Although few remember it today, an extraordinary thing happened during the influenza season of 1977. For the first time in the relatively short history of tracking flu, two subtypes of influenza A were found co-circulating the globe.
To understand how unexpected this was, all you need do is look at the graphic at the top of this post.
From 1918 through 1976 we’d seen three influenza A pandemics (1918, 1957, 1968) and each time the pandemic virus completely supplanted the previously circulating influenza A virus. The descendents of the 1918 H1N1 virus reigned supreme (and alone) until it was unseated by H2N2 in 1957. H2N2 held court until H3N2 pushed it aside eleven years later.
There were certainly influenza B viruses in the mix, but the norm appeared to be only one influenza A subtype each flu season.
In 1977, however, a second influenza A virus abruptly appeared, or rather - re-appeared – and began circulating along side H3N2. A throwback to the 1950s, the 1977 H1N1 `Russian flu’ was generally mild in adults, but hit children and adolescents born before 1957 the hardest.
This unusual turn of events happened one year after our 1976 H1N1 swine flu scare, when as a young paramedic, I got my first taste of pandemic planning (see my account in Deja Flu, All Over Again). What we dodged in 1976 turned into a frantic flu season for children, hospitals and EMS the following year.
Since 1977 we’ve seen two influenza A subtypes co-circulate every year. Even when the 2009 H1N1 pandemic virus completely supplanted the old (1977) H1N1 virus, H3N2 continued to circulate.
For years scientists have tried to explain how a virus – gone from the wild for 20 years – could just suddenly reappear. Particularly one that was practically identical to a strain last seen more than a quarter of a century before. The most popular theory has been that of an accidental release from a Russian or Chinese research facility, but solid evidence has been lacking..
Yesterday, in the journal mBio, two researchers from UPMC Center for Health Security published a paper that looks at the available evidence, and discusses several plausible scenarios. They also discuss its possible relevance (or lack thereof) to the GOF (Gain of Function) debates of today (see mBio: The Risks & Benefits Of `GOF’ Experimentation On Pathogens With Pandemic Potential).
It’s a fascinating report, so follow the link below to read:
The 1977-1978 influenza epidemic was probably not a natural event, as the genetic sequence of the virus was nearly identical to the sequences of decades-old strains. While there are several hypotheses that could explain its origin, the possibility that the 1977 epidemic resulted from a laboratory accident has recently gained popularity in discussions about the biosafety risks of gain-of-function (GOF) influenza virus research, as an argument for why this research should not be performed. There is now a moratorium in the United States on funding GOF research while the benefits and risks, including the potential for accident, are analyzed. Given the importance of this historical epidemic to ongoing policy debates, we revisit the evidence that the 1977 epidemic was not natural and examine three potential origins: a laboratory accident, a live-vaccine trial escape, or deliberate release as a biological weapon. Based on available evidence, the 1977 strain was indeed too closely matched to decades-old strains to likely be a natural occurrence. While the origin of the outbreak cannot be conclusively determined without additional evidence, there are very plausible alternatives to the laboratory accident hypothesis, diminishing the relevance of the 1977 experience to the modern GOF debate.