long it persists for is unknown. The symptoms can be serious and wide-ranging, affecting the lungs, heart, brain, kidneys, stomach and nervous system. Headaches, shortness of breath, sore throat and feeling exhausted are common. So is recovery followed by frequent relapses.
  575. >“We don’t know what is causing prolonged SARS2. Is it the ongoing initial illness, or is it an inflammatory reaction or is it a post-viral syndrome? We don’t know what the prognosis is or what the long-term consequences are. I wonder how many people are having prolonged illness and what the impact is on the workforce, for example. It’s scary to have an illness for which there isn’t any treatment and that doesn’t seem to be going away.”
  576. http://archive.is/OyRtB
  577.  
  578. Coronavirus may lurk deep in lungs after patients recover, study suggests
  579. http://archive.is/AoZZJ
  580.  
  581. >Most who "recovered" haven't actually recovered
  582. >researchers found mild to significant lung abnormalities on the chest computed tomography (CT) images of 94 percent of patients with coronavirus upon discharge from the hospital, suggesting follow-up monitoring of patients might be necessary.
  583. http://archive.is/H7oK5
  584.  
  585. SARS-CoV2 infects stem cells, halting lung recovery
  586. >Infection of stem cells and their subsequent loss can result in a decreased capacity for lung epithelial regeneration, which could be a determinant of SARS-CoV-2 pathogenicity
  587. http://archive.is/9oX2Q
  588.  
  589. Findings from Investigation and analysis of re-positive cases
  590. https://pastebin.com/raw/PHZ1y0rG
  591.  
  592. 24 y.o. disabled woman died in Catania - recovered after a first infection, got sick again (swab test - positive) and died
  593. http://archive.is/dScyA
  594.  
  595. Coronavirus After Effects? NY Doctor Develops Heart Disease After Recovery
  596. http://archive.is/CI7Bm
  597.  
  598. >The concomitant presence of fibrotic features on CT indicates the need for follow-up for evaluation of CHRONIC pulmonary complications.
  599. http://archive.is/BqeGn
  600.  
  601. In China, 20% discharged patients still exhaling SARS-CoV-2
  602. http://archive.is/0tZnp
  603.  
  604. Reactivation/chronic illness from SARS-CoV2
  605. >A proportion of recovered patients still exhibit as the virus carriers and the case of CD8+ lymphocytes dysfunction was reported. These clinical characters of SARS2 suggest that SARS-CoV-2 could lead to adoptive immune disorder while remain active viral replication.
  606. >The discrepancy of ORF8 between SARS-CoV-2 and SARS-CoV could at least partially be responsible for specific SARS2 clinical and pathological characteristics, which somehow behaves as a chronic viral infection."
  607. http://archive.vn/YHRTD
  608.  
  609. >Hallucinations
  610. >Possible Dementia
  611. >Confusion, aggression
  612. >potentially impaired memory and intellectual ability among recovered.
  613. >Recovered need to be monitored for a long time.
  614. http://archive.is/pLimM
  615.  
  616. Coronavirus has lingering effects on some people
  617. >An NHK survey has found that COVID-19 has lingering effects on some patients after testing negative for the virus and being discharged from hospital.
  618. >About 1,370 people were discharged or moved to other hospitals from the 18 hospitals by the end of May after symptomatic improvements. There were at least 98 people with problems that made daily life difficult. They accounted for about 7 percent.
  619. >Forty-seven people are experiencing respiratory function deterioration due to aftereffects of pneumonia caused by the virus, and six of them need the support of an oxygen inhalator at home.
  620. >There were 46 people who had lost muscle strength or had weaker mobility function over many days in hospital, and 27 people who had shown a cognitive decline due to old age. There were also cases of dysfunctions in the sense of smell and the higher brain.
  621. >Respondents also pointed out the need to recognize that people have continued to experience various problems after discharge from hospital and that a greater network of support is needed.
  622. http://archive.is/IOjDl
  623.  
  624. These people have been sick with coronavirus for more than 60 days.
  625. >Over the following weeks, Montano, 32, developed a fever, cough, stomach problems, and lost her sense of taste and smell like other sufferers of the novel coronavirus. Unlike most of them, though, her symptoms never went away. They kept coming and going in waves like a roller coaster that has kept her bed-bound for 78 days straight
  626. >Cara Schiavo, a 31-year-old social worker from Cedar Grove, N.J., came down with something that looked like pinkeye on March 15, and then wound up in the emergency room when she developed a fever and other symptoms. Since then, "I haven't had a day when I've been back to normal."
  627. >Matthew Long-Middleton, 35, a radio journalist in Kansas City, Mo., was struck with fever, chills and typical flu-like symptoms on March 11, and has never fully recovered. "I sometimes try to work from bed, but sometimes just sitting up is too much," he said.
  628. >Long-Middleton, a triathlete, describes the illness as "mercurial" with better days and hours. After a full month of being extremely sick in bed, he is better, but struggles with lingering symptoms, including profound weakness and what he called a "buzzing/tingling/vibration/tremor sensation" that can make it difficult to walk, much less return to cycling, swimming and running. "I'm better, but the hardest, most confusing thing about this is that I'm not well," he said this week.
  629. >"It's a pretty bad infection even in mild cases," said Avindra Nath, clinical director of the National Institute of Neurological Disorders and Stroke at the National Institutes of Health.
  630. http://archive.is/h6V1S
  631.  
  632.  
  633.  
  634.  
  635.  
  636.  
  637.  
  638.  
  639. ******* 10. SARS-CoV-2 and MIS-C (SARS2-induced Kawasaki-like disease) **************************
  640. >SARS-CoV-2 and MIS-C
  641.  
  642. Louisiana child's possible coronavirus-linked MIS-C death the first in state
  643. http://archive.is/dzjO0
  644.  
  645. 2 mysterious inflammatory syndrome cases turned out to be Kawasaki disease: KCDC
  646. http://archive.is/eBYPH
  647.  
  648. Yakima Child Diagnosed With Coronavirus-Related Syndrome
  649. http://archive.is/2PYDI
  650.  
  651. Redlands: Multisystem Inflammatory Syndrome In Children Related To SARS2
  652. http://archive.is/FhYfK
  653.  
  654. 8-year-old North Carolina girl dies after getting coronavirus
  655. >An 8-year-old North Carolina girl has died after she got sick with coronavirus and suffered a seizure that left her in a coma, according to a report.
  656. http://archive.is/hzU3W
  657.  
  658. Rare “Multisystem Inflammatory Syndrome in Children” cases affecting children are being reported across the globe
  659. http://archive.is/60dbp
  660.  
  661. 161 Severe Child SARS-CoV2 Syndrome Cases Now Being Investigated in NY: Docs Fear Undercount
  662. 92% of these children had antibodies
  663. http://archive.is/f2d48
  664.  
  665. >Symptoms include stomach pains, fever, rashes
  666. >heart damage all but confirmed
  667. >Six weeks asymptomatic incubation
  668. http://archive.is/HssbI (CNN, 20/05)
  669.  
  670. >Two cases at Seattle Children's, 13 and 10
  671. http://archive.is/DRuOy (KIRO7, 22/05)
  672.  
  673. >38% of cases have acute kidney injury
  674. >51% got myocardial impairment
  675. >75% went into shock
  676. http://archive.is/9Tg5H (DAIC, 20/05)
  677.  
