We are all interested in this new illness, COVID-19, whose nature is gradually being revealed. Will it have a prolonged recovery phase in some people, like glandular fever? If the sudden worsening at day 7 to 10 is due to a cytokine storm, would anti-TNF inhibitors administered early prevent this? Interestingly patients with inflammatory bowel disease on anti-TNF inhibitors, do better than those on other immunosuppressive treatments.(1)
What should we do about the hypercoagulable state?(2) Will COVID-19 lead to lung fibrosis in some patients, like Middle east Respiratory Syndrome, caused by another coronavirus?(3) But, beyond a few virologists, who has noticed that the spike protein of Sars-Cov-2, against which teams are competing to develop a vaccine, is highly homologous with a human HERV protein, syncytin-1.(4) What, indeed, are HERV proteins? What are HERVs?
HERVs are human endogenous retroviruses, that is to say retroviruses whose DNA, over millions of years, has become part of our DNA. All retroviruses, such as HIV, contain viral RNA which is transcribed into DNA and inserted into the host genome. Viral DNA normally leads to the production of more viral RNA, viral proteins and infective particles. In contrast HERV DNA, due to certain faults, is no longer translated into RNA and proteins. Astonishingly 8% of human DNA consists of these preserved but inactive retrovirus DNA sequences, more than is devoted to DNA coding known human proteins. HERVs have been called ’fossil viruses’. They are largely ‘selfish genetic elements’, that is to say that they are reproduced without any benefit to the host, but merely perpetuate themselves as genes.(5)
Will the COVID-19 pandemic trigger the expression of HERV proteins in some patients and lead to the emergence of new diseases as it wanes, just as occurred after the 1918 flu pandemic?
That very common disorder, schizophrenia, with a prevalence of 1% of the population, may be associated with the expression of HERVs.(13) It has been known for a long time that schizophrenia can be triggered by infection; there was a large surge in cases after the 1918 influenza pandemic.(14)
Three questions can now be asked about the remarkable homology recorded between SARS-CoV-2 spike protein and HER-W derived protein syncytin-1.(4) Firstly, is that why COVID-19 has adverse effects on pregnancy and child birth? (15) Secondly, is the protection women enjoy relative to men due to immune modulation by the expression of syncytin-1 during childbirth and placentation? If so, do nulliparous women not share that relative protection? It should be straightforward to find this out.
Finally, will the COVID-19 pandemic trigger the expression of HERV proteins in some patients and lead to the emergence of new diseases as it wanes, just as occurred after the 1918 flu pandemic? There are already suggestions that this might be the case for some neurological presentations.(16) Will somebody be measuring syncytin-1 in the CSF of these patients?
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