The IgA antibodies, which have higher avidity than IgG antibodies, can readily access mucosal viral antigens and are able to provide protection against heterologous strains [20]

The IgA antibodies, which have higher avidity than IgG antibodies, can readily access mucosal viral antigens and are able to provide protection against heterologous strains [20]. the second immunization, pigs were challenged with the antigenic variant Swine/MN/08 H1N1 (MN08) and the heterologous Swine/NC/10 H1N2 (NC10) influenza virus. Antibodies in serum and respiratory tract, lung lesions, virus shedding in nasal secretions and virus load in lungs were assessed. Intranasal administration of PAV induced challenge viruses specific-hemagglutination inhibition- and IgG antibodies in the serum and IgA and IgG antibodies in the respiratory tract. Importantly, intranasal administration of PAV provided protection against the antigenic variant MN08 and the heterologous NC10 swine influenza viruses as evidenced by significant reductions in lung virus load, gross lung lesions and significantly reduced shedding of challenge viruses in Rabbit Polyclonal to TACD1 nasal secretions. These results indicate that Poly I:C or its homologues may be effective as vaccine adjuvants capable of generating cross-protective immunity against antigenic variants/heterologous swine influenza viruses in pigs. Keywords: Inactivated swine influenza vaccines, Swine influenza virus, Vaccine adjuvants, Poly I:C 1.?Introduction The genetic diversity of swine influenza A virus (SIV) in North America has increased in the last two decades. However, the majority of the SIV infections in pigs are caused by subtypes H1N1, H1N2 and H3N2 [1]. Emergence of the H3N2 subtype containing a triple reassortment internal gene (TRIG) cassette contributed vastly to the generation of antigenic divergent reassortant viruses [2], [3]. The hemagglutinin (HA) gene in these H3N2 viruses was derived from the different seasonal human influenza viruses. Subtypes containing H1 also exhibited a high rate of divergence and are currently classified into clusters , , and . The emergence of the 2009 2009 H1N1 pandemic virus (H1N1 pdm09) and its subsequent reassortments with the recent H3N2 variant increased the antigenic variation of SIV [4], [5], [6], [7]. A Imidafenacin combination of some of the HA gene alleles and TRIG cassettes might be contributing towards survival and propagation of emerging SIV variants in pigs [8]. Establishment of these antigenic variants in the swine population poses a zoonotic threat as they can be transmitted to humans. Current vaccine approaches are inadequate to counter the antigenic diversity of SIV because the vaccine-derived protective immunity is typically strain-specific [9], [10]. Vaccination against SIV is routinely Imidafenacin employed in swine farms. Most of the commercial vaccines are Imidafenacin bivalent or trivalent and contain whole inactivated virus. The SIV strains used in these vaccines vary between regions and their protective efficacies depend on the strains prevalent in those areas. Although inactivated vaccines are effective against homologous strains, only limited protection is offered against heterologous strains [11], [12]. Moreover, inactivated SIV vaccines are also associated with development of vaccine-associated enhanced respiratory disease (VAERD) [13], [14]. This happens when the vaccine and challenge strains belong to the same subtype but differ due to antigenic drift. Another weakness of currently employed commercial inactivated vaccines is that these products are administered by an intramuscular route and do not induce adequate mucosal immunity [15]. This is important because cross-protective activity of influenza vaccines is largely correlated to mucosal immunity. Intranasal administration of live attenuated SIV vaccines containing virus with truncated NS1 protein [16] and modified HA protein [17], [18] developed both mucosal and humoral antibodies in Imidafenacin different animal species. Similarly, an intranasal inoculation of seasonal trivalent inactivated vaccine provided mucosal immunity in mice [19]. These vaccines provided protection against both homologous and heterologous strains. Intranasal vaccine administration induced a higher secretory IgA production when compared with administration by the parenteral route. The IgA antibodies, which have higher avidity than IgG antibodies, can readily access mucosal viral antigens and are able to provide protection against heterologous strains [20]. Furthermore, use of an effective mucosal adjuvant in conjunction with intranasal vaccine administration could enhance vaccine efficiency. Poly (I:C), a synthetic double-stranded RNA,.