  678. >2 Kids and a Teenager dead in New York
  679. http://archive.is/BN5Dm (CNN, 10/05)
  680. http://archive.is/fSqVH (RT, 10/05)
  681.  
  682. >15 cases in Paris, 70 in New York
  683. http://archive.is/txKpf (German tagesschau, 14/05)
  684.  
  685. >First fatality in France is a 14-year old with no underlying conditions
  686. http://archive.is/DPSIy (France24, 15/05)
  687.  
  688. >Researchers at the Imperial College London early in developing a test
  689. http://archive.is/VCEQx (FOX, 20/05)
  690.  
  691. >Kawasaki-like syndrome now called PMIS (paediatric multisystem inflammatory syndrome) or MIS-C (multisystem inflammatory syndrome in children)
  692. >20 cases in Bergamo, Italy with Kawasaki symptoms - more than the past 5 years combined
  693. >Other affected children develop persistent fevers
  694. http://archive.is/Z4guz (Al-Jazeera, 21/05)
  695.  
  696. MAY 13, 2020
  697. Italy:
  698. >An outbreak of severe Kawasaki-like disease at the Italian epicentre of the SARS-CoV-2 epidemic: an observational cohort study
  699. https://archive.is/DUu0f
  700.  
  701. Netherlands/UK:
  702. Kawasaki-like disease: emerging complication during the coronavirus pandemic:
  703. https://archive.is/d6jrV
  704.  
  705. MAY 14, 2020
  706. France:
  707. Outbreak of Kawasaki disease in children during coronavirus pandemic: a prospective observational study in Paris, France
  708. https://archive.is/Qn3Ne
  709. https://www.frontiersin.org/articles/10.3389/fimmu.2019.01156/full
  710.  
  711. USA:
  712. 15 children are hospitalized due to corona with Kawasaki disease symptoms in New York
  713. http://archive.vn/plfSj
  714.  
  715.  
  716.  
  717.  
  718.  
  719.  
  720. ******* 11. Lungs **************************
  721. >lungs
  722. Follow-up study of the pulmonary function and related physiological characteristics of SARS2 survivors 3 months after recovery
  723. >Three months after discharge, the degrees of radiological abnormalities were detected in 39 patients (70.91%), and their HRCT scan images were viewed
  724. >Thirteen patients (23.64%) showed bilateral involvement on chest HRCT scans. The lower right lobe was involved in 23 patients (41.82%), while lower left lobe and upper left lobe were involved in 12 patients (21.82%) and 11 patients (20%), respectively
  725. >lung function abnormalities were detected in 14 patients (25.45%). Anomalies were noted in TLC of 4 patients (7.27%), FEV1 of 6 patients (10.91%), FVC of 6 patients (10.91%), DLCO of 9 patients (16.36%), and small airway function in 7 patients (12.73%)
  726. >Fifty-five of the 77 COVID-19 survivors completed the study. Their mean (SD) age was 47.74 (15.49)
  727. >Common comorbidities included hypertension (6 cases, 10.91%), diabetes mellitus (2 cases, 3.64%) and cardiovascular diseases (2 cases, 3.64%). No underlying pulmonary diseases were observed on admission
  728. http://archive.is/kcZJh
  729. https://www.thelancet.com/action/showPdf?pii=S2589-5370%2820%2930207-8
  730.  
  731. Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections
  732. >Abnormal radiological findings confined to one lung were identified in 66.7% (14/21) of the asymptomatic individuals, whereas 33.3% (7/21) had abnormalities in both lungs.
  733. >The median duration of viral shedding in the asymptomatic group was 19 d (interquartile range (IQR), 15–26 d)
  734. >asymptomatic individuals had a weaker immune response to SARS-CoV-2 infection
  735. >Of the 37 asymptomatic individuals, the median age was 41 years (range, 8–75 years) and 22 were female
  736. http://archive.is/UVaXw
  737. https://www.nature.com/articles/s41591-020-0965-6.pdf
  738.  
  739. Prevalence of Asymptomatic SARS-CoV-2 Infection
  740. >Asymptomatic persons seem to account for approximately 40% to 45% of SARS-CoV-2 infections, and they can transmit the virus to others for an extended period, perhaps longer than 14 days
  741. >Asymptomatic infection may be associated with subclinical lung abnormalities, as detected by computed tomography
  742. http://archive.is/W7XGo
  743.  
  744. SARS-CoV2 infects stem cells, halting lung recovery
  745. >Infection of stem cells and their subsequent loss can result in a decreased capacity for lung epithelial regeneration, which could be a determinant of SARS-CoV-2 pathogenicity
  746. http://archive.is/9oX2Q
  747.  
  748. Netherlands: "thousands will have permanent lung damage"
  749. http://archive.is/9l46z
  750.  
  751. SARS2 Patient Gets Double Lung Transplant, Offering Hope for Others
  752. http://archive.is/0hgzL
  753.  
  754. SARS2‑associated invasive pulmonary aspergillosis (fungal infection in the lungs)
  755. http://archive.is/zT5JF
  756. https://www.atsjournals.org/doi/pdf/10.1164/rccm.202004-1038LE
  757.  
  758. Coronavirus patient puzzles New York doctors with rare symptoms
  759. >patient’s lungs indicated a fungal invasion
  760. >He developed a cytokine storm within a few hours of the disease’s onset, something that rarely happens so quickly
  761. http://archive.is/LF4oe
  762.  
  763. >Most who "recovered" haven't actually recovered
  764. >researchers found mild to significant lung abnormalities on the chest computed tomography (CT) images of 94 percent of patients with coronavirus upon discharge from the hospital, suggesting follow-up monitoring of patients might be necessary.
  765. itnonline.com/content/study-looks-ct-findings-covid-19-through-recovery
  766.  
  767. 14-Apr: Corona "ravages" lungs and affects brain
  768. https://archive.is/hypQs
  769.  
  770. 21-Mar: Lungs of young patients filled with blood
  771. https://archive.is/5hhjk
  772.  
  773. 24-Feb: Virus manifests as lung abnormalities
  774. https://archive.is/Nr8N7
  775. https://doi.org/10.1016/S1473-3099(20)30086-4
  776.  
  777. 22-Apr: Several "mild cases" actually suffered permanent lung damage
  778. https://archive.is/1eHDS
  779.  
  780. 17-Mar: Most "asymptomatic" cases actually have glassed lungs
  781. https://archive.is/SBCKv
  782. https://doi.org/10.1148/ryct.2020200110
  783.  
  784. 15-Mar: Survivors can be left with lung damage for 15 years
  785. https://archive.is/L0qJ3
  786.  
  787. 13-Mar: Survivors might suffer from reduced lung function
  788. https://archive.is/k3rYV
  789.  
  790. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis from coronavirus
  791. >In lungs from patients with Covid-19, the amount of new vessel growth — predominantly through a mechanism of intussusceptive angiogenesis — was 2.7 times as high as that in the lungs from patients with influenza (P<0.001).
  792. CONCLUSIONS
  793. >In our small series, vascular angiogenesis distinguished the pulmonary pathobiology of Covid-19 from that of equally severe influenza virus infection. The universality and clinical implications of our observations require further research to define.
  794. https://www.nejm.org/doi/full/10.1056/NEJMoa2015432
  795.  
  796. SARS-Cov2 enables anaerobic bacteria (Prevotella, et al) to colonize the lungs disrupting homeostasis - symptoms (ARDS, septic shock, blood clots,arterial stroke)
  797. https://www.docdroid.net/tnA9ZfW/sars-cov2enables-anaerobic-bacteria-prevotella-et-al-pdf
  798.  
