Prior Infections With Seasonal Influenza A/H1N1 Virus Reduced the Illness Severity and Epidemic Intensity of Pandemic H1N1 Influenza in Healthy Adults

A new influenza virus appeared in Mexico and the United States in April 2009 and caused outbreaks of influenza in humans [1, 2]. The virus was promptly identified as a swine-like influenza A (H1N1) virus and shown to be a triple reassortant virus containing genes from swine, human, and avian influenza A viruses [3]. The virus spread rapidly throughout North America and worldwide, causing the World Health Organization (WHO) to declare the spread as pandemic influenza [4]. Public health authorities mobilized for monitoring and control as the virus proceeded to cause epidemic influenza in the Southern and Northern Hemispheres during the spring and summer of 2009. Pandemic H1N1 influenza (pH1N1) peaked in the United States in October 2009, with minimal activity during the usual winter period of influenza [5]. Retrospective estimates of the medical impact for the United States for the period April 2009 to April 2010 are 60.8 million cases, 274 304 hospitalizations, and 12 469 deaths, less than some seasonal epidemics but substantial in children [6]. The hemagglutinin (HA) of the pH1N1 virus is a swine virus HA similar to the HA of viruses isolated from swine in North America in recent years and related to influenza A/H1N1 viruses that have circulated in swine since first detected in 1930 [7]. Antigenically related influenza A/H1N1 viruses circulated in humans from 1918 to 1956 and reappeared in 1977 as the “Russian flu” [8]. At that time, persons ≥25 years of age were “primed” for H1 antigens from prior A/H1N1 virus infections; they experienced very little clinical influenza during the 1977–1978 A/H1N1 virus epidemic [9]. Because A/H1N1 viruses had caused infections and influenza as well as having been included in the annual influenza vaccine since 1977, it seemed likely that large numbers of people would have a degree of immunity to the pH1N1 virus, with increasing susceptibility likely to increase with decreasing age. However, no specific age could be designated for full susceptibility as was possible in 1977. It seemed likely that young adults would have a high degree of susceptibility. A serological survey for specific antibody conducted by the Centers for Disease Control and Prevention had indicated very little pH1N1 antibody in them [10]. To assess the clinical and epidemiological impact of pH1N1 infections and to identify immunologic factors correlating with infections and illnesses, we conducted a prospective study of influenza in a young adult population. Here we describe the infections and illnesses in this population with the pH1N1 virus, assess the role of prior seasonal H1N1 infections in occurrences of infection and illness with the pH1N1 virus, and discuss the similarity of the pH1N1 experience with that of the “Russian” H1N1 influenza that emerged in 1977.