2009 Influenza A (H1N1) Virus
These colorized, negatively stained transmission electron micrographs depict a number of 2009 swine flu virions (left) and their ultrastructural morphology (right).
First described in April 2009, the virus appeared to be a new strain of H1N1 that resulted from reassortment, a process through which two or more influenza viruses swap genetic information by infecting the same host.1 Two of the genes often swapped code for the production of hemagglutinin (H) and neuraminidase (N) proteins. Hemagglutinin helps invading flu virions attach to a host cell, while neuraminidase lets new flu virions detach from their host cell to find new cells to infect. The 2009 H1N1 strain contained a unique mix of genetic material from birds, pigs and humans, and presented a never-before-seen combination of these proteins.2 As a result, people had virtually no immunity against the virus, and a pandemic soon followed the initial outbreak in Veracruz, Mexico.3
Unlike most strains of influenza, H1N1 does not disproportionately infect adults older than 60 years; this was an unusual and characteristic feature of the H1N1 pandemic.4 Even a small percentage of previously very healthy individuals developed pneumonia or acute respiratory distress syndrome (ARDS).5 A 2012 study led by an international group of scientists estimated 284,500 deaths worldwide associated with the 2009 H1N1 pandemic.6
References: (1) CDC; (2) Karen Kaplan, Los Angeles Times; (3) Donald G. McNeil Jr., New York Times; (4) Writing Committee of the WHO Consultation on Clinical Aspects of Pandemic (H1N1) 2009 Influenza; (5) WHO; (6) Fatimah S. Dawood, A. Danielle Iuliano, Carrie Reed, et al.
Photo credits: (left) Dennis Kunkel Microscopy, Inc. / Visuals Unlimited, Inc.; (right) Cynthia S. Goldsmith and Amanda Balish at the CDC.