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Bat-borne influenza viruses enter host cells by utilizing surface exposed MHC-II molecules of various species, including humans. Now, an international research team from Germany (Medical Center—University of Freiburg and Friedrich-Loeffler-Institut, island of Riems) and the United States (Colorado State University, Fort Collins and Kansas State University, Manhattan) addressed concerns about the zoonotic spill-over potential and discovered an unexpected high genetic plasticity of the bat influenza virus H18N11 with unpredictable consequences.
"Influenza viruses have an inherent high mutation rate," explains Prof. Martin Schwemmle of the Medical Center—University of Freiburg and coordinator of this study. "We therefore first tested the bat flu virus' genetic stability to assess its natural mutational potential in cell culture." To their surprise, within a short period of time all isolated viruses acquired specific amino acid mutations in the viral hemagglutinin (HA) and a truncated neuraminidase (NA) surface glycoprotein. The scientists performed further experiments and showed that these amino acids changes in HA enabled an NA independent viral growth. "Using a variety of mutant viruses, we finally demonstrated that in the absence of a mutated HA, functional NA is required for viral spread." While the role of the mysterious NA protein has been unknown so far, the researchers found some evidence that its...
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