  799. https://www.medrxiv.org/content/10.1101/2020.03.29.20041962v2
  800. Highly pathogenic coronavirus N protein aggravates lung injury by MASP-2-mediated complement over-activation
  801.  
  802. Coronavirus may lurk deep in lungs after patients recover, study suggests
  803. http://archive.is/AoZZJ
  804.  
  805. >SARS-Cov2 enables anaerobic bacteria (Prevotella, et al) to colonize the lungs disrupting homeostasis - symptoms (ARDS, septic shock, blood clots, arterial stroke) finds resonance, with key differences, in the ‘forgotten disease’ Lemierre Syndrome
  806. osf.io/usztn/
  807. >for the first time, SARS-CoV-2 invasion of the placenta, highlighting the potential for severe morbidity among pregnant women with coronavirus.
  808. medrxiv.org/content/10.1101/2020.04.30.20083907v1
  809.  
  810.  
  811.  
  812.  
  813.  
  814.  
  815. ******* 12. Brain and the nervous system **************************
  816. >brain and the nervous system
  817.  
  818. Nervous System Involvement in SARS-2: Results from a Retrospective Consecutive Neuroimaging Cohort
  819. >Results 185 patients with COVID-19 (62±14 years, 138 men) underwent neuroimaging. In total, 222 brain CT, 47 brain MRI and 7 spinal MRI scans were performed. Intra-axial susceptibility abnormalities were the most common finding (29 of 39 [74%, 95%-CI 58-87%]) in patients with brain MRI, often with an ovoid shape suggestive of microvascular pathology, and with a predilection to corpus callosum (23 of 39, [59%, 95%-CI 42-74%]) and juxtacortical areas (14 of 39, [36%, 95% CI 21-53%]). Ischemic and macrohemorrhagic manifestations were also seen, but vascular imaging did not reveal overt abnormalities. Dynamic susceptibility contrast perfusion MRI in 19 patients did not reveal consistent asymmetries between hemispheres or regions. Many patients (18 of 41 [44%, 95%-CI 28-60%]) had leukoencephalopathy and one patient had a cytotoxic lesion of the corpus callosum. Other findings included olfactory bulb signal abnormalities (7 of 37, 19%), prominent optic nerve subarachnoid spaces (20 of 36, 56%), and enhancement of the parenchyma (3 of 20, 15%), leptomeninges (3 of 20, 15%), cranial nerves (2 of 20, 10%), and spinal nerves (2 of 4, 50%)
  820. https://pubmed.ncbi.nlm.nih.gov/32729812/
  821.  
  822. StratNeuro seminar series: neurological symptoms of SARS-2 compilation
  823. https://news.ki.se/stratneuro-seminar-series-neurological-symptoms-of-covid-19
  824.  
  825. Risk of stroke in hospitalized SARS-CoV-2 infected patients: A multinational study
  826. >A total of 17,799 patients were included in meta-analyses. Among them, 156(0.9%) patients had a stroke—123(79%) ischaemic stroke, 27(17%) intracerebral/subarachnoid hemorrhage, and 6(4%) cerebral sinus thrombosis
  827. >Among the 156 stroke patients, 123 (79%) presented with acute ischaemic stroke, 27 (17%) with intracerebral/subarachnoid hemorrhage, and 6 (4%) with cerebral venous or sinus thrombosis (Table 2). We observed mean age of 68.6 (13.9) years among patients with ischaemic stroke, 62.5 (15.3) years in patients with intracranial hemorrhage, and 50.3 (12.9) in patients with cerebral venous thrombosis. Overall, 43 (27.6%) of the stroke patients presented to the medical centres with stroke-related symptoms as the chief complaint, without the prior diagnosis of SAR-CoV-2 infection.
  828. >results of this multi-national study on hospitalized patients with SARS-CoV-2 infection indicated an overall stroke risk of 0.5% (pooled risk: 0.9%)
  829. https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(20)30315-7/fulltext
  830.  
  831.  
  832.  
  833.  
  834. > SARS-CoV-2 could also enter the brain through the median eminence of the hypothalamus and other circumventricular organs, brain regions with a leaky BBB due to openings (fenestrae) in the capillary wall
  835. >The hypothalamus: target and culprit of immune dysregulation: The brain, the hypothalamus in particular, could also contribute to the immune dysregulation (Figure 3). Several cytokines upregulated in COVID-19 (IL-6, IL-1β, TNF) are powerful activators of the hypothalamic‐pituitary‐adrenocortical (HPA) axis
  836. >The mechanisms of these effects involve activation of the HPA, leading to the release of norepinephrine and glucocorticoids. These mediators act synergistically to induce splenic atrophy, T cell apoptosis, and NK cell deficiency. In the bone marrow, tyrosine hydroxylase and norepinephrine trigger a response in mesenchymal stromal cells, most likely through β3-adrenergic receptors, resulting in a reduction of cell retention (Iadecola et al., 2020). Downregulation of these factors, in concert with calprotectin release from damaged lungs, may increases hematopoietic stem cell proliferation skewed towards the myeloid lineage (emergency myelopoiesis) (Schulte-Schrepping et al., 2020; Silvin et al., 2020), which results in lymphopenia and neutrophilia, two key hematological features of COVID-19
  837. > SARS-CoV-2 unleashes a dysregulated systemic immune response (see Systemic inflammation and immune dysregulation), which can have delayed effects on the nervous system. These immune-mediated manifestations involve both the central and peripheral nervous system and occur typically after the acute phase of the infection subsides. In the CNS, reported cases in COVID-19 resemble classic post-infectiousi nflammatory conditions such as acute disseminated encephalomyelitis (Parsons et al., 2020) and acute necrotizing hemorrhagic encephalopathy (Poyiadji et al., 2020). Peripherally, several cases of Guillain-Barre syndrome, a neuropathy caused by an immune attack on peripheral nerves, have been reported in patients with recent COVID-19 (Toscano et al., 2020). Most reported cases describe classic features of this syndrome, such as generalized weakness, evidence of demyelination on nerve conduction studies and elevated proteins without white blood cells in CSF (Toscano et al., 2020). The Miller-Fisher variant of Guillain-Barre syndrome, characterized by cranial nerve involvement, has also been reported, including at least one case with detectable anti-ganglioside antibodies suggesting an immune attack on the peripheral nerves (Gutierrez-Ortiz et al., 2020). SARS-CoV-2 was not detected in any of the CSF samples (Toscano et al., 2020), supporting an immune mechanism rather than direct infection.
  838. > Emerging data seem to confirm this observation: in one multicenter study, patients with COVID-19 and acute respiratory distress syndrome had twice the incidence of thrombotic complications compared to a matched cohort with ARDS from other causes (Helms et al., 2020b). This also applies to thrombotic complications affecting the brain, since the proportion of COVID-19 related hospitalizations complicated by stroke seems much higher than that seen in influenza
  839. >In conclusion, the neurological manifestations of COVID-19 constitute a major public health challenge not only for the acute effects on the brain, but also for the long-term harm to brain health that may ensue.
  840. >These delayed manifestations are anticipated to be significant since they are likely to also affect patients who did not show neurological symptoms in the acute phase.
  841. https://www.sciencedirect.com/science/article/pii/S0092867420310709
  842.  
  843. SARS-2 can trigger myasthenia gravis, a neuromuscular disease
  844. http://archive.is/bEZdW
  845.  
