SARS-CoV2 (Continued)

SARS-CoV2 (Continued)  

     One of the puzzling features of this virus is that some infected people, while carrying a considerable viral load, and shedding infectious virions, nevertheless develop such trivial symptoms that they never notice they are infected. While other, of course, develop virally driven hyper-inflammation,  respiratory failure, and sometimes also kidney and heart failure.

     This variability in response is especially striking when it affects a whole nation-state. Thus the official WHO figures record that Vietnam, with a population of 97 million, has confirmed only 416 cases of COVID-19, and that none have died. (c.f. UK, population 67 million, 297,914 cases, 45,677 deaths on 24th July. )

Possible explanations for variable responses.

     The hypothesis of genetic variability in the human host, which supposes that the Vietnamese lack e.g. the ACE2 receptor site (See my SARS-CoV2 post), is more-or-less ruled out by anecdotal observations such as that of an asymptomatic carrier infecting 5 family members [1]. As also is the hypothesis of genetic variability among the circulating SARS-CoV2 strains, for the carrier would obviously infect the household with the strain she was carrying. 

     Could there be competition between two co-infecting viral strains, where one causes trivial, often negligible, symptoms but occupies all the binding sites? 

     Or could there be, in some people, residual anti-bodies at a sufficient titre from a previous infection by the same (or sufficiently similar) coronavirus?  This last seems the best hypothesis, and in the last 10 days has received some support. 

    The group of Antonio Bertoletti at the Duke-NUS Medical School in Singapore has just published in Nature [2] an online report showing that previous infection with a virus of the beta-coronavirus family can leave long-lasting and multispecific T cell immunity to the nucleocapsid structural protein (N protein, or NP, See my Coronavirus post) that can cross-react with the N protein of SARS-CoV2). This previous infection could be a harmless "common cold" member of the corona virus family, but in Singapore it was possible also to study survivors of the 2003 SARS pandemic. 

     Back in 2013 a group in Taiwan explored the antigenicity of the N protein of the mild common cold virus HCoV-OC43, and had found that the middle section was highly antigenic [3]. Well over 90% of healthy young adults contained antibodies in their serum against the N protein of this common virus. These antibodies were even found in cord-blood samples showing that newborn babies acquire some immunity against coronaviruses from their mothers. 

     We have already learnt that it is foolish to infect yourself deliberately with SARS-CoV2; you could become very ill or die. But there may be a beta-coronavirus, prevalent in Vietnam, that does protect you against COVID-19. And it may be that here in Britain a sufficiently recent 'common cold' may leave you with enough circulating antibodies to prevent or greatly limit the effect of SARS-CoV2 infection. 

References

[1]  Susan Lee,  Paula Meyler,  et al. (2020) Can J Anaesth. : 1–7. "Asymptomatic carriage and transmission of SARS-CoV-2: What do we know?". 

[2]  Le Bert N, Tan AT, Kunasegaran K, et al. (2020)  "SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls." [published online ahead of print]. Nature. 2020;10.1038/s41586-020-2550-z. doi:10.1038/s41586-020-2550-z.  

See also  Ruairi J. Mackenzie, Science Writer for Technology Networks (2020) “'Common Cold' Coronaviruses Could Help Produce Anti-SARS-CoV-2 Immune Cells." 

[3]  Fang-Ying Liang, Leng-Chieh Lin, (2013  J Virol Methods;187(2):413-20. "Immunoreactivity characterisation of the three structural regions of the human coronavirus OC43 nucleocapsid protein by Western blot: implications for the diagnosis of coronavirus infection. "