Latent infection of myeloid progenitors by human cytomegalovirus protects cells from FAS-mediated apoptosis through the cellular IL-10/PEA-15 pathway.

Latent infection of primary CD34(+) progenitor cells by human cytomegalovirus (HCMV) results in their increased survival in the face of pro-apoptotic signals. For instance, we have shown previously that primary myeloid cells are refractory to FAS-mediated killing and that cellular IL-10 (cIL-10) is an important survival factor for this effect. However, how cIL-10 mediates this protection is unclear. Here, we have shown that cIL-10 signalling leading to upregulation of the cellular factor PEA-15 mediates latency-associated protection of CD34(+) progenitor cells from the extrinsic death pathway.

Keywords

Antigens, CD34, Apoptosis, Apoptosis Regulatory Proteins, Cell Line, Cytomegalovirus, Cytomegalovirus Infections, Fas Ligand Protein, Humans, Interleukin-10, Intracellular Signaling Peptides and Proteins, Myeloid Cells, Phosphoproteins, Stem Cells, Virus Latency

Journal Title

J Gen Virol

Journal ISSN

0022-1317
1465-2099

Volume Title

96

Publisher

Microbiology Society

Publisher DOI

https://doi.org/10.1099/vir.0.000180

Rights and licensing

Except where otherwised noted, this item's license is described as Attribution 2.0 UK: England & Wales

Sponsorship

Medical Research Council (MR/K021087/1)
Medical Research Council (G0701279)

We gratefully acknowledge funding from the UK Medical Research Council (J.H.S. G:0701279) which supports the current research in our laboratory and also the support of NIHR UK Biomedical Research Centre (J.H.S.). We thank Linda Teague, Roy Whiston and Stuart McGregor Dallas for technical support and Stuart McGregor Dallas for providing validation data for figure 1.

Collections

Scholarly Works - Medicine
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