Year-end Sale % OFF 
Abstract
Viruses have evolved diverse strategies to manipulate cellular signaling pathways in order to promote infection and/or persistence. Human cytomegalovirus (HCMV) possesses a number of unique properties that allow the virus to alter cellular events required for infection of a diverse array of host cell types and long-term persistence. Of specific importance is infection of bone marrow derived and myeloid lineage cells, such as peripheral blood monocytes and CD34+ hematopoietic progenitor cells (HPCs) because of their essential role in dissemination of the virus and for the establishment of latency. Viral induced signaling through the Epidermal Growth Factor Receptor (EGFR) and other receptors such as integrins are key control points for viral-induced cellular changes and productive and latent infection in host organ systems. This review will explore the current understanding of HCMV strategies utilized to hijack cellular signaling pathways, such as EGFR, to promote the wide-spread dissemination and the classic life-long herpesvirus persistence.
Highlights
Human cytomegalovirus (HCMV) infection is a significant public health threat worldwide (Stagno et al, 1986; Bentz et al, 2006; Arvin, 2007; Nogalski et al, 2014; Fulkerson et al, 2021)
Infiltration of infected monocytes into host organ systems allows for viral spread to additional hosts through release of new virus in a variety of body fluids and spread to the bone marrow where latency is established in CD34+ hematopoietic progenitor cells (HPCs)
Integrins We previously described that viral engagement of β1 and β3 integrins are essential for infection of human peripheral monocytes via the interaction of the HCMV gH/gL/UL128-131 complex with these two integrin families [Figure 2 (Nogalski et al, 2013; Kim et al, 2016)]
Summary
Human cytomegalovirus (HCMV) infection is a significant public health threat worldwide (Stagno et al, 1986; Bentz et al, 2006; Arvin, 2007; Nogalski et al, 2014; Fulkerson et al, 2021). HCMVinfected monocytes are initially short lived and are nonpermissive for productive infection (Yurochko et al, 1989, 1990, 1992, 1995, 1997a,b, 1999; Taylor-Wiedeman et al, 1991; Mendelson et al, 1996; Hahn et al, 1998; Yurochko and Huang, 2000; Chan et al, 2010) To regulate these processes, HCMV utilizes a unique signalosome generated initially by the signaling downstream of gB/EGFR and pentamer/β1 and β3 integrin engagement at the cell surface and activation of EGFR and integrin dependent events post entry (Collins-McMillen et al, 2017b; Fulkerson et al, 2020). We hope to shed light on HCMV signaling through key cellular receptors, and how that signaling initiates productive infection and persistence in this review
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