  846. The S1 protein of SARS-CoV-2 crosses the blood-brain barrier in mice
  847. >radioiodinated S1 (I-S1) readily crossed the murine blood-brain barrier (BBB)
  848. >I-S1 from two commercial sources crossed the BBB with unidirectional influx constants of 0.287 +/- 0.024 microL/g-min and 0.294 +/- 0.032 microL/g-min and was also taken up by lung, spleen, kidney, and liver
  849. >I-S1 was uniformly taken up by all regions of the brain and inflammation induced by lipopolysaccharide reduced uptake in the hippocampus and olfactory bulb
  850. >I-S1 crossed the BBB completely to enter the parenchymal brain space, with smaller amounts retained by brain endothelial cells and the luminal surface
  851. >Studies on the mechanisms of transport indicated that I-S1 crosses the BBB by the mechanism of adsorptive transcytosis and that the murine ACE2 receptor is involved in brain and lung uptake, but not that by kidney, liver, or spleen
  852. >I-S1 entered brain after intranasal administration at about 1/10th the amount found after intravenous administration and about 0.66% of the intranasal dose entered blood
  853. >ApoE isoform or sex did not affect whole brain uptake, but had variable effects on olfactory bulb, liver, spleen, and kidney uptakes
  854. http://archive.is/yejLn
  855. https://www.biorxiv.org/content/10.1101/2020.07.15.205229v1.full.pdf
  856.  
  857. Neurological manifestations of SARS2 in children
  858. >Findings In a case series of 4 children with COVID-19 and neurological symptoms, all 4 patients had signal changes in the splenium of the corpus callosum on neuroimaging and required intensive care admission for the treatment of COVID-19 pediatric multisystem inflammatory syndrome.
  859. >Meaning Children with COVID-19 may present with new neurological symptoms involving both the central and peripheral nervous system and splenial changes on imaging, in the absence of respiratory symptoms; this diagnosis should be considered within the differential diagnosis of splenial lesions.
  860. http://archive.is/xAAnb
  861.  
  862. Central nervous system manifestations of COVID-19: A systematic review
  863. >Neuroinvasion of SARS-CoV2 may partially explain why some patients develop respiratory failure.
  864. >While neurological manifestations of COVID-19 have not been studied appropriately yet, it is highly likely that some of these patients, particularly those who suffer from a severe illness, have CNS involvement and neurological manifestations. Precise and targeted documentation of the neurological symptoms (e.g., headache, dizziness, etc.) and signs (e.g., change in mental status, meningeal signs, etc.), detailed clinical, neurological, and electrophysiological investigations (e.g., EEG) of the patients (particularly those with a change in mental status), attempts to isolate SARS-CoV-2 from CSF, and autopsies of the COVID-19 victims may clarify the roles played by this virus in causing neurological manifestations.
  865. http://archive.is/G2zeQ
  866.  
  867. The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in vitro models of the human blood–brain barrier
  868. >Key to our findings is the demonstration that S1 promotes loss of barrier integrity in an advanced 3D microfluid model of the human BBB, a platform that most closely resembles the human physiological conditions at this CNS interface. Subsequent analysis also showed the ability for SARS-CoV-2 spike proteins to trigger a pro-inflammatory response on brain endothelial cells that may contribute to an altered state of BBB function. Together, these results are the first to show the direct impact that the SARS-CoV-2 spike protein could have on brain endothelial cells; thereby offering a plausible explanation for the neurological consequences seen in COVID-19 patients.
  869. http://archive.is/SboeP
  870.  
  871. 'Silent' neurological damage: May lead to future health problems
  872. >3 stages of neurological deficits caused by coronavirus.
  873. >Damage to the epithelial cells of the nose and mouth begins.
  874. >1st stage:Temporary loss of smell and taste.
  875. >2nd: Inflammation caused by a cytokine storm begins in lungs. Can spread to other organs and cause blood clots, leading to stroke
  876. >3rd: Inflammation damages a protective layer in the blood vessels of the brain, allowing blood content, and virus particles to invade the brain.
  877. >Doctors suggest MRI brain scans and follow ups with these patients
  878. >Patients with severe inflammation develop seizures, confusion, coma or encephalopathy which alters the function/structure of the brain. This increases risk of Parkinson's disease/Alzheimer's/Multiple sclerosis
  879. >Fotuhi says patients who COVID caused gave brain impairments in should be monitored for cognitive decline, attention deficit, brain fog or Alzheimer's disease
  880. >A French study found 84% of ICU patients with COVID had positive abnormalities on their neurological exams. 15% of patients who leave the ICU have residual neurological deficits, including poor attention and difficulties with decision-making and behavior control
  881. >Anywhere from 1/3 to 59% of hospitalized COVID-19 patients will experience confusion, dizziness, headaches, mini strokes and paralysis
  882. >Mini strokes may lead to a slowness in thinking
  883. Strokes in the young
  884. >"Patients in their 30s are having massive strokes more commonly seen in 80 year olds
  885. >2 unusual findings: Massive strokes in both hemispheres of the brain;also in both arteries and veins
  886. >Mortality rate of stroke patients with COVID: 42%-higher than the typical 10% rate
  887. >Coronavirus may enter cells by attaching to a protein abundant in cells that line the bodies blood vessels, heart/kidney/lungs.
  888. >Also, virus could be affecting cells' ability to control brain blood-flow. Also possibility: inflammation of blood vessels causes mini blood clots in the vessels.
  889. archive.is/PitHD
  890.  
  891.  
  892. Reactivation/neurodamage of SARS2 mirrors Nipah virus
  893. http://archive.is/p6nOm
  894.  
  895. Longterm neurological consequences of SARS2
  896. http://archive.is/6cwbT
  897.  
  898. Review: neuropsychiatric aspects of SARS2
  899. http://archive.is/2wBXi
  900.  
  901. SARS2 is "neurotoxin-like"
  902. >We recently reported that many of the clinical manifestations of severe COVID-19 could be explained by dysregulation of the NCS. In this study, we present an amino acid sequence in the receptor binding domain of the SARS-CoV-2 Spike glycoprotein which is homologous to a sequence of a snake venom toxin.
  903. http://archive.is/QKJc8
  904.  
  905. Axonal damage in olfactory structures of the CNS
  906. http://archive.is/3ROVq
  907.  
  908. Altered mental status and strokes are the most common neurological symptoms in SARS2 patients
  909. http://archive.is/uojaw
  910.  
  911. Olfactory transmucosal SARS-CoV-2 invasion as port of Central Nervous System entry in SARS2 patients
  912. >Subsequently, SARS-CoV-2 follows defined neuroanatomical structures, penetrating defined neuroanatomical areas, including the primary respiratory and cardiovascular control center in the medulla oblongata.
  913. http://archive.is/wP4o6
  914.  
  915. SARS2 can directly attack neurons
  916. >This study provides direct evidence that SARS human coronavirus is capable of infecting the central nervous system, and that Mig might be involved in the brain immunopathology of SARS.
  917. https://academic.oup.com/cid/article/41/8/1089/377612
  918.  
  919. >Of 725 consecutive hospitalized patients with COVID-19, 108 (15%) had acute neurological symptoms requiring neuroimaging
  920. https://pubs.rsna.org/doi/10.1148/radiol.2020201933
  921.  
