PROJECT TITLE :
Computational Study of Interdependence Between Hemagglutinin and Neuraminidase of Pandemic 2009 H1N1
Influenza sort A viruses are classified into subtypes based on their two surface proteins, hemagglutinin (HA) and neuraminidase (NA). The HA protein facilitates the viral binding and entering a number cell and also the NA protein helps the release of viral progeny from the infected cell. The complementary roles of HA and NA entail their collaboration, that has important implications for viral replication and fitness. The HA protein from early strains of pandemic 2009 H1N1 of swine origin preferentially binds to human type receptors with a weak binding to avian sort receptors. This virus caused many human deaths in December 2013 in Texas, USA, which motivated us to investigate the changes of genetic features that might contribute to the surged virulence of the virus. Our time series analysis on the strains of this virus collected from 2009 to 2013 implied that the HA binding preference of this virus in USA, Europe, and Asia has been the characteristic of swine H1N1 virus since 2009. But, its characteristic of seasonal human H1N1 and its binding avidity for avian kind receptors each were on steady rise and had a clear increase in 2013 with American strains having the sharpest surge. The first modification may enhance the viral transmission and replication in humans and therefore the second may increase its ability to cause infection deep in lungs, which would possibly account for the recent human deaths in Texas. In light of HA and NA coadaptation and evolutionary interactions, we tend to also explored the NA activity of this virus to reveal the functional balance between HA and NA throughout the course of virus evolution. Finally we have a tendency to identified amino acid substitutions in HA and NA of the virus that were vital for the observed evolution.
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