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Influenza A Virus Essay

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In the human body, there are commensal bacteria serving as part of the normal flora. Various viruses can interact with these bacteria in order promote their infectivity. Poliovirus can bind with bacterial lipopolysaccharide (LPS) for stabilization to prevent premature RNA release and improve cell attachment to host cell through the poliovirus receptor. For retroviruses, specifically MMTV (mouse mammary tumor virus), binding to LPS improve their chances of successful transmission. MMTV-bound LPS get binds to toll-like receptor 4, which is a pattern recognition receptor of LPS. This event eventually leads to the induction of interleukin-10 (IL-10), which is an immune response inhibitory cytokine. By producing IL-10, it allows MMTV to go undetected by the …show more content…

Furthermore, bacteria and virus interactions extend beyond the binding of virus with normal intestinal microbiota. Through the co-infection on influenza A virus and Streptococcus pneumoniae, it increases chances of mortality. It is important to note that the two are working together rather than through any direct binding to increase infectivity. Prior infection with Influenza A virus allows for colonization of S. pneumoniae in the nasopharynx. Sialic acid, a non-reducing sugar, is released from cells and mucus after cleavage by influenza neuraminidase. The sialic acid serves as a nutrient source for S. pneumoniae for colonization. In addition, a deficient of the S. pneumoniae’s neuraminidase, NanA (neuraminidase A), which is essential for breaking down of sialic acid to allow for adherence to host cells can decrease colonization. During co-infection, influenza virus can partially restore nasal colonization of NanA-deficient pneumococci. Co-infection is also beneficial for the virus since it can decrease specific influenza antibodies. Another study also present that having respiratory syncytial virus (RSV) can increase the risk for acute otitis

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