During March 2013–February 24, 2017, annual epidemics of avian influenza A (H7N9) in China resulted in 1,258 avian influenza A (H7N9) virus infections in humans being reported to the World Health Organization (WHO) by the National Health and Family Planning Commission of China and other regional sources (1). During the first four epidemics, 88% of patients developed pneumonia, 68% were admitted to an intensive care unit, and 41% died (2). Candidate vaccine viruses (CVVs) were developed, and vaccine was manufactured based on representative viruses detected after the emergence of A (H7N9) virus in humans in 2013. During the ongoing fifth epidemic (beginning October 1, 2016),* 460 human infections with A (H7N9) virus have been reported, including 453 in mainland China, six associated with travel to mainland China from Hong Kong (four cases), Macao (one) and Taiwan (one), and one in an asymptomatic poultry worker in Macao (1). Although the clinical characteristics and risk factors for human infections do not appear to have changed (2, 3), the reported human infections during the fifth epidemic represent a significant increase compared with the first four epidemics, which resulted in 135 (first epidemic), 320 (second), 226 (third), and 119 (fourth epidemic) human infections (2). Most human infections continue to result in severe respiratory illness and have been associated with poultry exposure. Although some limited human-to-human spread continues to be identified, no sustained human-to-human A (H7N9) transmission has been observed (2, 3).

CDC analysis of 74 hemagglutinin (HA) gene sequences from A (H7N9) virus samples collected from infected persons or live bird market environments during the fifth epidemic, which are available in the Global Initiative on Sharing All Influenza Data (GISAID) database (4, 5), indicates that A (H7N9) viruses have diverged into two distinct genetic lineages. Available fifth epidemic viruses belong to two distinct lineages, the Pearl River Delta and Yangtze River Delta lineage, and ongoing analyses have found that 69 (93%) of the 74 HA gene sequences to date have been Yangtze River Delta lineage viruses. Preliminary antigenic analysis of recent Yangtze River Delta lineage viruses isolated from infections detected in Hong Kong indicate reduced cross-reactivity with existing CVVs, whereas viruses belonging to the Pearl River Delta lineage are still well inhibited by ferret antisera raised to CVVs. These preliminary data suggest that viruses from the Yangtze River Delta lineage are antigenically distinct from earlier A (H7N9) viruses and from existing CVVs. In addition, ongoing genetic analysis of neuraminidase genes from fifth epidemic viruses indicate that approximately 7%–9% of the viruses analyzed to date have known or suspected markers for reduced susceptibility to one or more neuraminidase inhibitor antiviral medications. The neuraminidase inhibitor class of antiviral drugs is currently recommended for the treatment of human infection with A (H7N9) virus. Antiviral resistance can arise spontaneously or emerge during the course of treatment. Many of the A (H7N9) virus samples collected from human infections in China might have been collected after antiviral treatment had begun.