Abstract
Human cytomegalovirus (HCMV) has evolved a number of mechanisms for long-term co-existence within its host. HCMV infects a wide range of cell types, including fibroblasts, epithelial cells, monocytes, macrophages, dendritic cells, and myeloid progenitor cells. Lytic infection, with the production of infectious progeny virions, occurs in differentiated cell types, while undifferentiated myeloid precursor cells are the primary site of latent infection. The outcome of HCMV infection depends partly on the cell type and differentiation state but is also influenced by the composition of the immune environment. In this review, we discuss the role of early interactions between HCMV and the host immune system, particularly cytokine and chemokine networks, that facilitate the establishment of lifelong latent infection. A better understanding of these cytokine signaling pathways could lead to novel therapeutic targets that might prevent latency or eradicate latently infected cells.
Highlights
Human cytomegalovirus (HCMV) is a member of the Herpesviridae family that is widespread in the general population
There are more than fifty different interleukins (ILs), a group of cytokines that were initially defined by the fact that they were secreted from white blood cells
There was reduced horizontal acquisition of Rhesus cytomegalovirus (RhCMV) and significantly altered long-term immunity after those macaques became infected [94]. This result hints at the role of RhcmvIL-10 in establishing persistent or latent infections and suggests that immunization against cmvIL-10 could be a beneficial approach in HCMV vaccine development
Summary
Human cytomegalovirus (HCMV) is a member of the Herpesviridae family that is widespread in the general population. Despite a vigorous immune response to HCMV, the virus is never cleared and instead establishes lifelong latent infection in the host [2]. Reactivation is limited by host immune responses, clinical reactivation events may occur in the immunosuppressed. Primary HCMV infection usually occurs in epithelial cells at the mucous membranes of the oropharynx, while latency is established in CD34+ myeloid progenitor cells [2]. In these undifferentiated cells, the lytic replication cycle is prevented by suppressing the transcriptional activity of the Major. Cytokines are small extracellular proteins that facilitate communication between immune cells, regulating their growth, maturation, and response to infection [5]. The roles of representative members of each group in HCMV infection and latency are described below
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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.
