Immune response to poxvirus infections in various animals.
The study of infections of vertebrate animals by poxviruses has remained a dynamic area of research for the last century. The host range of poxviruses vary from extremely narrow to exceedingly broad, and they have been shown to enter their host by either the respiratory route or through the skin. The severity of infection varies dramatically from one species to another, causing anywhere from a local, self-limiting infection, to a devastating systemic disease, such as smallpox. Although the immune response to poxvirus infections are very similar to that seen in other viral infections, the poxviruses, unlike most other viruses (with the exception of Herpes viruses), are able to defend themselves. They have been shown to carry a repertoire of proteins involved in immune evasion and immune modulation. Poxviruses encode proteins involved in blocking many of the strategies employed by the host to combat viral infections; they encode for proteins that block activity of many chemokines, cytokines, serine proteases, and even complement. Traditionally, different animal models have been used to study the pathogenesis of poxvirus infections, and the characterization of virulence genes using mutant poxviruses. Additionally, new animal models are being developed to study the possible therapeutic uses many of these poxvirus immune modulating proteins might have. This review discusses the host immune response against poxvirus infections in various animals, the viral counter response to the host, and the animal models used to study poxvirus infection and immune modulating proteins.
Smith
Scott A
SA
Department of Microbiology and Immunology, University of Louisville School of Medicine, KY, USA.
Kotwal
Girish J
GJ
D000818:Animals; D000914:Antibodies, Viral / Q000276:immunology; D000920:Antibody-Dependent Cell Cytotoxicity / Q000276:immunology; D002642:Chick Embryo; D003165:Complement System Proteins / Q000502:physiology; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000276:immunology; D007372:Interferons / Q000502:physiology; D007694:Killer Cells, Natural / Q000276:immunology; D051379:Mice; D018448:Models, Immunological; D011212:Poxviridae / Q000145:classification / Q000254:growth & development / Q000472:pathogenicity*; D011213:Poxviridae Infections / Q000150:complications / Q000276:immunology / Q000662:veterinary*; D011817:Rabbits; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D014616:Vaccinia virus / Q000254:growth & development / Q000276:immunology; D012901:Variola virus / Q000254:growth & development / Q000276:immunology; D014780:Viruses / Q000145:classification / Q000276:immunology
D000914:Antibodies, Viral; D016207:Cytokines; D003165:Complement System Proteins; D007372:Interferons