The emergence of influenza A (H3N2)v virus: what we learned from the first wave.

Swine influenza was first recognized clinically in pigs at the time of the 1918 Spanish Flu pandemic [1]. From 1918 to 1998, swine influenza was almost exclusively caused by the influenza A (H1N1) classic swine virus; this virus circulated in pigs with little genetic drift [1–3] for more than 70 years. In 1998, severe influenza-like illness (ILI) was observed in pigs in the United States. The causative agent was determined to be a reassortant influenza A (H3N2) virus with human HA, NA, and PB1 gene segments [1, 3], likely transmitted from people to pigs at some earlier point. The increase in genetic diversity of the virus in the US swine population and the inclusion of human influenza genes in swine viruses has important implications for human health, including the enhanced potential for virus adaptation and cross-species transmissibility. Currently circulating subtypes of influenza A viruses in swine include (H1N1), (H1N2), and (H3N2); all have caused disease in humans. Results of diagnostic testing of more than 6000 specimens from a large midwestern academic reference laboratory from 2009 to 2012 indicate an increase in the frequency of influenza A (H3N2) virus infection in swine in 2011, with prevalence reaching approximately 26% [4]. Following the 2009 H1N1 pandemic in humans, these influenza A(H3N2) viruses experienced a notable genetic reassortment. Phylogenetic analysis indicates that the influenza A (H3N2) virus acquired theM, ormatrix, gene from the 2009 pandemic influenza A (H1N1) virus (A(H1N1) pdm09) and that the proportion of influenza A (H3N2) viruses with the A(H1N1)pdm09 M gene became more prevalent. In 2009, <5% of swine influenza A (H3N2) viruses contained the A(H1N1)pdm09 M gene, and in 2011 more than half of all swine influenza A H3N2 viruses contained the A(H1N1)pdm09 M gene [4]. It appears that both symptomatic and asymptomatic pigs can shed virus and transmit infection to other pigs and humans [5, 6]. In a recent study by Bowman et al, 83% of pigs tested at agricultural fairs from which influenza was recovered did not show signs of ILI [7]. From December 2005 to June 2011, 21 human cases of swine influenza A virus infection (henceforth known as variant infection, abbreviated influenza subtype lowercase v [8]) were reported to the Centers for Disease Control and Prevention by state and local health departments. Twelve were H1N1v virus infections, 1 was an H1N2v virus infection, and 8 were H3N2v virus infections. All were triple-reassortant swine-origin viruses with genes from human, avian, and swine influenza viruses. From 2005 to 2008, 1 to 5 cases were identified every year. However, in recent years identifications have increased for the following reasons: the of adoption of novel influenza A virus infection as a reportable disease in the United States in 2007, the availability of improved influenza diagnostic tests at state health departments, and a greater awareness of the pandemic potential of swine influenza after the 2009 H1N1 pandemic. Most of these cases had direct swine contact, were children and adolescents, and recovered from their illness after a few days. Only 3 of these 21 infections were transmitted from person to person (CDC, unpublished data). Correspondence: David L. Swerdlow, MD, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Mailstop A-27, 1600 Clifton Rd, NE, Atlanta, GA 30333 ([email protected]). Clinical Infectious Diseases 2013;57(S1):S1–3 Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2013. DOI: 10.1093/cid/cit324