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The H2N2 virus that was identified was found to be similar to H2N2 viruses that circulated in humans in 1957-1958 at the beginning of the so-called "Asian" influenza pandemic. Influenza A virus (IAV) is a major cause of respiratory infections worldwide, with the most severe cases occurring in the very young and in elderly individuals [[1]]. Unlike the seasonal IAV age risks noted above, pandemic IAV infections often disproportionately kill young adults, as has been well documented for the 1918 [[1], [5]], 1968 [[6]], and even the 2009 [[7], [9]] pandemics. Seasonal IAV was responsible for an average of 12,000-52,000 deaths annually between 2010 and 2020 in the U.S. before the onset of the COVID-19 pandemic, according to the Centers for Disease Control and Prevention, with preventive measures addressing the latter respiratory infection also reducing the impact of seasonal influenza. [Extracted from the article]

The current studies were undertaken to determine the susceptibility of human alveolar macrophages (AMs) to influenza A virus (IAV) infection in comparison with autologous peripheral blood-derived monocytes-macrophages (PBMs). AMs and PBMs were exposed to IAV in vitro and examined for their ability to bind and internalize IAV, and synthesize viral proteins and RNA. PBMs but not AMs demonstrated binding and internalization of the virus, synthesizing viral proteins and RNA. Exposure of AMs in the presence of a sialidase inhibitor or anti-IAV antibody resulted in viral protein synthesis by the cells. Exposure of AMs to fluorescein isothiocyanate-labeled IAV in the presence of anti-fluorescein isothiocyanate antibody also resulted in viral protein synthesis. Thus, human AMs are apparently not susceptible to direct infection by a human IAV but are likely to be infected indirectly in the setting of exposure in the presence of antibody that binds the challenging strain of IAV. [ABSTRACT FROM AUTHOR]