TY - JOUR
T1 - Functional implications of mitochondrial reactive oxygen species generated by oncogenic viruses
AU - Choi, Young Bong
AU - Harhaj, Edward William
N1 - Publisher Copyright:
© 2014, Higher Education Press and Springer-Verlag Berlin Heidelberg.
PY - 2014/12/5
Y1 - 2014/12/5
N2 - Between 15% and 20% of human cancers are associated with infection by oncogenic viruses. Oncogenic viruses, including HPV, HBV, HCV and HTLV-1, target mitochondria to influence cell proliferation and survival. Oncogenic viral gene products also trigger the production of reactive oxygen species which can elicit oxidative DNA damage and potentiate oncogenic host signaling pathways. Viral oncogenes may also subvert mitochondria quality control mechanisms such as mitophagy and metabolic adaptation pathways to promote virus replication. Here, we will review recent progress on viral regulation of mitophagy and metabolic adaptation and their roles in viral oncogenesis.
AB - Between 15% and 20% of human cancers are associated with infection by oncogenic viruses. Oncogenic viruses, including HPV, HBV, HCV and HTLV-1, target mitochondria to influence cell proliferation and survival. Oncogenic viral gene products also trigger the production of reactive oxygen species which can elicit oxidative DNA damage and potentiate oncogenic host signaling pathways. Viral oncogenes may also subvert mitochondria quality control mechanisms such as mitophagy and metabolic adaptation pathways to promote virus replication. Here, we will review recent progress on viral regulation of mitophagy and metabolic adaptation and their roles in viral oncogenesis.
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U2 - 10.1007/s11515-014-1332-0
DO - 10.1007/s11515-014-1332-0
M3 - Review article
AN - SCOPUS:84916218348
SN - 1674-7984
VL - 9
SP - 423
EP - 436
JO - Frontiers in Biology
JF - Frontiers in Biology
IS - 6
ER -