ABSTRACT
In March 2009, cases of influenza-like illness in Mexico caused by a novel H1N1 virus
containing genes from swine, avian, and human influenza strains were reported. Within
several weeks, 2009 H1N1 disseminated rapidly and was the predominant influenza strain
globally. On June 11, 2009, the World Health Organization declared that criteria for
an influenza pandemic had been met. Concern that this pandemic would rival the 1918
pandemic was high. Fortunately, that was not the case. Influenza-related disease activity
peaked in late October to November 2009. By August 2010, the H1N1 influenza virus
had moved into the postpandemic period. During the 2010–2011 season, influenza A H3N2
has been the predominant serotype, but the 2009 H1N1 continues to co-circulate with
H3N2 and B strains. In contrast to previous seasonal influenza strains, the novel
2009 H1N1 strain preferentially affected young adults, with a clustering of severe
and fatal cases in adults between the ages of 30 and 50 years. Additionally, H1N1
displayed a heightened potential for severe lung injury as well as gastrointestinal
symptoms. Risk factors for severe disease included obesity, morbid obesity, pregnancy,
immunosuppression, asthma (in children), chronic obstructive pulmonary disease, neurological
disorders, other comorbidities, HIV-infection, poverty, and lack of access to care.
However, >25% of deaths were in previously healthy individuals. Molecular tools for
identifying 2009 H1N1 were rapidly developed, but the volume of samples quickly overwhelmed
available laboratory services. Further, in the early phases of the pandemic, the volume
of patients presenting to emergency rooms, acute care clinics, and physician's offices
overwhelmed health care resources. Fortunately, most cases were mild; in the United
States, only one in 400 required intensive care unit care, and one in 2000 died. Because
most infected individuals have mild, self-limited disease, the risk/benefit assessment
for early access to antiviral agents must balance the potential benefit for reducing
transmission, disease severity, and burden on health care providers against the potential
for dissemination of viral resistance and drug-related adverse events. Monovalent
vaccines against 2009 H1N1 were developed and ready for distribution by September
2009, but initial supplies were inadequate to impact the bulk of cases that occurred
in the Northern Hemisphere between April and September 2009. Continued efforts to
develop universal vaccines and improve access to effective vaccines are critical.
KEYWORDS
Novel 2009 H1N1 - influenza - swine influenza - pandemic
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Philip LaRussaM.D.
Department of Pediatrics, College of Physicians and Surgeons, Columbia University
Black Bldg. 4-442, 650 W. 168th St., New York, NY 10032
eMail: plarussa@columbia.edu