Ever since its sudden and surprising appearance on the world stage in the spring of 2009, the pandemic influenza A (H1N1) virus has challenged the medical and scientific communities in ways we rarely encounter. Of the many unanswered questions that remain about this novel virus, perhaps the most intriguing is that of how it originated and, most importantly, that of how we can limit its dissemination in the human population. The exact geographic origin of the pandemic influenza A (H1N1) virus and the precise time and events that led to its emergence are still unknown and may never be resolved. The first isolate to be identified by the Centers for Disease Control and Prevention (CDC) on April 15 was obtained from a 10-y-old boy from San Diego County, CA. Within days, there was a successful characterization of the full genetic composition of the eight RNA segments of the viral genome. Six of the genes were similar to segments previously found in a swine influenza strain known to circulate in North America, causing sporadic infections in persons with exposure to pigs. Swine influenza viruses have previously only rarely been transmitted to humans and had not shown the ability to be transmitted from person-to-person. The current swine virus is an exception. This may be due to the fact that it represents a multiple reassortant, containing RNA segments from classical swine influenza, Eurasian swine influenza, avian influenza, and avian via human to pig. Although reassortment of swine lineages seems to have occurred years before its emergence in humans, the precise timing of the immediate origin of the epidemic remains unclear (1).
At this writing, it also remains unclear how much morbidity and mortality to expect from H1N1 influenza. Based on comparisons to the 1957 pandemic, the CDC estimates that H1N1 could strike up to 40% of US population in the next 2 y and that the death toll might rise to several hundred thousand. In the United States, as of September 10, the CDC was reporting 9079 hospitalizations and 593 deaths related to H1N1. Globally, the World Health Organization was reporting 254,206 cases and at least 2,837 deaths. In contrast to seasonal influenza, current evidence indicates that this virus causes more severe illness among young people, with the highest attack rate being in children aged younger than 5 y. In the United States, most deaths were in at least one of two groups: aged younger than 5 y, and/or those with high-risk chronic medical condition. Notably, among children with high-risk conditions, the majority had neurodevelopmental disabilities (e.g. developmental delay or cerebral palsy). Other high-risk conditions appearing to predispose to more severe disease include asthma, chronic obstructive airways disease, obesity, or pregnancy. The elderly may be relatively protected because of multiple previous exposures to H1N1 virus, through either repeated natural infections or immunization. Although the severity of disease does not seem to be much worse than seasonal influenza, the H1N1 strain does have a predilection to infect the lower respiratory tract and, interestingly, the gastrointestinal tract.
