1977 Russian Flu Pandemic
Strictly speaking, there was a fourth pandemic in the 20th century, an H1N1 strain which appeared in 1977. This was a "benign" pandemic, primarily involving persons born after the 1950, because the older population had protective immunity resulting from prior experience with H1N1 strains. The Russian Flu began in May 1977, when influenza A/H1N1 viruses isolated in northern China spread rapidly, and caused epidemic disease in children and young adults (< 23 years) worldwide. Russian, or later red influenza or red flu, first came to attention in November 1977, in the Soviet Union. However, it was later reported as having first occurred in northeastern China in May of that year. In May 1977, influenza viruses in northern China spread rapidly and caused epidemic disease in children and younga dults.
By January 1978, the virus had spread around the world. From November 1977 through mid-January 1978 the population younger than 25 years in the Union of Soviet Socialist Republics experienced a widespread epidemic of mild influenza (Russian flu) caused by an H1N1 virus similar to the virus that circulated worldwide during the early 1950s. Outbreaks of Russian flu occurred in school populations and military recruits in the United States starting in mid-January. Many other countries reported outbreaks of H1N1 virus in the winter of 1978.
It quickly became apparent that this rapidly spreading epidemic was almost entirely restricted to persons younger than about 25 years of age. The age distribution was attributed to the absence of H1N1 viruses in humans after 1957 and the subsequent successive dominance of the H2N2 and then the H3N2 subtypes. The 1977 virus was similar to other A/H1N1 viruses that had circulated prior to 1957. In 1957, the A/H1N1 virus was replaced by the new A/H2N2 viruses. Because of the timing of the appearance of these viruses, persons born before 1957 were likely to have been exposed to A/H1N1 viruses and to have developed immunity against A/H1N1 viruses. Therefore, when the A/H1N1 reappeared in 1977, many people over the age of 23 had some protection against the virus and it was primarily younger people who became ill from A/H1N1 infections. By January 1978, the virus had spread around the world, including the United States. Because illness occurred primarily in children, this event was not considered a true pandemic. Vaccine containing this virus was not produced in time for the 1977-78 season, but the virus was included in the 1978-79 vaccine.
The Russian flu strain expected to be predominant during the 1978-79 flu season was not, and a slightly different strain called Brazil flu became predominant. The 1978-79 flu strains in total primarily attacked individuals under age 26. Only a small portion of those over age 65 and the chronically ill over age 26 were attacked. Not only did the predicted Russian flu not become predominant as expected, but also the predicted population group to be most seriously affected was attacked infrequently. HEW had predicted, based on past experience, that the 1978-79 flu would be most severe in the chronically ill and those over 65 years of age. However, the population attacked most frequently were people under 26 years of age, and the disease consequences were generally mild in those attacked.
Although the Russian flu vaccine used during the program is expected to provide some protection against Brazilian flu, the level of protection provided is uncertain. According to CDC, flu immunizations should be completed by late November for optimal program effectiveness. The 1978-79 flu program was originally planned to meet this schedule. However, by the end of November, fewer than 600,000 doses had been administered.
When antigenic and molecular characterization of this virus showed that both the HA and NA antigens were remarkably similar to those of the 1950s, this finding had profound implications. Where had the virus been that it was relatively unchanged after 20 years? If serially (and cryptically) transmitted in humans, antigenic drift should have led to many changes after two decades. Reactivation of a long dormant infection was a possibility, but the idea conflicted with what was known of the biology of the virus, in which a latent phase has not been found. Had the virus been in a deep freeze? This was a disturbing thought because it implied concealed experimentation with live virus, perhaps in a vaccine. Delayed mutation and consequent evolutionary stasis in an animal host were not unreasonable, but in what host? And if a full-blown epidemic did originate, it would be the first to do so in the history of modern virology, and a situation quite unlike the contemporary situation with H5N1 and its protracted epizootic phase. Thus, the final answer to the 1977 epidemic is not yet known.