Antibody and inflammatory response-mediated severity of pandemic 2009 (pH1N1) influenza virus.

Influenza A virus causes significant morbidity and mortality each year worldwide due to antigenic drift, punctuated by infrequent pandemics following antigenic shift. H1N1 subtype of pandemic 2009 (pH1N1) influenza virus lineages has continued to circulate in humans and raised severe concerns about its pandemic developments. The pathogenesis of the disease and its progression as post-infectious sequelae is not well understood. Moderate inflammatory response protects against the ill effects and hyper-inflammatory response promotes the pathogenesis in disease progression. Samples were screened by RT-PCR and classified in pandemic 2009 (pH1N1), Influenza A virus infected patient. Further antibody titer was analyzed by hemagglutination inhibition assay and cytokine/chemokine response by Cytometric bead array assy. Screening of 216 patients shows 63 were belongs to pH1N1 influenza virus infection and 47 were Influenza A virus infected and 106 samples were negative for these viruses, were used as a disease control. Apart from that 100 samples were taken for healthy control. Lower antibody titer was found in patient infected with pH1N1/Influenza A virus and expression of cytokines (IL-6, IL-8, and IL-10) and chemokine MCP-1 was higher in patient infected with pH1N1 compare to healthy/disease control however there was no significant difference observed in the expression of pro-inflammatory cytokines TNF-α and antiviral cytokine IFN-γ in pH1N1 influenza virus infected patients.