Cytokines Induced During Influenza Virus Infection

Influenza A virus is one of the major human pathogens. The influenza infection can pass out without any subclinical symptoms or infestation can appear in upper respiratory tract as well as in lower respiratory tract where it can result in lethal outcome. Both innate and adaptive immune responses are activated shortly after infection providing protection against infection. Many activities of the cells of innate and adaptive immunity are coordinated by cytokines. However, inordinate or disbalanced immune response may result in overproduction of cytokines as well as chemokines which can lead to severe inflammation, including excessive recruitment of neutrophils and mononuclear cells at the site of infection. These may damage lung tissue, reduce respiratory capacity, and cause severe disease and mortality. Recently, the role of cytokines induced by virus infection has been reevaluated. While moderate inflammatory response protects against development of severe illness, the hyper-inflammatory response can elevate the disease progression. In this mini-review, we summarized the data on cytokines and chemokines induced in the sera of hospitalized patients infected with human and avian influenza viruses and define their possible role in pathogenesis. Interleukin IL-6 and chemokines CCL-2/MCP-1, CCL-4/MIP-1 beta, CXCL-8/IL-8, CXCL-9/MIG, and CXCL-10/IP-10 are associated with pathogenicity of both avian (H5N1 and H7N9) and human (pdmH1N1 and H3N2) viruses. Chemokines CCL-2/MCP-1, CXCL-8/IL-8, CXCL-9/MIG, and CXCL-10/IP-10 are also related with mortality. These cytokines may be used as targets for new, more complex therapy in the extenuation of unfavorable effects of hyper inflammatory response.