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-1β, 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.
Keywords: Cytokines, chemokines, interferon, influenza virus, interleukin, immunity, pathogenesis, macrophage, NK cell, T cell, B cell.
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