Influenza A, B and C are the most important genera of the Orthomyxoviridae family, casusing both pandemic and seasonal disease in humans. Influenza A viruses are enveloped, single-stranded RNA viruses with a segmented genome (Table 1 ) [1] . They are classified into subtypes on the basis of the antigenic properties of the hemagglutinin (HA) and neuraminidase (NA) glycoproteins expressed on the surface of the virus [1, 2] . Influenza A viruses are characterized by their pathogenicity, with highly pathogenic avian influenza (HPAI) causing severe disease or death in domestic poultry [3] . Molecular changes in the RNA genome occur through two main mechanisms: point mutation (antigenic drift) and RNA segment reassortment (antigenic shift) [4, 5] . Point mutations cause minor changes in the antigenic character of viruses and are the primary reason a vaccination for influenza A is given yearly. Reassortment occurs when a host cell is infected with two or more influenza A viruses, leading to the creation of a novel subtype. The influenza subtypes of the 1957 (H2N2) and 1968 (H3N2) pandemics occurred through reassortment, while the origins of the 1918 (H1N1) pandemic are unclear.