Epidermal growth factor receptor is not required for human cytomegalovirus entry or signaling.

Epidermal growth factor receptor is not required for human cytomegalovirus entry or signaling. Research Abstract Details 

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Epidermal growth factor receptor is not required for human cytomegalovirus entry or signaling. Abstract Text:

Marisa K Isaacson,Adam L Feire,Teresa Compton,

Human cytomegalovirus (HCMV) can bind, fuse, and initiate gene expression in a diverse range of vertebrate cell types. This broad cellular tropism suggests that multiple receptors and/or universally distributed receptors mediate HCMV entry. Our laboratory has recently discovered that certain beta1 and beta3 integrin heterodimers are critical mediators of HCMV entry into permissive fibroblasts (A. L. Feire, H. Koss, and T. Compton, Proc. Natl. Acad. Sci. USA 101:15470-15475, 2004). It has also been reported that epidermal growth factor receptor (EGFR) is necessary for HCMV-mediated signaling and entry (X. Wang, S. M. Huong, M. L. Chiu, N. Raab-Traub, and E. E. Huang, Nature 424:456-461, 2003). Integrins are known to signal synergistically with growth factor receptors, and this coordination was recently reported for EGFR and beta3 integrins in the context of HCMV entry (X. Wang, D. Y. Huang, S. M. Huong, and E. S. Huang, Nat. Med. 11:515-521, 2005). However, EGFR-negative cell lines, such as hematopoietic cells, are known to be infected by HCMV. Therefore, we wished to confirm a role for EGFR in HCMV entry and then examine any interaction between beta1 integrins and EGFR during the entry process. Surprisingly, we were unable to detect any role for EGFR in the process of HCMV entry into fibroblast, epithelial, or endothelial cell lines. Additionally, HCMV did not activate the EGFR kinase in fibroblast cell lines. We first examined HCMV entry into two EGFR-positive or -negative cell lines but observed no increase in entry when EGFR was expressed to high levels. Physically blocking EGFR with a neutralizing antibody in fibroblast, epithelial, or endothelial cell lines or blocking EGFR kinase signaling with a chemical inhibitor in fibroblast cells did not inhibit virus entry. Lastly, we were unable to detect phosphorylation of EGFR in fibroblasts cells in response to HCMV stimulation. Our findings demonstrate that EGFR does not play a significant role in HCMV entry or signaling. These results suggest that specific integrin heterodimers either act alone as the primary entry receptors or interact in conjunction with an additional receptor(s), other than EGFR, to facilitate virus entry.

Epidermal growth factor receptor is not required for human cytomegalovirus entry or signaling. Publishing Authors By Initials

MK Isaacson,AL Feire,T Compton,

For similar biological phenomena, cell phenomena, and immunity: biological phenomena: microbiologic phenomena: viral physiology: virus internalization research abstracts see: biological phenomena, cell phenomena, and immunity: biological phenomena: microbiologic phenomena: viral physiology: virus internalization research

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MEDLINE DATE:

Epidermal growth factor receptor is not required for human cytomegalovirus entry or signaling. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Journal of virology

VOLUME: 81

Page Numbers: 6241-7

Journal Abbreviation: J. Virol.

ISSN: 0022-538X

DAY: 11

MONTH: 04

YEAR: 2007

Epidermal growth factor receptor is not required for human cytomegalovirus entry or signaling. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 113724

Epidermal growth factor receptor is not required for human cytomegalovirus entry or signaling. Keywords Mesh Terms:

KEYWORDS: Virus Internalization

MESH TERMS: metabolism

Chemical & Substance for Abstract: Epidermal growth factor receptor is not required for human cytomegalovirus entry or signaling. Information

Substance Name: Receptor, Epidermal Growth Factor

Registry Number: EC 2.7.1.112

Grant and Affiliation Information for Epidermal growth factor receptor is not required for human cytomegalovirus entry or signaling.

AFFILIATION: McArdle Laboratory for Cancer Research, University of Wisconsin-Madison Medical School 53706, USA.

Country: United States

AGENCY: United States NIAID

GRANT: R01 AI034998-10A1

ACRONYM: AI

MEDLINETA: J Virol

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