LAUSR

Human infections with H7N9 viruses can cause severe pneumonia and even death. To characterize the epidemiology and genetics of the H7N9 viruses circulating during from October 2016 to April 2017 in Suzhou, China, all pharyngeal swab samples were collected from severe acute respiratory infections (SARI) cases during this fifth wave of infection, and we amplified the H7N9 H7 and N9 genes using a real-time polymerase chain reaction (PCR). Positive samples were subjected to virus isolation and gene sequencing to analyze the evolution and variation of the H7N9 strains. The epidemiological features of H7N9 patients have not changed and there were no significant mutations in the key sites of the hemagglutinin (HA) gene sequence, but we identified the K526R and E627 K substitutions in the PB2 protein. In the neuraminidase (NA) protein, drug-resistant mutations (R294 K and H276Y) occurred in a few strains. Most of the H7N9 viruses isolated from Suzhou had no drug resistance mutations, but it is necessary to closely monitor and analyze the probable emergence of mutations and the spread of resistant strains. The reduction of the N-glycosylation site at position 42 of NA was observed in some strains.