In nature, the flu does not remain unchanged for 27 years as it circulates. So the reality that the “Russian influenza” was almost identical to the earlier stress eventually resulted in the conclusion that the Russian influenza was most likely the outcome of a lab leak or possibly a failed effort to inoculate people with live attenuated virus.
In a research paper released in the journal Nature in 1978, a group of scientists from The City University of New York discovered that the 1977 infection was genomically similar to the 1950 virus– nearly as though the viral development had been frozen in time.
It may be possible for an accidental anomaly to establish that resembles a variant from the past– but the scientists deemed it was not plausible to speculate that such back anomalies unintentionally produced a pressure so similar to something that distributed 27 years back.
This next bit is quite striking in light of existing events:
A 1978 research study by researchers from the Chinese Academy of Medical Sciences showed that the virus mostly impacted those listed below the age of 20– offering assistance to the theory that those above that age had currently been exposed to the very same infection prior to, and therefore had established immunity.
In the very same paper, however, the team dismissed the lab leak theory in one sentence, stating that none of the “laboratories worried” had been working or keeping with the H1N1 for a long time.
In 1977 an influenza broke out in northeast China which eventually spread to Russia and then around the world. Researchers who analyzed its DNA concluded it was almost identical to a previous stress of the flu virus which had triggered a break out between 1949 and 1950.
But as this 2015 paper explains, a laboratory leakage (or additionally a stopped working immunization effort with live attenuated infection) is now thought about the most likely explanation for the Russian flu as alternate descriptions have actually been discovered to be unconvincing. Once again, see if this does not sound familiar:
A biosafety lapse in a research lab is now usually cited as the cause of the 1977-1978 reemergence of the H1N1 influenza infection pressure (Fig. 2). The evidence in favor of this possibility is the clear abnormal origin of the virus and its temperature level of sensitivity, recommending lab manipulations. At the time of the epidemic, however, the World Health Organization omitted the laboratory mishap possibility after discussions with influenza infection laboratory researchers in the Soviet Union and China, finding that “the laboratories worried either had never ever kept H1N1 infection or had actually not dealt with it for a very long time”
Theres a graphic demonstrating how numerous theories have actually been proposed and talked about by scientists for many years. Since about 2008, the laboratory leak appears to be the dominant description:
The author of the paper appears to believe its more likely the release was the outcome of a vaccine trial using live attenuated virus which wasnt sufficiently attenuated.
There are two elements that point to the 1977 epidemic as arising from vaccine difficulty or trials: (i) live attenuated influenza virus (LAIV) research was extensive at the time, and (ii) a 1976 H1N1 swine influenza break out was feared to have pandemic capacity and caused a resurgent interest in H1N1 defense and research study (12 ).
In between 1962 and 1973, nearly 40,000 kids took part in 8 LAIV trials in the USSR (13 ). Researchers at the Peking Vaccine and Serum Institute in China likewise performed medical trials using live vaccines throughout the same time period (1 ). Furthermore, 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 frequently able to regain virulence upon administration to people and cause illness (16 ). In addition, lots of stress isolated from the 1977 break out (for example, the A/Tientsin/78/ 77 isolate) were temperature level sensitive (ts), meaning that the infection could not reproduce at greater temperature levels. Temperature level sensitivity usually occurs only after a series of laboratory controls, typical in generation of LAIVs, and is utilized as a biological marker of attenuation. While not all of the 1977-1978 strains were temperature sensitive, a comparison of all 1977 strains reveals a greater prevalence of the ts phenotype than in 1950 stress, supporting the claim that the outbreak may have arised from efforts at attenuation for vaccine purposes (1, 17).
Whatever the precise cause, most professionals now believe that the “Russian flu” of 1977 was triggered by a virus which had actually been collected at some point around 1950, worked on in a laboratory and then essentially launched back into the world by accident. The Russians and the Chinese rejected having done any such thing and the WHO supported those denials at the time, but 3 years later on most scientists now think the denials should be false. Influenza infections simply do not hibernate for 27 years and then suddenly cause an outbreak in a the same kind.
At the time of the epidemic, nevertheless, the World Health Organization omitted the laboratory mishap possibility after discussions with influenza infection laboratory researchers in the Soviet Union and China, discovering that “the labs concerned either had never ever kept H1N1 infection or had not worked with it for a long time”
In addition, lots of pressures isolated from the 1977 break out (for example, the A/Tientsin/78/ 77 isolate) were temperature delicate (ts), indicating that the virus could not reproduce at higher temperature levels. Whatever the specific cause, a lot of professionals now think that the “Russian influenza” of 1977 was triggered by a virus which had actually been gathered sometime around 1950, worked on in a laboratory and then basically launched back into the world by mishap. Flu viruses merely do not hibernate for 27 years and then all of a sudden trigger an outbreak in an unchanged form.
Scientists who examined its DNA concluded it was nearly identical to a previous strain of the flu infection which had caused a break out between 1949 and 1950.