Adrian Hugo Aginagalde
Spokesperson of the Spanish Society of Preventive Medicine, Public Health and Health Management (SEMPSPGS), Head of Service of the Epidemiological Surveillance and Health Information Unit of Gipuzkoa and, previously, Head of Service of the Population Screening Programmes Unit at the Ministry of Health
This work attempts, through RNA sequencing of samples from people who died at the time and the molecular clock technique, to determine the timing of the mutation and the degree of similarity to the circulating H1N1 influenza.
This is compatible with the hypothesis that has been used historically so far. According to this, there must have been a mutation between autumn and winter 1918 that increased its virulence compared to the virus circulating between spring and summer 1918. It was known that such a mutation must have occurred, although there was no evidence for it, but that the genetic distance must not have been sufficiently high for those who had been infected in the first wave not to retain immunity in the second. At the same time, the data are consistent with what is known about H1N1 influenza viruses, namely that prior to 2009 they were related to the 1918 virus.
It is interesting that they have not only used samples from people buried in the permafrost, as was previously the case, but have also incorporated pieces preserved in the Museums of the History of Medicine. This makes it possible to broaden the geographical scope of the study and to better study the differences between the virus samples circulating on both sides of the Atlantic.
It confirms that acute respiratory virus infections do not disappear, but displace previous serotypes and become seasonalised, causing increases in mortality in the following winters. Also that there is no herd immunity in these viruses to block transmission and that there is no natural (or intrinsic) tendency to reduce their virulence.
It is the disappearance of the extraordinary risk factors that favour transmission and increase vulnerability (such as a World War), as well as the decrease in the number of susceptible people, that causes its impact to diminish; but without disappearing, generating occasional excess mortality higher than expected in subsequent winters and without mutations that increase its benignity.