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Host Specific Subversion Of The MAPK‐Dependent Apoptotic Response To B Virus Infection
Author(s) -
FarahAbraham Rachael,
Hilliard Julia
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb181
Subject(s) - biology , p38 mitogen activated protein kinases , apoptosis , virus , microbiology and biotechnology , mapk/erk pathway , protein kinase r , interferon , signal transduction , virology , viral replication , immune system , protein kinase a , phosphorylation , immunology , genetics , mitogen activated protein kinase kinase
B virus (Macacine herpesvirus 1) is an alphaherpesvirus indigenous to Old World monkeys & is closely related to HSV‐1. B virus produces mild/no disease in its natural host. When transmitted to humans, it replicates at the site of injury & invades the CNS/travels directly to the CNS. In humans high morbidity & mortality are associated in 80% untreated cases. Five major signaling pathways can be activated after infection, inclusive of the MAPK pathway. Early stimulation of one/more of these pathways leads to the induction of cytokines & apoptosis. Apoptotic induction plays an important role in host‐pathogen interaction & adaptive immune responses. This study investigated host‐specific regulation of B virus induced apoptosis via p38 & JNK (MAPK) pathways in cells derived from the natural & foreign host. Our data suggest that macaque & human cells temporally differ in the induction of p38 & JNK. The overall early induction & downstream phosphorylation of factors associated with apoptotic events are significantly greater in cells derived from the foreign host. The use of specific inhibitors demonstrated that inhibition of p38 resulted in a decrease in virus replication & lowered levels of proteins associated with apoptosis. By investigating the role of B virus viral genes in the differential induction & regulation of the MAPK pathway early after infection, we can further elucidate virus‐induced host specific modulations.