Viral infection.
The relationship between viruses and the cellular stress response is a multifaceted and complex phenomenon which depends on the structural and genetic characteristics of the virus, on the type of infection, as well as on the environmental conditions. It is now well documented that infection of mammalian cells by several types of RNA and DNA viruses often results in alterations of the cellular stress response. Interactions between stress proteins and viral components have been described in a large variety of experimental models at different stages of the viral life cycle, depending on the type of virus and host cell. The presence of heat shock proteins in intact virions has also been described. On the other hand, induction of HSP expression by hyperthermia or other agents results in alterations of the virus replication cycle during acute or persistent infections of mammalian cells, and a possible role of heat shock proteins in the beneficial effect of fever and local hyperthermia during acute infection has been hypothesized. This chapter describes the different aspects of the interaction between viruses and the stress response, and discusses the possible role of stress proteins in the control of virus replication and morphogenesis.
Santoro
M G
MG
Institute of Experimental Medicine, CNR, Rome, Italy.
D000163:Acquired Immunodeficiency Syndrome / Q000378:metabolism; D000818:Animals; D000998:Antiviral Agents / Q000494:pharmacology; D004267:DNA Viruses / Q000378:metabolism*; D005334:Fever; D005786:Gene Expression Regulation / Q000235:genetics; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D011454:Prostaglandins A / Q000494:pharmacology; D012328:RNA Viruses / Q000378:metabolism*; D013312:Stress, Physiological
D000998:Antiviral Agents; D006360:Heat-Shock Proteins; D011454:Prostaglandins A