  922. https://www.biorxiv.org/content/10.1101/2020.05.20.106575v1
  923. >SARS-CoV-2 targets cortical neurons of 3D human brain organoids and shows neurodegeneration-like effects
  924.  
  925. Unusual behavior
  926. >Serious impairments of the brain
  927. >Loss of ability to speak
  928. >Abnormal swelling and inflammation in the brain found.
  929. >Patients staring into space.
  930. https://www.nytimes.com/2020/04/01/health/coronavirus-stroke-seizures-confusion
  931.  
  932. Coronavirus broadly neuroinfectious
  933. http://archive.is/CIAyJ
  934.  
  935. Coronavirus: Neuropsychiatric symptoms and potential immunologic mechanisms
  936. http://archive.vn/OWIPo
  937.  
  938. Psychiatric and neuropsychiatric presentations associated with severe coronavirus infections: a systematic review and meta-analysis with comparison to the coronavirus pandemic
  939. https://www.thelancet.com/pdfs/journals/lanpsy/PIIS2215-0366(20)30203-0.pdf
  940.  
  941. Coronavirus infects the brain. Can lead to:
  942. >Acute Encephalopathy
  943. >Seizures / Status Epilepticus
  944. >Acute Hemorrhagic Necrotizing Encephalopathy
  945. >Ischemic Stroke / Intra Cerebral Hemorrhage / Cerebral Venous Sinus Thrombosis
  946. >Encephalitis
  947. >Demyelinating lesions
  948. >Guillain-Barré Syndrome / Miller Fisher Syndrome
  949. >Posterior Reversible Encephalopathy Syndrome
  950. >Subjective neurological symptoms
  951. https://ictalgroup.org/2020/04/08/spectrum-of-neurological-manifestations-associated-with-sars-cov-2-infections/
  952.  
  953. Ischemic brain damage in SARS2 patients
  954. http://archive.is/UALgD
  955.  
  956. >Coronavirus is attacking the TAU axon so that little fibrous connection between the soma is getting disrupted.
  957. >induces of neuronal death
  958. https://www.biorxiv.org/content/10.1101/2020.05.20.106575v1.full.pdf
  959.  
  960. Brainstem involvement in fatal SARS2 cases
  961. http://archive.is/Q46iL
  962.  
  963. Neuropilin-1 facilitates SARS-CoV-2 cell entry and provides a possible pathway into the central nervous system
  964. >SARS-CoV-2 infected NRP1-positive cells in the olfactory epithelium and bulb. In the olfactory bulb infection was detected particularly within NRP1 positive endothelial cells of small capillaries and medium-sized vessels.
  965. >Studies in mice demonstrated, after intranasal application, NRP1-mediated transport of virus-sized particles into the central nervous system.
  966. >Thus, NRP1 could explain the enhanced tropism and spreading of SARS-CoV-2
  967. https://www.biorxiv.org/content/10.1101/2020.06.07.137802v1.full.pdf
  968.  
  969. SARS brain damage can be categorized using a new 3-stage 'NeuroCovid' framework
  970. >Evidence of SARS2’s dangerous impact on the central nervous system continues to mount, and one neurological expert is proposing a new system that classifies such brain damage into three distinct stages. “We are learning that a significant number of hospitalized SARS2 patients have various degrees of brain impairment,” Fotuhi, who is also the medical director of NeuroGrow Brain Fitness Center in Virginia, added in a statement.
  971. >More than two dozen case reports cited in the analysis detail neurological symptoms in patients infected with the novel virus, including stroke, seizures, confusion, dizziness, paralysis, and coma. One study of more than 700 patients, published early last month in Radiology, found that 59% of patients experienced an altered mental state, 31% suffered a stroke, and a separate 15% had serious neurological symptoms requiring brain or spine imaging.
  972. >NeuroCovid Stage I: Virus damage is contained to epithelial cells in the nose and mouth, and primary symptoms include loss of smell and taste.
  973. >NeuroCovid Stage II: Inflammation begins to flood the body, beginning in the lungs and moving through the blood vessels toward all the patient’s organs. This “cytokine storm” causes blood clots which can result in small or large strokes.
  974. >NeuroCovid Stage III: The cytokine storm damages the blood-brain barrier, allowing virus particles to infiltrate the brain leading to seizures confusion, coma, or encephalopathy.
  975. “Our experience with previous forms of coronaviruses suggests that in the long-term patients may develop depression, insomnia, Parkinson’s disease, memory loss, or accelerated aging in the brain,” Fotuhi added.
  976. http://archive.is/SSgIe
  977.  
  978. One autopsy study found particles of the SARS-CoV-2 virus in the neurons of a specimen of frontal lobe, Spudich and her colleagues report in their review. “Neurons were found to have viral particles packed in dilated vesicles” and, once the virus gets into neuronal tissue “it could begin a cycle of viral budding,” inflicting further damage to neurons.
  979. http://archive.is/bgASn
  980.  
  981. Brain scans of a 25-year-old patient with Covid-19 have shown how a "viral brain invasion" appears to have temporarily changed areas of her brain.
  982. >Published in JAMA Neurology, doctors describe what they say is the first evidence to show in vivo brain alteration due to the SARS-CoV-2 virus, and that it demonstrates that anosmia – loss of smell – can present as the dominant symptom of Covid-19.
  983. >The authors describe the case of an Italian female radiographer who started experiencing symptoms of the virus after working in a Covid-19 ward.
  984. >Her case was relatively mild and no fever was present, but a Magnetic Resonance Imaging (MRI) scan revealed inflammation in her olfactory bulb, the neural structure of the brain involved in olfaction (the sense of smell), which was "suggestive of a viral infection".
  985. >"To our knowledge, this is the first report of in vivo human brain involvement in a patient with COVID-19 showing a signal alteration compatible with viral brain invasion in a cortical region [...] that is associated with olfaction,"
  986. >"Based on the MRI findings, including the slight olfactory bulb changes, we can speculate that SARS-CoV-2 might invade the brain through the olfactory pathway and cause an olfactory dysfunction of sensorineural origin," though they stress the need for further testing to confirm.
  987. >“We know from previous research that some individuals who have had SARS-CoV-2 infection may develop neurological and psychiatric symptoms,"
  988. >"What remains to be seen is to what extent symptoms are due to viral infection of the brain itself, or secondary effects including inflammation in the brain triggered by the immune system’s response to the virus, and in others stroke due to blood becoming more likely to clot for example."
  989. archive.is/pTZuJ
  990.  
  991. The way the coronavirus messes with smell hints at how it affects the brain
  992. >But so far, details remain elusive about how SARS-CoV-2, the coronavirus that causes COVID-19, can infiltrate and shut down the body’s smelling machinery. One recent hint comes from a young radiographer who lost her sense of smell. She had signs of viral infection in her brain.
  993. >No one knows whether SARS-CoV-2 can infect nerve cells in the brain directly, and if so, whether the virus’s route to the brain can sometimes start in the nose.
  994. >“There’s something unusual about the relationship between COVID-19 and smell,” says neuroscientist Sandeep Robert Datta. Colds can prevent smelling by stuffing the nose up with mucus. But SARS-CoV-2 generally leaves the nose clear.
