2012
DOI: 10.1189/jlb.0112040
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Human cytomegalovirus induction of a unique signalsome during viral entry into monocytes mediates distinct functional changes: a strategy for viral dissemination

Abstract: Review on the viral entry process of HCMV and the potential role of receptor-ligand interactions in modulating monocyte biology. HCMV pathogenesis is a direct consequence of the hematogenous dissemination of the virus to multiple host organ sites. The presence of infected monocytes in the peripheral blood and organs of individuals exhibiting primary HCMV infection have long suggested that these blood sentinels are responsible for mediating viral spread. Despite monocytes being “at the right plac… Show more

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Cited by 62 publications
(89 citation statements)
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“…4F), indicating that increased transcription is not the only mechanism regulating protein expression. Nonetheless, since we have previously shown gH-initiated signaling to cross talk with EGFR (19), these data suggest that EGFR activation through both direct gB binding and indirect gH cross talk, as well as integrin activation through gH, is required for the increase in Mcl-1 and HSP27 mRNA levels.…”
Section: Fig 4 Hcmv-initiated Signaling Increasesmentioning
confidence: 81%
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“…4F), indicating that increased transcription is not the only mechanism regulating protein expression. Nonetheless, since we have previously shown gH-initiated signaling to cross talk with EGFR (19), these data suggest that EGFR activation through both direct gB binding and indirect gH cross talk, as well as integrin activation through gH, is required for the increase in Mcl-1 and HSP27 mRNA levels.…”
Section: Fig 4 Hcmv-initiated Signaling Increasesmentioning
confidence: 81%
“…Myeloid differentiation factors granulocyte macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF) block the activation of caspase 3 prior to the 48-h viability checkpoint (14,17). Similarly, we found that HCMV infection inhibited the activation of caspase 3 for the first 48 h postinfection (hpi), facilitating an antiapoptotic state and promoting monocyte-to-macrophage differentiation (14,18,19). The survival of infected short-lived monocytes is crucial for viral spread since, unlike monocytes, macrophages are permissive to viral replication (20)(21)(22)(23).…”
mentioning
confidence: 74%
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