In the highly cited 2006 review of Taubenberger and Morens it is mentioned that:

The impact of this pandemic was not limited to 1918–1919. All influenza A pandemics since that time, and indeed almost all cases of influenza A worldwide (excepting human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, including "drifted" H1N1 viruses and reassorted H2N2 and H3N2 viruses. The latter are composed of key genes from the 1918 virus, updated by subsequently incorporated avian influenza genes that code for novel surface proteins, making the 1918 virus indeed the "mother" of all pandemics. [Until Covid-19]

With the appearance of a new H2N2 pandemic strain in 1957 ("Asian flu"), the direct H1N1 viral descendants of the 1918 pandemic strain disappeared from human circulation entirely, although the related lineage persisted enzootically in pigs. But in 1977, human H1N1 viruses suddenly "reemerged" from a laboratory freezer (9). They continue to circulate endemically and epidemically.

It citest a somewhat obscure paper for that 1977 event. I've actually read the 1978 paper (now) but it leaves me somewhat more confused. It says this about the putative origins of the re-emergence:

The close similarity in both the HA and NA of A/USSR/77-like strains with a 1950 reference virus raises many questions as to the origin of the current H1N1 genes. Because antigenic drift has been observed in animal influenza viruses of several subgroups that have been isolated over a period of years ((16) and R. G. Webster, personal communication), it has been considered unlikely that the H1N1 virus could have been maintained in an animal reservoir for a quarter century without undergoing detectable mutation. Therefore, some have speculated that the epidemic may have resulted from a man-made event. However, it must be noted that the Hav1 antigen of fowl plague virus and the Heq1 antigen of equine influenza virus, which appear to be distantly related (17), have been stable for many years in viruses isolated from birds and horses, respectively ((18) and unpublished results). Chemical studies of all genes in the A/USSR/77-like isolates are, therefore, being done to further examine the question of the origin of this virus (personal communication from Drs. W. Bean, P. Palese, and C. Scholtissek).

The contrast between the homogeneity of antigenic specificity of the HA in 1977-1978 isolates of H1N1 influenza and the antigenic heterogeneity of the HA in viruses in the 1950-1951 epidemics does suggest, however, that current H1N1 viruses arose from a single source. This is also supported by the observed uniformity of avidity of the HAS in 1977-1978 isolates, since avidity also is believed to be a genetic characteristic of influenza viruses (7). Variant viruses that co-circulated in 1950-1951 presumably arose by mutation and evolution from strains widely seeded in the human population during the preceding years, as has also been observed more recently for H3N2 influenza A strains (19).

Note added in proof: Preliminary results of analysis of about 500 H1N1 strains of influenza A virus isolated from about February to May 1978 suggest that approximately 5% of the viruses exhibit minor antigenic drift away from the A/USSR/77 reference strain, and that several distinguishable groups of such variants may be detected. None of the variants, however, appear to resemble A/England/1/51 or other H1N1 strains isolated in the period of former prevalence of such viruses. Presumably, therefore, the newer variants represent examples of mutants of the A/USSR/77-like virus which have appeared following its spread through large segments of the human population.

While this paper entertains the idea of a laboratory release, it doesn't quite seem to fully back it up. So, has any additional research been done since then on the matter, that can (better) explain what Taubenberger and Morens [seem to] claim about the 1977 event?

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We have a more plausible reason for the reappearance in 1977 of H1N1. The thesis is that a live attenuated version of H1N1 (LAIV) was used by Chinese scientists who innoculated several 1000s military recruits. It likely was not attenuated correctly and reverted to a more virulent form in-vivo leading to the epidemic.

Between 1962 and 1973, almost 40,000 children participated in eight LAIV trials in the USSR (13). Scientists at the Peking Vaccine and Serum Institute in China also carried out clinical trials using live vaccines during the same time period (1). Additionally, there are records of the mass production of a live H1N1 vaccine in Odessa, USSR, in 1977 (14, 15). In the early days of research in the 1940s, LAIVs were often able to regain virulence upon administration to humans and cause disease (16). In addition, many strains isolated from the 1977 outbreak (for example, the A/Tientsin/78/77 isolate) were temperature sensitive (ts), meaning that the virus could not replicate at higher temperatures. Temperature sensitivity generally occurs only after a series of laboratory manipulations, typical in generation of LAIVs, and is used as a biological marker of attenuation. While not all of the 1977-1978 strains were temperature sensitive, a comparison of all 1977 strains shows a higher prevalence of the ts phenotype than in 1950 strains, supporting the claim that the outbreak may have resulted from attempts at attenuation for vaccine purposes (1, 17). The possibility that the 1977-1978 strain could have resulted from a LAIV trial was also mentioned in a personal communication from C. M. Chu, renowned virologist and the former director of the Chinese Academy of Medical Sciences to Peter Palese, who described “the introduction of this 1977 virus [as] the result of vaccine trials in the Far East involving the challenge of several thousand military recruits with live H1N1 virus” (18). Whether this involved an ineffectively attenuated vaccine or a laboratory-cultivated challenge strain, the deliberate infection of several thousand people with H1N1 would be a plausible spark for the outbreak.


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  • Nice find (aside: threat of funding cuts, a great motivator to do research on an otherwise nearly forgotten subject.) – Fizz Apr 16 at 21:56
  • Just out of interest, if H1N1 disappeared from human circulation entirely, as reported in the 1978 paper cited in the question, why would USSR and China be conducting LAIV trials on children and military recruits? – Chris Rogers Apr 17 at 9:53

According to a 1992 review the conclusion of release from a freezer is one obtained by elimination of alternatives:

Where was this virus for 27 years? The possible explanations include preservation in a frozen state, preservation in an animal reservoir, or retention in an integrated, as yet undetected form in the genetic material of a human or lower animal. The animal reservoir option is unlikely, for the accumulation of mutations would have continued. There is no evidence for integration of influenza genetic material into the host genome, leaving the most likely explanation that in 1977 the H1N1 virus was reintroduced to humans from a frozen source.

According to a 2009 (academic) blog the actual lab/source of the release was never found and the Chinese and Russians/Soviets strongly denied it came from one of their labs:

This possibility has been denied by Chinese and Russian scientists, but remains to this day the only scientifically plausible explanation.

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Found this in Wikipedia long ago although might not be what you're looking for.

The 1977–1978 Russian flu epidemic was caused by strain Influenza A/USSR/90/77 (H1N1). It infected mostly children and young adults under 23; because a similar strain was prevalent in 1947–57, most adults had substantial immunity. Because of a striking similarity in the viral RNA of both strains – one which is unlikely to appear in nature due to antigenic drift – it was speculated that the later outbreak was due to a laboratory incident in Russia or Northern China, though this was denied by scientists in those countries. The virus was included in the 1978–79 influenza vaccine.


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