By Joe Yasin
Published 2020-05-29
For some time I have been wondering why the effects of COVID 19 is so different amongst different people, even those of similar ages and conditions. And why, if Covid-19 is supposed to be so infectious, when some people get infected in the confined space of a cruise ship or a naval ship, they don’t ALL get infected? Are we not, according to the epidemiologists, all supposed to be a naïve population.
A related issue is why, when recently looked at, London is now estimated to have a much lower R factor (of around 0.4) than the rest of the UK (of around 0.7 to 0.8). Initially, the R factor in London was supposed to be between 0.5 and 1 – similar to what it is currently outside London. But if it is now 0.4, the R factor appears to have come down in London, while, until very recently (after this change in R), nothing much has changed in the London lockdown measures. They have not tightened, rather they have relaxed, which should increase the value of R rather than reduce it.
So WHY has the R factor come down? The conventional explanation is that the pool of people to be infected had shrunk substantially. But, everything else being the same, it would have had to shrink by 3/7, or 43% for R to fall from 0.7 to 0.4.
But this does not match HM Government’s estimates of infection data – 17% for London and 5% for the rest of the country – implying that the uninfected has only dropped from 95% in the rest of the country to 83% in London – implying the pool of uninfected has only dropped by 13% (12 percentage points), not the 43%, which would be needed to create the fall in R seen in London.
So how can the reduction in the ‘uninfected’ pool seen be reconciled with the observed reduction in R?
Work in progress at La Jolla Institute for Immunology in California may help explain this paradox in this paper https://www.sciencedirect.com/science/article/pii/S0092867420306103
Essentially, what is proposed is that a large proportion of the ‘uninfected’ pool may not be uninfected at all. They may actually be resistant or even immune to COVID 19 because they have previously been infected by a different, but related virus – a relatively harmless variant of the common cold – that gives some protection through cross-reactive T-cells against COVID 19. In effect, a large proportion of the population may have been protected by a natural vaccine!
This effect has been observed in the context of the 2009 H1N1 influenza pandemic. The La Jolla paper states “The presence of cross-reactive T cells was found to correlate with less severe disease (Sridhar et al., 2013; Wilkinson et al., 2012). The frequent availability of cross-reactive memory T cell responses might have been one factor contributing to the lesser severity of the H1N1 flu pandemic (Hancock et al., 2009). Cross-reactive immunity to influenza strains has been modelled to be a critical influencer of susceptibility to newly emerging, potentially pandemic, influenza strains (Gostic et al., 2016). Given the severity of the ongoing COVID-19 pandemic, it has been modelled that any degree of cross-protective coronavirus immunity in the population could have a very substantial impact on the overall course of the pandemic, and the dynamics of the epidemiology for years to come (Kissler et al., 2020).”
If this is indeed the case, the future is much more cheerful than anticipated in the worst scenarios. It means that initially COVID 19 probably infects those who are most susceptible (who have NOT been naturally immunised by the cold virus). But then it hits the barrier of perhaps 40-60% of the population who have previously been infected by that cold virus and are more resistant to attack by the COVID 19 virus. Because of this cold infection, the pool of the ‘naïve’ population would be much smaller than supposed, and the rate of infection (and the R factor) would decline rapidly. If this is the case, the 17% infected in London will reduce the uninfected pool much more than has been supposed, and the disease will die out in London faster than expected.
A resurgence in the winter is possible, but not inevitable, as COVID 19 may be relatively stable and may not mutate as fast as seasonal flu (https://www.livescience.com/coronavirus-mutation-rate.html ). So the existing resistance should last over the coming winter. If the cold virus gets you before COVID 19 does, that will be the end of it as a serious threat.
Much of this is speculative based on stitching together indicative data, and much more work needs to be done by immunologists to explore this hypothesis. But the concept of cross-reactive immunity seems extremely important for this pandemic and any new ones that emerge in the future, and work in the area would seem to be a high priority. Meanwhile, reality will unfold, possibly at a faster rate than the research.
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