Drowning in Coronavirus Research, Part 26

By June 24, 2020 Commentary

More research on potential cross-reactivity of antibodies from the common, pre-existing strains of coronavirus and the current one.  (Medrxiv Paper)  The authors were looking for commonality among various proteins.  There was commonality for all, but the greatest commonality with the original SARS virus, the MERS virus and then with two of the seasonal coronaviruses.  There was less commonality in the receptor binding domain than in other parts of the spike protein or the rest of the virus.  Having established some commonality, the researchers examined the extent of functional cross-reactivity.  In samples collected from healthy volunteers before 2019, there was minimal reactivity with the SARS, MERS or current coronavirus strain.  There was strong reactivity to the seasonal coronaviruses.  There was a low level of reactivity to the new virus strain.  T cells were not tested.

This is further research on what the immune response looks like across the spectrum of coronavirus infection.  (Medrxiv Paper)   They examined over a period of time 28 healthy persons who had been contacts of those with confirmed infections, 20 persons who were asymptomatic, 8 with mild disease and 8 with severe disease.  Those who were asymptomatic had more of a natural killer cell (a type of immune cell) response and a lower antibody response, compared to people with severe disease.  People with asymptomatic disease also had a more significant T cell response.  Many of these patients may have fought off the infection before it reached the lower respiratory tract through generalized antibodies and natural killer cells, limiting the development of antibody defenses.  The authors take a leap to suggesting this may limit population immunity development.  Since it does appear that memory T cells are activated even in mild cases, and that most people fight off infection with their general immune system, not sure what difference it makes if they don’t have a strong antibody response.  I would also note the couple of studies which have found that typical antibody assays measure at too high a threshold.

A paper that looked at prevalence of infection among Swedish health care workers.  (Medrxiv Paper)   The antibody survey indicated that about 19% of 2149 workers had been infected.  Need to add the T cell check.

This study looked at sources of transmission of the typical seasonal coronavirus.   (WO Study)   Using United Kingdom data, the authors attempted to estimate where people acquired the infection.  The UK has a network like the influenza-like illness network in the US.  Using data derived from that network on confirmed common coronavirus infections, the authors estimated that over 90% of infections were acquired outside the home, with household transmission playing a secondary role.   Not sure how relevant this is to the current strain, as the common ones infect children at high rates, and the current strain does not, probably because of cross-reactive immune defenses from those common infections.

This paper claims that face-mask wearing is associated with lower death rates.  (Medrxiv Paper)   Another questionable modeling study trying to identify correlations with death rates, which the authors say were obesity, being over age 80 and mask wearing.   The authors emphasized the mask-wearing.  And how did they measure actual use of masks–purely by self-reported surveys done by other researchers.  Totally unreliable data.

This study examined antibody prevalence in a hard-hit region of Italy.  (Medrxiv Paper)   4174 out of 4550 inhabitants were tested.  Testing was fairly restricted early on in Italy and there were only 184 confirmed infections, with a high hospitalization and death rate.  Overall 22% were positive.  There was a significantly lower positive rate for children.



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