TY - JOUR
T1 - Apoptosis
T2 - An innate immune response to virus infection
AU - Everett, Helen
AU - McFadden, Grant
N1 - Funding Information:
Supported by the National Cancer Institute and the Medical Research Council of Canada (MRC). We were previously supported by the Alberta Heritage Foundation for Medical Research, and G.M. is currently a Senior Scientist of the MRC. We thank Michele Barry for insightful comments, and D’vorah Elias for help with the manuscript.
PY - 1999/4/1
Y1 - 1999/4/1
N2 - Viruses can induce apoptosis of infected cells either directly, to assist virus dissemination, or by inadvertently triggering cellular sensors that initiate cell death. Cellular checkpoints that can function as 'alarm bells' to transmit pro- apoptotic signals in response to virus infections include death receptors, protein kinase R, mitochondrial membrane potential, p53 and the endoplasmic reticulum.
AB - Viruses can induce apoptosis of infected cells either directly, to assist virus dissemination, or by inadvertently triggering cellular sensors that initiate cell death. Cellular checkpoints that can function as 'alarm bells' to transmit pro- apoptotic signals in response to virus infections include death receptors, protein kinase R, mitochondrial membrane potential, p53 and the endoplasmic reticulum.
UR - http://www.scopus.com/inward/record.url?scp=0032894113&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032894113&partnerID=8YFLogxK
U2 - 10.1016/S0966-842X(99)01487-0
DO - 10.1016/S0966-842X(99)01487-0
M3 - Review article
C2 - 10217831
AN - SCOPUS:0032894113
SN - 0966-842X
VL - 7
SP - 160
EP - 165
JO - Trends in microbiology
JF - Trends in microbiology
IS - 4
ER -