G. ZIMMER¹, E. MOREIRA², H. BOLTE², S. LOCHER¹, M. JUOZAPAITIS², T. AYDILLLO³, A. GARCÍA-SASTRE³, M. SCHWEMMLE<sup>2

1</sup>Institute of Virology and Immunology (IVI), Mittelhäusern, Switzerland, ²Institute of Virology, Medical Center, University of Freiburg, Freiburg, Germany, ³Icahn School of Medicine at Mount Sinai, New York, New York, USA

Two novel influenza A-like viral genome sequences have been recently identified in South American fruit bats and provisionally designated “H17N10” and “H18N11”. All efforts to isolate infectious virus from bats or to generate these viruses by reverse genetics have failed to date. Vesicular stomatitis virus (VSV) pseudotyped with bat influenza virus glycoproteins were used to identify cell lines that are susceptible to bat influenza virus infection. Madin-Darby canine kidney type II (MDCK II) cells were found to support replication of H18 but not H17 pseudotype virus. Entry in these cells was dependent on a low-pH triggered membrane fusion activity and sialidase pre-treatment did not abrogate infection. In contrast to conventional influenza A viruses infection occurred preferentially at the basolateral site. Cells of varies species revealed limited susceptibility to HA pseudotype virus infection with the notable exception of human U87-MG, SK-Mel 28 and Calu3 cells. Although to very low levels, infectious H18N11 but not H17N10 virus was recovered from transfected cells and passaged on MDCK II cells. Infection with H18N11 virus was efficiently neutralized by anti-H18 but not by anti-H17 immune sera. H18N11 preferentially infected polarized MDCK II cells from the basolateral site and sialidase pre-treatment did not abrogate HA18N11 infection, highlighting marked differences to conventional influenza A viruses. The ability of H18N10 to infect human cells might indicate increased zoonotic potential of these bat influenza A-like viruses.