Influenza is one of the major respiratory virus that causes nearly annual epidemics and occasional pandemics. Influenza epidemics generally occur in the winter months in the Northern hemisphere and May-September in the Southern hemisphere (Cox et al, 2004). This virus belongs to the genus Orthomyxovirus in the family of Orthomyxoviridae. Influenza A viruses are enveloped RNA virus with eight RNA segments that encodes for upto 11 viral genes ( Lamb &Krug ,2001, Fields virology, 4th edt. ).The genome is segmented, with 8 RNA fragments (7 for influenza C). There are 4 antigens present, the hemagglutinin (HA), neuraminidase (NA), the matrix (M) and the nucleocapsid proteins. HA and NA are the major antigenic proteins which classify influenza
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(Hovden et al,2007). Influenza infection is initiated by the viral hemagglutinin (HA) binding to sialic acid receptors on the surface of the host cell. This is widely acceptable that the human-specific HA subtypes selectively bind to the α(2,6)-sialic acid linkage, while the avian-specific HA subtypes selectively bind to the α(2,3)-sialic acid linkage. This selective binding is the key determinant for the host tropism (Garcia Sastre., 2010). The HA protein binds to sialic acid-containing receptors on the host cell surface and mediates fusion of the viral envelope with the endosomal membrane after receptor-mediated endocytosis ( Lakadamyali et al. , 2004). The NA protein plays a crucial role late in infection by removing sialic acid from sialyloligosaccharides, thereby releasing newly assembled virions from the cell surface and preventing the self-aggregation of virus particles (Watanbe et al, 2010). ).M2 is a very minor component of the envelope, with only 16 to20 molecules per virion. Underneath the lipid bilayer lies the matrix protein (M1), a major structural protein. Within the virus shell are eight viral ribonucleoprotein (vRNP) complexes, each composed of viral RNA associated with the nucleoprotein NP and the three components of the viral RNA polymerase complex (PB2, PB1, and PA) (Samji T. ,2009).
(Hovden et al,2007). Influenza infection is initiated by the viral hemagglutinin (HA) binding to sialic acid receptors on the surface of the host cell. This is widely acceptable that the human-specific HA subtypes selectively bind to the α(2,6)-sialic acid linkage, while the avian-specific HA subtypes selectively bind to the α(2,3)-sialic acid linkage. This selective binding is the key determinant for the host tropism (Garcia Sastre., 2010). The HA protein binds to sialic acid-containing receptors on the host cell surface and mediates fusion of the viral envelope with the endosomal membrane after receptor-mediated endocytosis ( Lakadamyali et al. , 2004). The NA protein plays a crucial role late in infection by removing sialic acid from sialyloligosaccharides, thereby releasing newly assembled virions from the cell surface and preventing the self-aggregation of virus particles (Watanbe et al, 2010). ).M2 is a very minor component of the envelope, with only 16 to20 molecules per virion. Underneath the lipid bilayer lies the matrix protein (M1), a major structural protein. Within the virus shell are eight viral ribonucleoprotein (vRNP) complexes, each composed of viral RNA associated with the nucleoprotein NP and the three components of the viral RNA polymerase complex (PB2, PB1, and PA) (Samji T. ,2009).