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

Emma Poole | Zendy; Jonathan C. Lau | Zendy; John Sinclair | Zendy

Open Access

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

Author(s) -

Emma Poole,

Jonathan C. Lau,

John Sinclair

Publication year - 2015

Publication title -

journal of general virology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.55

H-Index - 167

eISSN - 1465-2099

pISSN - 0022-1317

DOI - 10.1099/vir.0.000180

Subject(s) - biology , progenitor cell , human cytomegalovirus , cd34 , apoptosis , immunology , myeloid , myeloid cells , downregulation and upregulation , cytomegalovirus , microbiology and biotechnology , virology , cancer research , stem cell , virus , herpesviridae , biochemistry , gene , viral disease

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.

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