Airborne Aids

Even if it seems quite far fetched to some, at least personally and until the facts dictate otherwise, I tend to view the resulting disease COVID-19 that emanates from an infection with SARS-Cov-2 as a form of airborne acquired immunodeficiency syndrome.

See for example:

SARS-CoV-2 RNA reverse-transcribed and integrated into the human genome

Liguo Zhang, Alexsia Richards, Andrew Khalil, Emile Wogram, Haiting Ma, Richard A. Young, Rudolf Jaenisch

doi: https://doi.org/10.1101/2020.12.12.422516

Abstract

Prolonged SARS-CoV-2 RNA shedding and recurrence of PCR-positive tests have been widely reported in patients after recovery, yet these patients most commonly are non-infectious. Here we investigated the possibility that SARS-CoV-2 RNAs can be reverse-transcribed and integrated into the human genome and that transcription of the integrated sequences might account for PCR-positive tests. In support of this hypothesis, we found chimeric transcripts consisting of viral fused to cellular sequences in published data sets of SARS-CoV-2 infected cultured cells and primary cells of patients, consistent with the transcription of viral sequences integrated into the genome. To experimentally corroborate the possibility of viral retro-integration, we describe evidence that SARS-CoV-2 RNAs can be reverse transcribed in human cells by reverse transcriptase (RT) from LINE-1 elements or by HIV-1 RT, and that these DNA sequences can be integrated into the cell genome and subsequently be transcribed. Human endogenous LINE-1 expression was induced upon SARS-CoV-2 infection or by cytokine exposure in cultured cells, suggesting a molecular mechanism for SARS-CoV-2 retro-integration in patients. This novel feature of SARS-CoV-2 infection may explain why patients can continue to produce viral RNA after recovery and suggests a new aspect of RNA virus replication.

Competing Interest Statement:

The authors have declared no competing interest. https://www.biorxiv.org/content/10.1101/2020.12.12.422516v1




Yet more interesting indictators that point approximately in the same direction:

SARS-CoV-2 invades host cells via a novel route: CD147-spike protein https://www.biorxiv.org/content/10.1101/2020.03.14.988345v1

Infection of human lymphomononuclear cells by SARS-CoV-2 https://www.biorxiv.org/content/10.1101/2020.07.28.225912v1.full

The analysis of the long-term impact of SARS-CoV-2 on the cellular immune system in individuals recovering from COVID-19 reveals a profound NKT cell impairment https://www.medrxiv.org/content/10.1101/2020.08.21.20179358v1

The ORF8 Protein of SARS-CoV-2 Mediates Immune Evasion through Potently Downregulating MHC-I https://www.biorxiv.org/content/10.1101/2020.05.24.111823v1

Multi-organ impairment in low-risk individuals with long COVID https://www.medrxiv.org/content/10.1101/2020.10.14.20212555v1

Spike glycoprotein and host cell determinants of SARS-CoV-2 entry and cytopathic effects https://www.biorxiv.org/content/10.1101/2020.10.22.351569v1

Single-cell analyses reveal SARS-CoV-2 interference with intrinsic immune response in the human gut https://www.biorxiv.org/content/10.1101/2020.10.21.348854v1

An insertion unique to SARS-CoV-2 exhibits superantigenic character strengthened by recent mutations https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7263503/

Immunologically distinct responses occur in the CNS of COVID-19 patients https://www.biorxiv.org/content/10.1101/2020.09.11.293464v1


And

SARS-CoV-2 Uses CD4 to Infect T Helper Lymphocytes https://www.medrxiv.org/content/10.1101/2020.09.25.20200329v1

ORF3a mediated-incomplete autophagy facilitates SARS-CoV-2 replication https://www.biorxiv.org/content/10.1101/2020.11.12.380709v1

Anti-SARS-CoV-2 IgG from severely ill COVID-19 patients promotes macrophage hyper-inflammatory responses https://www.biorxiv.org/content/10.1101/2020.07.13.190140v1

Persistent SARS-CoV-2 presence is companied with defects in adaptive immune system in non-severe COVID-19 patients. https://www.medrxiv.org/content/10.1101/2020.03.26.20044768v1

Post Viral syndrome Covid-19 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7320866/

The neuroinvasive potential of SARS-CoV2 may play a role in the respiratory failure of COVID-19 patients https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7320866/

Cognitive deficits in people who have recovered from COVID-19 https://www.medrxiv.org/content/10.1101/2020.10.20.20215863v1

Human cardiac stromal cells exposed to SARS-CoV-2 evolve into hyper-inflammatory/pro-fibrotic phenotype and produce infective viral particles depending on the levels of ACE2 receptor expression https://www.medrxiv.org/content/10.1101/2020.11.06.20226423v1

SARS-CoV-2 D614 and G614 spike variants impair neuronal synapses and exhibit differential fusion ability https://www.biorxiv.org/content/10.1101/2020.12.03.409763v1

Clinically identifiable autoreactivity is common in severe SARS-CoV-2 Infection https://www.medrxiv.org/content/10.1101/2020.10.21.20216192v2


​Unusual Medications used for Sars-Cov-2

Glecaprevir and Maraviroc (Hiv Medications) are high-affinity inhibitors of SARS-CoV-2 main protease

https://pubmed.ncbi.nlm.nih.gov/32441299/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7268261/

Pharmacologic profiling reveals lapatinib(Breast Cancer Drug) as a novel antiviral against SARS-CoV-2 in vitro https://www.biorxiv.org/content/10.1101/2020.11.25.398859v1

Ribavirin(Hep-C Drug) shows antiviral activity against SARS-CoV-2 and downregulates the activity of TMPRSS2 and the expression of ACE2 In Vitro https://www.biorxiv.org/content/10.1101/2020.12.04.410092v1