  995. >Recent studies have begun to identify the cells in the olfactory epithelium, a slender sheet of tissue that lines part of the nasal cavity, that seem vulnerable to SARS-CoV-2 infection. Smell-supporting cells called sustentacular cells are likely targets, scientists report in two new papers
  996. >“Obviously we don’t know for sure, but at this point, it appears that the smell losses associated with SARS-CoV-2 are probably due to its impact on the supporting cells, the non-neuronal cells, in the olfactory epithelium,”
  997. >If SARS-CoV-2 doesn’t target olfactory receptor neurons directly, that could be good news. That’s because, as far as neurons go, olfactory receptor neurons are unusual — they live outside of the brain, but keep one foot inside it. This precarious straddle renders them — and the brain itself — vulnerable to infections. Other pathogens, including a different coronavirus and a brain-eating amoeba (SN: 7/20/15), can use these neurons, and their message-sending axons that reach the brain, as conduits to the brain. “The big open question is whether or not the SARS-CoV-2 virus can move along olfactory neuronal axons to the brain,”
  998. archive.is/nt1aW
  999.  
  1000. Coronavirus can infect the brain and replicate, new study claims
  1001. >The coronavirus is capable of infecting the brain and then replicating within the cells — with virus levels increasing tenfold within three days, a new study has found.
  1002. >The new research, which is under peer review at the journal Altex but not yet published, looked at potential neurological effects of the illness by injecting the virus into lab-grown brains, which are developed from human stem cells
  1003. >“It is really critical to know that our most precious organ can be directly affected by the virus”
  1004. >Hartung and his team discovered once the virus entered neurons in the artificial brains, it made copies of itself, the report said. The levels of the virus were found to increase 10 times in just three days.
  1005. >But the research was unable to prove whether the virus can get past the blood-brain barrier of the brain that protects the organ against many viruses and chemicals, as well as often prevents infections.
  1006. >Though the lab-grown brains share many features with real ones, they lack the blood-brain barrier, according to the report.
  1007. >“Whether or not the Sars-Cov-2 virus passes this barrier has yet to be shown, but it is known that severe inflammations, such as observed in Covid-19 patients, make the barrier disintegrate,” Hartung told the newspaper.
  1008. >More research into the neurological impacts of the virus could have important implications for treating patients, the report said.
  1009. >If the virus does infect the brain, certain medications would not be effective since some cannot get past the blood-barrier, according to the report.
  1010. archive.is/iya1x
  1011.  
  1012.  
  1013.  
  1014. ******* 13. Cardiovascular system
  1015. Coronavirus May Be a Blood Vessel Disease, Which Explains Everything
  1016. archive.is/jwj8w
  1017.  
  1018. SARS-CoV-2: the vasculature unleashed
  1019. http://archive.is/mPNwP
  1020. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7240244/pdf/41577_2020_Article_343.pdf
  1021.  
  1022. SARS-CoV-2 (as a blood disease): hemoglobin, iron, and hypoxia beyond inflammation
  1023. >Scientific literature has pointed out two potential pathophysiological mechanisms:
  1024. >i) severe acute respiratory syndrome-coronavirus-2 (SARS-CoV- 2) interaction with hemoglobin molecule, through CD147, CD26 and other receptors located on erythrocyte and/or blood cell precursors;
  1025. >ii) hepcidin-mimetic action of a viral spike protein, inducing ferroportin blockage. In this translational medicinebased narrative review, the following pathologic metabolic pathways, deriving from hemoglobin denaturation and iron metabolism dysregulation, are highlighted:
  1026. >i) decrease of functioning hemoglobin quote;
  1027. >ii) iron overload in cell/tissue (hyperferritinemia);
  1028. >iii) release of free toxic circulating heme;
  1029. >iv) hypoxemia and systemic hypoxia;
  1030. >v) reduction of nitric oxide;
  1031. >vi) coagulation activation; vii) ferroptosis with oxidative stress and lipoperoxidation;
  1032. >viii) mitochondrial degeneration and apoptosis.
  1033. >A few clinical syndromes may follow, such as pulmonary edema based on arterial vasoconstriction and altered alveolo-capillary barrier, sideroblastic-like anemia, endotheliitis, vasospastic acrosyndrome, and arterio- venous thromboembolism. We speculated that in COVID-19, beyond the classical pulmonary immune-inflammation view, the occurrence of an oxygen-deprived blood disease, with iron metabolism dysregulation, should be taken in consideration.
  1034. http://archive.is/MowCB
  1035. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7267810/pdf/cp-10-1-1271.pdf
  1036.  
  1037. Chilblain-like lesions likely associated with COVID-19: a Canadian case presentation
  1038. >Physical examination was notable for several violaceous nodules bilaterally on the dorsal aspect of the toes with associated dusky discolouration of the toes. The lesions were tender to palpation
  1039. http://archive.is/Bp8Aw
  1040. https://www.cambridge.org/core/services/aop-cambridge-core/content/view/371460DD28788768539AE46D17B5AEFD/S1481803520004236a.pdf/chilblainlike_lesions_likely_associated_with_covid19_a_canadian_case_presentation.pdf
  1041.  
  1042. A case report: SARS2 transmission and blood transfusion
  1043. >a 21-year-old man with very severe aplastic anaemia who received apheresis platelet transfusion from an individual who was subsequently diagnosed with COVID-19. Our patient tested negative for COVID-19 and is awaiting allogeneic stem cell transplantation
  1044. http://archive.is/2aaxH
  1045.  
  1046. SARS2, like SARS1, is believed to be a form of viremia in humans. Although we have no existing data on the case in animals, it is certainly possible that the virus can also be housed within their bloodstreams like humans
  1047. http://archive.is/lylIy
  1048. http://archive.is/jaiCO
  1049.  
  1050. >SARS-CoV-2 Attacks Hemoglobin In Red Blood Cells, Rendering It Incapable Of Transporting Oxygen
  1051. >The research discovered that some of these proteins are to hijack the red blod cells and remove the Iron ions from the heme groups (HBB) and replace themselves with it. This makes the hemoglobin unable to transport oxygen.
  1052. http://archive.is/3hx2C
  1053.  
  1054. http://archive.is/lXGfS
  1055. In platelet-deficient plasma, 5HTA acts in a manner similar to platelet factor 2 in accelerating the conversion of fibrinogen to fibrin.
  1056. Fibrinogen > fibrin is what causes coagulation
  1057. >http://archive.is/mgpke
  1058. Hematological changes are common in patients with SARS2, which include reduced lymphocyte count and platelet count but normal white blood cell count.
  1059. >http://archive.is/1npDg
  1060. Total leukocytes were increased and lymphocytes decreased.
  1061.  
  1062. >NYC Boy Had No Underlying Conditions — 5 Days Later, He Was on a Ventilator After Cardiac Arrest
  1063. nbcnewyork.com/news/local/nyc-boy-had-no-underlying-conditions-5-days-later-he-was-on-a-ventilator-after-cardiac-arrest/2402127/?amp
  1064.  
  1065.  
  1066.  
  1067. ******* 14. Kidneys
  1068.  
  1069. The coronavirus is damaging kidneys. Doctors worry that some survivors will need dialysis forever
  1070. >Two studies of New York patients found that 68% to 76% of intensive care patients with COVID-19 had kidney damage. In one, a third of ICU patients needed dialysis, a process in which a machine performs the kidney’s blood-filtering work
  1071. >Doctors said the kidneys suffer along with the rest of the body. “The kidney is kind of an innocent bystander sometimes,” Boyle said. “If the rest of the body isn’t doing well, the kidney feels it too.”
  1072. >Whether the coronavirus directly attacks kidney cells is controversial. Some studies find no sign of the virus in kidney tissue, but a recent Lancet study found viral RNA in 60% of 63 autopsy samples and in 72% of samples from patients with acute kidney injury.
