Short communicationHerpesvirus saimiri has a gene specifying a homologue of the cellular membrane glycoprotein CD59
References (35)
- et al.
Virology
(1990) - et al.
Cell
(1988) - et al.
J. Mol. Biol.
(1990) - et al.
Mol. Immunol.
(1989) - et al.
Immunol. Today
(1989) - et al.
Arch. Virol.
(1992) - et al.
J. Virol.
(1986) - et al.
J. Virol.
(1984) - et al.
Science
(1985)
J. Virol.
J. Virol.
J. Virol.
EMBO J.
Nucleic Acids Res.
Nucleic Acids Res.
Science
Cited by (87)
Sequestration of host-CD59 as potential immune evasion strategy of Trichomonas vaginalis
2015, Acta TropicaCitation Excerpt :Thus, it is necessary to determine how CD59 is anchored to the parasites surface will be further investigated. There are numerous reports of bacteria, viruses, and parasites overcoming complement by having CD59-like molecules via acquisition of complement inhibitors or by lysis of complement proteins directly (Albrecht et al., 1992; Würzner, 1999). For example, the Herpes virus, Hepatitis C virus, and HIV escape from complement via capsid incorporation of CD59 obtained from the host (Saifuddin et al., 1997; Amet et al., 2012; Ejaz et al., 2012).
Viral regulators of complement activation: Structure, function and evolution
2014, Molecular ImmunologyCitation Excerpt :As expected, the mimics of complement regulatory proteins are found only in viruses with a larger coding capacity like poxviruses and herpesviruses. These viruses have been found to express homologs of the regulators of complement activation (RCA) (Mullick et al., 2003b) as well as non-RCA (CD59 (Albrecht et al., 1992; Bramley et al., 1997) and HSV gC (Friedman et al., 1984)) proteins. In the present review, we provide an overview on the structure, function and evolution of the virus-encoded RCA (vRCA) proteins.
Complement and its role in protection and pathogenesis of flavivirus infections
2008, VaccineCitation Excerpt :To minimize recognition and/or destruction by complement several different families of viruses have evolved strategies to evade or exploit complement to establish infection (reviewed in [83–87]). Complement evasion mechanisms include: (a) use of complement receptors to enhance viral entry or suppress adaptive immune response (e.g., HIV, West Nile virus (WNV), measles virus, adenoviruses, herpesviruses, enteroviruses, hepatitis B and C viruses [88–126]); (b) expression of viral proteins that directly inhibit complement (e.g., herpesviruses, coronaviruses, and astroviruses [127–136]); (c) modulation of expression of complement regulators on host cells to prevent complement-dependent lysis (e.g., herpesviruses [137–139]); (d) incorporation of human regulators on the surface of virions to protect from complement-mediated virolysis (e.g. HIV, HTLV, cytomegalovirus, and vaccinia virus [140–146]); (e) recruitment of soluble complement regulatory proteins to the virion or infected cell surface (e.g., WNV and HIV [147–151]); (f) expression of viral decoy proteins that structurally or functionally mimic complement regulatory proteins (e.g., poxviruses and herpesviruses [152–159]. A single virus may utilize several independent strategies to escape from recognition and targeting by complement and modulate the immune response to establish persistent infection.
T-cell transformation and oncogenesis by γ2-herpesviruses
2005, Advances in Cancer ResearchThe relevance of complement to virus biology
2004, Virology
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