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Within a month of its emergence in Mexico in April 2009, pandemic influenza A (H1N1) virus (“swine flu”) had sickened 64 U.S. residents in six states (MMWR Morb Mortal Wkly Rep 2009; 58:431). Analysis of representative strains yielded genes from swine, avian, and human influenza viruses, but no homology to circulating seasonal human subtypes (JW Pediatr Adolesc Med May 8 2009). Symptoms were typical of influenza.
During 2009, ages of affected patients spanned a wide range, but attack rates were high among children and adolescents, with clusters of cases in schools and universities (JW Infect Dis Jul 1 2009). In the adult population, pregnant women and people with chronic underlying medical conditions seemed particularly vulnerable (JW Infect Dis May 27 2009), and mortality rates were considerably higher among hospitalized adults than among hospitalized infants and children (JW Gen Med Nov 19 2009).
Tracing the path of the virus has been complicated by unreliable diagnostic tests, which are always a problem with influenza. Standard antigen-based rapid influenza A tests have sensitivity of about 50% compared with gold standard culture or PCR techniques. But a rapid test for 2009 H1N1 virus performed even worse, with a sensitivity of 11% compared with PCR, and even PCR appeared to be relatively unreliable for case identification (JW Infect Dis Oct 14 2009). One small outbreak among a group of travelers showed patterns of transmission consistent with droplet or fomite, but not airborne, transmission (JW Infect Dis Oct 14 2009).
In serologic studies, researchers found negligible levels of protective immunity to 2009 H1N1 virus among infants and children, even in those who had received standard seasonal vaccines. Among adults, protective antibodies were more common, especially in those born before 1950 and in those who were vaccinated against the 1976 swine flu strain (JW Gen Med Sep 17 2009).
The discovery that just a single dose of two different inactivated vaccine candidates could produce protective titers seemed likely to smooth the path toward universal vaccination. However, manufacturing difficulties supervened, and the initial vaccine supplies have been targeted to the highest-risk groups, including schoolchildren and pregnant women (JW Gen Med Sep 17 2009).
Meanwhile, use of antiviral agents has been widespread, including off-label use of oseltamivir (Tamiflu) for prolonged courses in seriously ill patients and, in November 2009, emergency release of the investigational agent peramivir (JW Infect Dis Nov 4 2009). Neuraminidase resistance has been reported in a few H1N1 isolates (JW Pediatr Adolesc Med Sep 16 2009), and prospective studies have yet to confirm the benefit of prolonged neuraminidase inhibitor use in patients with severe H1N1 infections.
As of mid-October 2009, the CDC estimates that 22 million people in the U.S. have contracted H1N1 virus, resulting in approximately 98,000 hospitalizations and 3900 deaths. Whether the H1N1 toll will differ substantially from the usual seasonal flu morbidity and mortality awaits final tabulations. In the meantime, public health officials, journalists, and ordinary citizens have had experience coping with the uncertainty that accompanies an emerging infection. If the 2009 H1N1 flu proves not to be “the big one,” at least we have had a dress rehearsal for the real thing.