Unknown

Dataset Information

0

Latent Cytomegalovirus-Driven Recruitment of Activated CD4+ T Cells Promotes Virus Reactivation.


ABSTRACT: Human cytomegalovirus (HCMV) infection is not cleared by the initial immune response but persists for the lifetime of the host, in part due to its ability to establish a latent infection in cells of the myeloid lineage. HCMV has been shown to manipulate the secretion of cellular proteins during both lytic and latent infection; with changes caused by latent infection mainly investigated in CD34+ progenitor cells. Whilst CD34+ cells are generally bone marrow resident, their derivative CD14+ monocytes migrate to the periphery where they briefly circulate until extravasation into tissue sites. We have analyzed the effect of HCMV latent infection on the secretome of CD14+ monocytes, identifying an upregulation of both CCL8 and CXCL10 chemokines in the CD14+ latency-associated secretome. Unlike CD34+ cells, the CD14+ latency-associated secretome did not induce migration of resting immune cell subsets but did induce migration of activated NK and T cells expressing CXCR3 in a CXCL10 dependent manner. As reported in CD34+ latent infection, the CD14+ latency-associated secretome also suppressed the anti-viral activity of stimulated CD4+ T cells. Surprisingly, however, co-culture of activated autologous CD4+ T cells with latently infected monocytes resulted in reactivation of HCMV at levels comparable to those observed using M-CSF and IL-1β cytokines. We propose that these events represent a potential strategy to enable HCMV reactivation and local dissemination of the virus at peripheral tissue sites.

SUBMITTER: Jackson SE 

PROVIDER: S-EPMC8072157 | biostudies-literature |

REPOSITORIES: biostudies-literature

Similar Datasets

| S-BSST619 | biostudies-other
| S-EPMC3826617 | biostudies-literature
| S-EPMC6437071 | biostudies-literature
| S-EPMC5972543 | biostudies-literature
| S-EPMC5445581 | biostudies-literature
| S-EPMC6436878 | biostudies-literature
| S-EPMC3311280 | biostudies-literature
2022-02-15 | GSE179864 | GEO
| S-EPMC8143188 | biostudies-literature
| S-EPMC3989168 | biostudies-literature