Immune evasion by herpes simplex virus type 1, strategies for virus survival.
Many viruses capable of persistent or recurrent infections have evolved strategies to evade host immunity. Viral evasion molecules target components of innate and acquired immunity, including complement proteins, natural killer cells, MHC Class I or Class II molecules and antibody. Our work focuses on HSV-1 glycoproteins gC and gE that impair antibody and complement responses. gC inhibits complement activation by binding C3b and blocking activities mediated by this pivotal complement protein, while gE binds the IgG Fc domain, blocking Fc-mediated activities, including complement activation and antibody-dependent cellular cytotoxicity. HSV-1 mutant viruses that lack the ability to bind C3b, IgG Fc, or both are much less virulent than wild-type virus in a murine model. These HSV-1 immunoevasins help explain the virus' ability to produce recurrent infections despite intact immunity. Strategies to prevent immune evasion may be required to develop successful HSV vaccines.
Friedman
Harvey M
HM
University of Pennsylvania, Philadelphia, PA 19104-6073, USA. hfriedma@mail.med.upenn.edu
D000818:Animals; D000914:Antibodies, Viral; D005260:Female; D006561:Herpes Simplex / Q000276:immunology / Q000517:prevention & control / Q000821:virology; D018259:Herpesvirus 1, Human / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity*; D022283:Herpesvirus Vaccines / Q000302:isolation & purification; D007116:Immunization, Passive; D051379:Mice; D008807:Mice, Inbred BALB C; D009154:Mutation; D009500:Neutralization Tests; D014759:Viral Envelope Proteins / Q000235:genetics / Q000276:immunology; D014774:Virulence / Q000235:genetics / Q000276:immunology
D000914:Antibodies, Viral; D022283:Herpesvirus Vaccines; D014759:Viral Envelope Proteins; C044768:glycoprotein E, herpes simplex virus type 1; C038535:glycoprotein gC, herpes simplex virus type 1