Immune evasion strategies of Kaposi's sarcoma-associated herpesvirus.
To establish lifelong infection in the presence of an active host immune system, herpesviruses have acquired an impressive array of immune modulatory mechanisms that contribute to their success as long-term parasites. Kaposi's sarcoma-associated herpesvirus (KSHV) is the most recently discovered human tumor virus and is associated with the pathogenesis of Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease. KSHV has acquired a battery of genes to assist in viral survival against the host immune response. These viral gene products target a variety of host immune surveillance mechanisms, including the cytokine-mediated immune response, apoptosis, natural killer (NK) cell killing and T cell-mediated responses. This review summarizes our understanding of the role of these viral proteins in the escape from host immune surveillance, which ultimately contributes to lifelong infection and pathogenesis of KSHV.
Means
R E
RE
Department of Microbiology and Molecular Genetics, Tumor Virology Division, New England Regional Primate Research Center, Harvard Medical School, 1 Pine Hill Drive, Southborough, MA 01772, USA.
Choi
J K
JK
Nakamura
H
H
Chung
Y H
YH
Ishido
S
S
Jung
J U
JU
D000818:Animals; D017209:Apoptosis; D016207:Cytokines; D005814:Genes, Viral; D006566:Herpesviridae Infections / Q000276:immunology*; D019288:Herpesvirus 8, Human / Q000235:genetics / Q000276:immunology*; D006801:Humans; D007110:Immunity, Active / Q000235:genetics; D007113:Immunity, Innate / Q000235:genetics; D007372:Interferons; D007694:Killer Cells, Natural; D013602:T-Lymphocytes, Cytotoxic; D014764:Viral Proteins / Q000276:immunology; D014779:Virus Replication
D016207:Cytokines; D014764:Viral Proteins; D007372:Interferons