Cluster of Oseltamivir-Resistant and Hemagglutinin Antigenically Drifted Influenza A(H1N1)pdm09 Viruses, Texas, USA, January 2020
Teena Mohan, Ha Nguyen, Krista Kniss, Vasiliy P. Mishin, Angiezel Merced-Morales, Jennifer Laplante, Kirsten St. George, Patricia Blevins, Anton Chesnokov, Juan A. De La Cruz, Rebecca Kondor, David E. Wentworth, Larisa V. Gubareva
Abstract
R esistance to antiviral drugs for infl uenza is an on- going public health concern. The neuraminidase (NA) inhibitor oseltamivir is the most prescribed antiviral drug for controlling infl uenza. However, during 2007-2009, oseltamivir-resistant infl uenza A(H1N1) viruses rapidly spread worldwide (1). Molecular mechanisms implicated in this event were acquisition of NA-permissive mutations that alleviated deleterious fi tness effects of the resistance-conferring mutation NA-H275Y (N1 numbering) (2); changes that improved balance of hemagglutinin (HA) and NA activities (3); and a "hitchhiking" mechanism, in which HA antigenic drift promoted the spread of oseltamivir-resistant viruses (4). Oseltamivir-resistant H1N1 viruses were later displaced by the 2009 pandemic virus, infl uenza A(H1N1)pdm09 (pH1N1), which was antigenically distinct and oseltamivir sensitive (5). The emergence and transmission of oseltamivir-resistant pH1N1 carrying a NA-H275Y mutation was fi rst reported early in the 2009 pandemic (6). In the following years, transmission of oseltamivir-resistant viruses within healthcare settings and communities, or between close contacts, was occasionally observed (1); clusters were reported in Australia in 2011 ( Despite these incidents, widespread circulation of oseltamivir-resistant viruses has yet to occur.