2009
DOI: 10.1073/pnas.0908787106
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Activation of EGFR on monocytes is required for human cytomegalovirus entry and mediates cellular motility

Abstract: Human cytomegalovirus (HCMV) rapidly induces a mobile and functionally unique proinflammatory monocyte following infection that is proposed to mediate viral spread. The cellular pathways used by HCMV to initiate these biological changes remain unknown. Here, we document the expression of the epidermal growth factor receptor (EGFR) on the surface of human peripheral blood monocytes but not on other blood leukocyte populations. Inhibition of EGFR signaling abrogated viral entry into monocytes, indicating that EG… Show more

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Cited by 170 publications
(309 citation statements)
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“…1). [38][39][40] CD90 has also been linked to HCMV entry, possibly through interaction with HCMV envelope associated glycoproteins. 41 Interestingly, HCMV infection strongly up-regulates expression of PDGFR and CD61, slightly increases CD90 but has no effect on CD29 or EGFR.…”
Section: Discussionmentioning
confidence: 99%
“…1). [38][39][40] CD90 has also been linked to HCMV entry, possibly through interaction with HCMV envelope associated glycoproteins. 41 Interestingly, HCMV infection strongly up-regulates expression of PDGFR and CD61, slightly increases CD90 but has no effect on CD29 or EGFR.…”
Section: Discussionmentioning
confidence: 99%
“…For example, EGFR mediates the uptake of cytomegalovirus by monocytes and influenza A virus by epithelial cells (18,19). Also, HER2 signaling stimulates endothelial cell invasion by Neisseria meningitidis and neuronal demyelination in response to Mycobacterium leprae (20,21).…”
Section: Discussionmentioning
confidence: 99%
“…Understanding how HCMV overcomes these biological barriers following infection may provide clues to the underlying causes of HCMV pathogenesis and persistence. Our laboratory has provided molecular evidence for how HCMV evolved to deal with these biological barriers (16)(17)(18)(19)(20)(21)(22).We have shown that the biological changes in HCMV-infected monocytes are triggered by the binding of gB to EGFR (19) and binding of the gH/gL/UL128-131 complex to β1 and β3 integrins (7, 18). These receptor-ligand interactions trigger the EGFR and integrin signaling cascades, promoting enhanced motility and viral entry into monocytes (16,19).…”
mentioning
confidence: 99%
“…Understanding how HCMV overcomes these biological barriers following infection may provide clues to the underlying causes of HCMV pathogenesis and persistence. Our laboratory has provided molecular evidence for how HCMV evolved to deal with these biological barriers (16)(17)(18)(19)(20)(21)(22).…”
mentioning
confidence: 99%
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