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9.1.1 Effects on biosynthetic pathways
Virus infection to a host cell inhibits its DNA and/or RNA, and its protein synthesis. Sometimes it also causes breakage and fragmentation of host chromosome. Moreover it also changes the growth characteristics, shape, and surface protein expression of the infected host cell. Viruses often subvert the host biosynthetic pathway for their own benefits at the cost of cellular macromolecules.
Virus infection to a cell forms many early proteins that mediate the changes in cellular biochemical pathways. Viral nucleic acid contains specific signal sequences that help in migration of nucleic acids to different cellular locations. In addition, it also contains some motifs that bind to regulators of cellular transcriptional machinery. Therefore many viral early proteins contain binding sites for a wide range of cellular transcriptional factor. These interactions and bindings are very important for the activation of virus protein synthesis and production of progeny viruses. The biochemical events sometimes include glycosylation and phosphorylation of viral proteins. These modifications are often associated with the increase or decrease of the pathogenicity and virulence of the viruses. Generally virus alters the cascades that are involved in the synthesis of protein kinases and secondary messengers (cyclic AMP,cyclic GMP, etc). Occasionally virus triggers the cells to overproduce regulatory proteins that changes the cellular biochemical pathways. These regulatory proteins may be transforming growth factors, interleukins, cytokines, NF-kβ or TNFα and TNFβ (HIVand Herpesviruses). In some viral infections cellular mRNA get degraded (Influenza virus). Alternatively herpesviruses and reoviruses inhibit the cellular DNA synthesis. Interestingly Pox virus degrades the host DNA with the help of virus associated DNase.
9.1.2 Effects on cell morphology
Changes evident in a cell following the virus infection are called cytopathic effects (CPE). There are various kinds of CPE depending on type of infection. For example, detachment of cells from monolayer, rounding of cells, formation of syncytia (multinucleated cells formed after fusion of nuclei) and nuclear or cytoplasmic inclusion bodies formation.