[[Image:Innate viral response.jpg|thumb|right|150px|Innate response to dsRNA - B. Catchpole, RVC 2008]]
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Because viruses invade host cells to take over a host's cellular machinery, the innate system has a more difficult time detecting viruses as foreign agents. However, there is a give-away element of the viral attack that the innate system can recognize: the '''double-stranded RNA''' (dsRNA) produced by a virus in its replication phase. Because mammalian cells only ever produce single-stranded RNA, the presence of dsRNA signals a foreign intruder. dsRNA can be detected by TLR-3R on the cell surface or intracellularly by the presence of dsRNA-dependent protein kinase.
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The innate response to viral attack also depends on the presence of '''Type-1 Interferons''', which are produced by all cells on recognition of a viral attack. Interferons serve to increase degradation of mRNA, inhibit protein synthesis, and increase the effectiveness of the adaptive response by increasing antigen presentation to antibody.
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Lastly, the final line of defense for the innate response to viruses lies in the actions of [[Lymphocytes#Natural Killer (NK) Cells|'''Natural Killer (NK) cells''']]. These warriors monitor the production of [[MHC - WikiBlood|MHC]] (Major Histocompatibility Complex) on the surface of cells, which is produced as part of the adaptive response. A cell whose cellular machinery is compromised by viral infection will experience a drop in the amount of MHC it produces. When a cell's MHC production drops, NK cells are triggered to phagocytose these cells. As such, this is a non-specific targeting based simply on the ability of a cell to function normally, which also lends them to playing a role in targeting malignant cells. NK cells are incapable of directly targeting viral infection.