title: Viral immune evasion: a masterpiece of evolution.
abstract: Coexistence of viruses and their hosts imposes an evolutionary pressure on both the virus and the host immune system. On the one hand, the host has developed an immune system able to attack viruses and virally infected cells, whereas on the other hand, viruses have developed an array of immune evasion mechanisms to escape killing by the host's immune system. Generally, the larger the viral genome, the more diverse mechanisms are utilized to extend the time-window for viral replication and spreading of virus particles. In addition, herpesviruses have the capacity to hide from the immune system by their ability to establish latency. The strategies of immune evasion are directed towards three divisions of the immune system, i.e., the humoral immune response, the cellular immune response and immune effector functions. Members of the herpesvirus family are capable of interfering with the host's immune system at almost every level of immune clearance. Antibody recognition of viral epitopes, presentation of viral peptides by major histocompatibility complex (MHC) class I and class II molecules, the recruitment of immune effector cells, complement activation, and apoptosis can all be impaired by herpesviruses. This review aims at summarizing the current knowledge of viral evasion mechanisms.
authors.affiliation: Department of Experimental Immunology, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: Mireille T M
authors.initials: MT
authors.lastname: Vossen
authors.forename: Ellen M
authors.initials: EM
authors.lastname: Westerhout
authors.forename: Cécilia
authors.initials: C
authors.lastname: Söderberg-Nauclér
authors.forename: Emmanuel J H J
authors.initials: EJ
authors.lastname: Wiertz
mesh_terms: D000818:Animals; D000917:Antibody Formation; D017951:Antigen Presentation; D017209:Apoptosis; D005075:Biological Evolution; D003167:Complement Activation; D016207:Cytokines / Q000096:biosynthesis; D007109:Immunity; D007111:Immunity, Cellular; D008954:Models, Biological; D015398:Signal Transduction; D015163:Superinfection / Q000276:immunology; D014777:Virus Diseases / Q000276:immunology; D014780:Viruses / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity*
chemical_list: D016207:Cytokines