From 2016 to 2017, more than 500 shelter cats in New York, USA were infected with H7N2 feline influenza virus derived from A / H7N2 low pathogenic avian influenza virus, resulting in respiratory disease.Two people, including a veterinarian, were also infected and had mild respiratory symptoms.There was concern about the emergence of a new pandemic virus, but it has since converged.The research group is now investigating the mutations required for the efficient growth of this cat virus in the human respiratory tract.

　When the virus was continuously passaged in cultured human respiratory cells, mutations were found in the head region responsible for the receptor binding of the glycoprotein HA (erythroagglutinin) on the surface of the virus and the stalk region responsible for the membrane fusion activity.On the other hand, mutations also occurred in the transmembrane domain of NA (neuraminidase), which is responsible for the release of the virus from cells.

　Next, when each mutant virus was created and investigated by the reverse genetics method, each recombinant virus in which mutations were introduced separately into the HA head, HA stalk, and NA transmembrane regions was propagated to varying degrees. The improvement of sex was recognized.As a result of investigating the mechanism of improvement of proliferation of each mutant virus, the pH requirement of HA membrane fusion activity and HA-NA functional balance (regulators of virus proliferation and cell / host specificity) were determined as receptors for human respiratory cells. Mutations that adapt to the environment have proved to be important for gaining their proliferative potential.

　These mutations identified this time are expected to contribute significantly to virus monitoring, which is responsible for predicting pandemic surveillance.

Paper information:[Viruses] Adaptation of the H7N2 Feline Influenza Virus to Human Respiratory Cell Culture