  1073. >Another possibility, Negoianu said, is that blood clotting caused by COVID-19 damages kidneys.
  1074. https://archive.is/jZGAO
  1075.  
  1076. Outcomes for Patients With SARS-2 and Acute Kidney Injury: A Systematic Review and Meta-Analysis
  1077. https://www.kireports.org/article/S2468-0249(20)31336-X/fulltext#%20
  1078.  
  1079. >Kidney function on admission predicts in-hospital mortality in COVID-19
  1080. > Results Baseline eGFR was under 60 mL/min/1.73m2 in 61 patients (18.2%). Acute kidney injury occurred in 29.1% of the patients. In-hospital mortality was calculated as 12.8%
  1081. >mean age 55.0 ±15.9
  1082. http://archive.is/qV9Yk
  1083.  
  1084. SARS2 is indicated to aggravate preexisting non-respiratory conditions based on a kidney study
  1085. >renal tropism is a potential explanation of commonly reported new clinical signs of kidney injury in patients with Covid-19,5 even in patients with SARS-CoV-2 infection who are not critically ill.
  1086. >Our results indicate that SARS-CoV-2 has an organotropism beyond the respiratory tract, including the kidneys, liver, heart, and brain, and we speculate that organotropism influences the course of Covid-19 disease and, possibly, aggravates preexisting conditions.
  1087. http://archive.is/HLzvR
  1088.  
  1089. >SARS-CoV-2 has a receptor binding domain specifically designed for the human angiotensin converting enzyme-2 receptor (ACE2) found in lungs, kidneys, intestines and blood vessels
  1090. >SARS-CoV-2 has a furin polybasic cleavage site not found in any closely-related bat coronaviruses as well as other artificially inserted charged amino acids that enhance the virus’ ability to bind to and enter human cells by forming “salt bridges” between the virus and the cell surface
  1091. >he SARS2 pandemic is revealing neurological, haematological and immunological pathogenicity, which cannot be explained by infectivity via the ACE2 receptor alone
  1092. >SARS-CoV-2 binding to the bitter/sweet receptors in the upper respiratory tract provides a perfect location for transmission by coughing
  1093. >oral and upper respiratory infection can lead to transmission to the lower respiratory tract, gastrointestinal effects and a cascade of inflammation-producing immunological responses
  1094. http://archive.li/NUN4Y
  1095. >These data reveal the biological structure of SARS-CoV-2 Spike and confirm that accumulated charge from inserts
  1096. and salt bridges are in surface positions capable of binding with cell membrane components other than the ACE2
  1097. receptor
  1098. >Analysis of the Spike protein of SARS-CoV-2 shows 78.4% similarity with human-like (HL) epitopes
  1099. >antibodies can only recognize 5-6 amino acids and therefore a 6 amino acid rolling window search for
  1100. antibody epitopes was performed. A search so tailored to match against all human known proteins will give a 78.4%
  1101. human similarity to the SARS-CoV-2 Spike protein, i.e if all epitopes on the 1255 amino acid long SARS-CoV-2 Spike
  1102. protein can be used by antibodies then there will be 983 antibody binding sites which also could bind to epitopes on
  1103. human proteins
  1104. https://www.cambridge.org/core/services/aop-cambridge-core/content/view/DBBC0FA6E3763B0067CAAD8F3363E527/S2633289220000083a.pdf/biovacc19_a_candidate_vaccine_for_covid19_sarscov2_developed_from_analysis_of_its_general_method_of_action_for_infectivity.pdf
  1105.  
  1106.  
  1107. An online survey of 151 medical professionals who fell ill in March found 68 are still unable to work. A further 26 went back, only to stop again when symptoms returned.
  1108. >It appears coronavirus may be a chronic condition. How long it persists for is unknown. The symptoms can be serious and wide-ranging, affecting the lungs, heart, brain, kidneys, stomach and nervous system. Headaches, shortness of breath, sore throat and feeling exhausted are common. So is recovery followed by frequent relapses.
  1109. >“We don’t know what is causing prolonged SARS2. Is it the ongoing initial illness, or is it an inflammatory reaction or is it a post-viral syndrome? We don’t know what the prognosis is or what the long-term consequences are. I wonder how many people are having prolonged illness and what the impact is on the workforce, for example. It’s scary to have an illness for which there isn’t any treatment and that doesn’t seem to be going away.”
  1110. http://archive.is/OyRtB
  1111.  
  1112. Dead, Recovered, and Dying
  1113. >Research: 1 in 20 SARS2 patients experience long-term on-off symptoms. It’s unclear whether long-term means 2 months, or 3 or longer. The best parallel is dengue fever.
  1114. >“These people may be going back to work and not performing at the top of their game,” Spector says. “There is a whole other side to the virus which has not had attention because of the idea that ‘if you are not dead you are fine.’”
  1115. >SARS2 is a “multi-system disease” which can potentially affect any organ. It causes microvascular problems and clots. Lungs, brain, skin, kidneys and the nervous system may be affected. Neurological symptoms can be mild (headache) or severe (confusion, delirium, coma).
  1116. http://archive.is/yG2Xx
  1117.  
  1118.  
  1119.  
  1120.  
  1121. ******* 15. SARS-CoV-2 and Male/Female Sterility/Fertility/Hormonal system
  1122.  
  1123. Italian males recovering from mild SARS-CoV-2 show no evidence of SARS-CoV-2 in semen despite prolonged nasopharyngeal swab positivity
  1124. >median age - 42
  1125. http://archive.is/t6vQg
  1126.  
  1127. Abnormal findings in testicular tissue of SARS2 patients, SARS-CoV-2 mostly undetected
  1128. >study included 12 patients, with an average age of 65 years
  1129. >Despite the lack of direct viral injury to the sperm-containing cells, the damage to the Sertoli cells and androgen-producing Leydig cells can cause the seminiferous tubules to atrophy, and eventually, cause reduced or no sperm formation in recovered SARS2 patients
  1130. http://archive.is/IBzKU
  1131.  
  1132. Potential Male Sterility
  1133. >Coronavirus can damage men's fertility by triggering changes to sperm-making cells in the testicles
  1134. >Researchers examined the testicular tissue of 2 men who died of coronavirus
  1135. >Ten of the 12 were positive for coronavirus in their lungs, but only one had virus in his testes.
  1136. >Although there were no signs of virus in the other's testes, cells involved in sperm production showed signs of damage and swelling that could impair fertility
  1137. >The most disturbing changes they found in men who were covid-positive were to the seminiferous tubules, small structures in the testes that produce and maintain sperm. Cells had 'ballooning' change, meaning they'd be come stretched and deformed.
  1138. >Although patients had normal spage while they were sick with coronavirus, the scientists are concerned that the damage to the seminiferous could lead to 'eventual reduced or even absent [sperm production] in patients who have recovered from COVID-19
  1139. >Because some cells in the testes have the same ACE2 receptors that allow the virus to attack lung cells, men have been warned not to donate sperm.
  1140. >Men who had COVID-19 also had lower counts of Leydig cells, which pump out hormones needed in sperm production.
  1141. >And inflammation was seen throughout the testes.
  1142. http://archive.is/lR8Lu
  1143.  
