The 1968 H3N2 pandemic resulted from influenza A/Hong Kong/1968 virus. The H3N2 virus contained two genes derived from the six genes from the A(H2N2) virus, associated with the 1957 H2N2 pandemic, and the avian influenza A virus. In the United States, the experience with the epidemic was unlike in any other country. A less severe second pandemic wave occurred in the 1969-1970 season, while 70 percent of additional epidemic influenza deaths and influenza occurred in the 1968-1969 season (Taylor et al. 64). However, the pandemic only had a 0.5% mortality rate and had a brief duration (Taylor et al. 66). Although the infection had comparatively low deaths, the virus was highly contagious, an issue that enabled its speedy global spreading.
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The virus originated in Hong Kong in July but first appeared in the U.S. in September and remains a circulating flu to date. In the U.S., the clinical attack rates between member states varied. For example, in Milwaukee, Wisconsin, the reports from the public health authorities showed a 43 percent illness attack rate (Jester et al. 671). A 40 percent illness attack rate was chronicled in Georgia, and the Californian retirement community residents revealed a 10 percent infection rate (Jester et al.671). The infection rates may have reflected some preexisting immunity within the older population. Worsening of underlying health conditions and complications as cardiac failure, diabetes, and chronic obstructive pulmonary disease were major contributors to mortality rates in the U.S.
Investigations by the U.S. public health reported that influenza activity increased dramatically in October 1968. The public health identified the first chronicled case in the country in Needles, California, where more than one-third of the population reported having Influenza-like illness (ILI) (Taylor et al. 69). The amount of absenteeism in school increased with the spread of the infection with the peak week of the epidemic, December 14 and January 11, resulting in most states falling to influenza. Based on a survey among nearly 7000 high school students, the findings showed “the median duration of illness was five days, although cough and prostration in some cases persisted as long as three weeks” (Jester et al. 671). Beyond increased screening and the school closure, the significance of the flu was minimal since there were little widespread changes.
The advent of antiviral medications and expansion of influenza vaccine options, in the 1960s, offered the U.S. an arsenal against the pandemic (Jester et al. 672). Studies show that on November 15, 1968, vaccine manufacturers released the first lot of 110000 H3N2 vaccine doses, with another 15 million doses becoming available by the peak of the pandemic in January 1969 (Wu et al. 45). A study of prison inmates showed that “all indicators of a therapeutic effect of amantadine approached or achieved statistical significance” (Jester et al. 672). The 1983 Mayo Clinic Symposium revealed that antiviral medication on influenza, especially amantadine, was beneficial in minimizing the effects of H3N2. The use of the vaccine enabled the people to survive the pandemic. However, the H3N2 virus remains in circulation to date and is considered a seasonal influenza strain.
The H3N2 flu originated in Hong Kong, had a brief duration, and was responsible for a 0.5 percent mortality rate. The pandemic started on July and by January it had reached its peak. However, its effect was controlled through vaccination, that became available by the peak of the pandemic. Despite school closure and screening, the significance of the epidemic was minimal to the global society and with the vaccination, the people survived the flu, which remains a seasonal influenza strain to date.
Jester, Barbara, Timothy M. Uyeki, and Daniel B. Jernigan. “Fifty Years of Influenza A(H3N2) Following the Pandemic of 1968.” American journal of public health vol. 110, no. 5, (2020): 669-676.
Taylor, Charles A, Christopher Boulos, and Matthew J. Memoli. “The 1968 Influenza Pandemic and Covid-19 Outcomes.” Medrxiv. 2021.
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Wu, Nicholas C, Jakub Otwinowski, Andrew J. Thompson, Corwin M. Nycholat, Armita Nourmohammad, and Ian A. Wilson. “Major Antigenic Site B of Human Influenza H3n2 Viruses Has an Evolving Local Fitness Landscape.” Nature Communications, vol. 11, no. 1, 2020.