[Immune evasion of alphaherpesviruses].
Alphaherpesviruses represent the largest subfamily of the herpesviruses and comprise many different, closely related pathogens of man and animal, including herpes simplex virus (cold sores, genital lesions) and varicella-zoster virus (chickenpox, shingles) in man, pseudorabies virus orAujeszky's disease virus in pigs (neurological and respiratory symptoms, abortion), equine herpesvirus type 1 (neurological and respiratory symptoms, abortion), and bovine herpesvirus type 1 (respiratory symptoms, abortion). Typical for alphaherpesviruses, and for herpesviruses in general, is their ability to persist in a non-replicative, latent state in their host during its entire lifetime. Specific stimuli can lead to reactivation of these viruses from their latent state, which can lead to renewed spread within and between hosts and recurrent symptoms. This recurrent replication and spread implies that herpesviruses have evolved techniques to delay and avoid recognition and elimination by the immune system, so-called immune evasion mechanisms. In the current manuscript, different alphaherpesvirus immune evasion mechanisms will be reviewed that have been discovered and elucidated at our research group based on pseudorabies virus and that interfere with the antiviral activity of virus-specific antibodies. Investigating immune evasion mechanisms leads to novel insights in the interactions between viruses, host cells, and the immunity, but can also lead to novel avenues in the design of strategies to interfere with viral infections.
Favoreel
H W
HW
Vakgroep Virologie Parasitologie en Immunologie, Faculteit Diergeneeskunde, Universiteit Gent, Merelbeke.
D018138:Alphaherpesvirinae / Q000276:immunology*; D000818:Animals; D006561:Herpes Simplex / Q000276:immunology; D006562:Herpes Zoster / Q000276:immunology; D006566:Herpesviridae Infections / Q000276:immunology / Q000635:transmission / Q000821:virology*; D006801:Humans; D018139:Simplexvirus / Q000276:immunology; D013045:Species Specificity; D014775:Virus Activation; D017735:Virus Latency; D014779:Virus Replication