  1144. SARS-CoV-2 and the male reproductive system
  1145. >There is the theoretical possibility that testicular damage and subsequent infertility may result following SARS2 infection, and also the possibility of sexual transmission, as SARS-CoV-2 has been identified in the semen of infected patients
  1146. http://archive.is/ftKXB
  1147.  
  1148. SARS-CoV-2 Could Impact Male Fertility
  1149. >A first hypothesis is that the virus could enter the testicle and lead to alterations in testicular functionality.
  1150. >A second hypothesis is that the binding of the virus to the ACE2 receptor, could cause an excess of ACE2 and give rise to a typical inflammatory response.
  1151. http://archive.is/Ley3e
  1152.  
  1153. SARS-CoV-2: Testosterone and Frailty in Males
  1154. >males seem to not only be more susceptible to the infection compared to female subjects, at least in western countries, but their case fatality rate attributable to SARS‐CoV‐2 infection is also highest.
  1155. >the different hormonal milieu could have a more profound pathophysiological role in association with SARS‐CoV‐2, with endogenous testosterone leaving men more prone to develop more serious complications related to the SARS‐CoV‐2 infection.
  1156. >Another option is that SARS‐CoV‐2 infection per se causes an acute stage of male hypogonadism, the depletion of androgenic action triggering serious or an even fatal course of the disease
  1157. http://archive.is/yQ6Ix
  1158.  
  1159. Male coronavirus patients suffer from testosterone and dihydrotestosterone deficiencies
  1160. >critically ill male SARS2 patients suffer from severe testosterone and dihydrotestosterone deficiencies. Both androgens are required to mount antiviral immune responses to combat infection in males
  1161. >Out of 35,the vast majority of male SARS2 patients present low testosterone (68.6%) and low dihydrotestosterone (48.6%) levels.
  1162. >In contrast, out of 10, most female SARS2 patients have elevated testosterone levels (60%) without alterations in dihydrotestosterone levels.
  1163. >Both, female and male SARS2 patients may present elevated estradiol levels (45.7% in males and 40% in females)
  1164. http://archive.is/TUsgC
  1165. https://www.medrxiv.org/content/10.1101/2020.05.07.20073817v1.full.pdf
  1166.  
  1167. Potential influence of SARS-CoV-2/ACE2 on the female reproductive system
  1168. >2019-nCoV may infect the ovary, uterus, vagina and placenta through the ubiquitous expression of ACE2. Moreover, 2019-nCoV/ACE2 may disturb the female reproductive functions, resulting in infertility, menstrual disorder and fetal distress
  1169. http://archive.is/Zpi3L
  1170. https://watermark.silverchair.com/gaaa030.pdf
  1171.  
  1172. Placentas from coronavirus-positive pregnant women show injury
  1173. >there are increased rates of maternal vascular malperfusion features and intervillous thrombi, suggesting a common theme of abnormal maternal circulation, as well as an increased incidence of chorangiosis. These findings provide mechanistic insight into the observed epidemiologic associations between COVID-19 in pregnancy and adverse perinatal outcomes
  1174. http://archive.is/BPmbv
  1175. http://archive.is/leYDk
  1176. https://watermark.silverchair.com/aqaa089.pdf
  1177.  
  1178. >Study: Baby Was Infected With SARS2 in Womb
  1179. >Strongly suggests that Covid-19 can be transmitted in utero.
  1180. >A baby born in a Paris hospital in March to a mother with SARS2 tested positive and developed symptoms of inflammation in his brain
  1181. >Dr. De Luca said the virus appeared to have been transmitted through the placenta of the 23-year-old mother.
  1182. archive.is/3GLAK
  1183.  
  1184.  
  1185.  
  1186. ******* 16. Studies on masks
  1187.  
  1188. Aerosol Filtration Efficiency of Common Fabrics Used in Respiratory Cloth Masks
  1189. http://archive.is/bCbv5
  1190.  
  1191. Cloth and medical masks help reduce transmission of SARS‐CoV‐2
  1192. http://archive.is/7Ofi1
  1193. http://archive.is/lFzwo
  1194. http://archive.is/OqSXP
  1195.  
  1196. ******* 17. Info on testing for SARS-CoV-2 infection
  1197.  
  1198. Antibody tests for Covid-19 wrong up to half the time, CDC says
  1199. >Antibody tests used to determine if people have been infected in the past with Covid-19 might be wrong up to half the time (More than half even), the US Centers for Disease Control and Prevention said in new guidance posted on its website.
  1200. >Antibody tests, often called serologic tests, look for evidence of an immune response to infection. "Antibodies in some persons can be detected within the first week of illness onset," the CDC says.
  1201. >"They are not accurate enough to use to make important policy decisions, the CDC said.
  1202. >"Serologic test results should not be used to make decisions about grouping persons residing in or being admitted to congregate settings, such as schools
  1203. https://archive.vn/6Se4r
  1204.  
  1205. Will antibody tests for the coronavirus really change everything?
  1206. >Some commercial antibody tests have recorded specificities as low as 40% early in the infection.
  1207. https://archive.vn/mJOrA
  1208.  
  1209. Official antibody test kit manual
  1210. >Positive results may be due to past or present infection with non-SARS-CoV-2 coronavirus strains (Cold, flu, etc...)
  1211. >A negative result may occur for an individual subject indicates absence of DETECTABLE anti-COVD-19 antibodies. However, a negative test result does not preclude the possibility of exposure to or infection with COVID-19.
  1212. https://archive.vn/et9NHm
  1213.  
  1214. ******* 18. Pancreas
  1215. Pancreatic injury
  1216. https://www.jwatch.org/na51331/2020/04/17/serologic-evidence-pancreatic-injury-covid-19
  1217. https://www.sciencedirect.com/science/article/pii/S142439032030154X
  1218. https://www.sciencedirect.com/science/article/pii/S2214388220300448
  1219.  
  1220. ******* X. Other
  1221.  
  1222. D614G Strain
  1223. Individuals infected with earlier SARS-CoV-2 coronavirus strains could be defenseless against the more aggressive European strains with the D614G mutations.
  1224. >Antibodies found in blood of individuals who have fought the disease previously failed to stop the D614G strain.
  1225. >The mutant form was collected from Beijing's current outbreak
  1226. >Dr Ailong said that there is an urgent need to determine what threat this mutation poses to people who have recovered from a different form of the virus. Also worrisome is that the new strain could actually be more worse the second time round in patients who were previously infected with the milder strains and recovered
  1227. >The strain with the D614G mutation began spreading in Europe in early Feb and by May was the dominant strain around the world, presenting in 70% of sequenced samples in Europe and North America. It is now in India, Iran, Middle-East and Brazil
  1228. >12% of the newly infected in Beijing are in critical condition
  1229. >Virus was found in the mouths of imported salmon among other places.
  1230. >Dr Huang and his team selected a strain of the virus that had previously circulated China and manipulated it to create a man-made version containing the mutation
  1231. >They extracted antibodies from 41 blood samples from recovered patients and pitched them against the mutant. All failed to fight the new strain.
  1232. >San Diego report reveals D614G mutation has the potential to increase the number of spike proteins on the coronavirus and boost its ability to infect human cells by a factor of 10.
  1233. >1 of the concerns now is whether the mutated D614G strain will devastate vaccine development since the current vaccines reaching final trials are based on the Wuhan strain.D614G mutation could reduce the effectiveness of vaccines that target the virus’ spike protein
  1234. >It must be noted that here are also other strains with mutations on them being discovered, with another 2 more that might be even more potent.
  1235. archive.is/A1j7I
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