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Article: Latent human cytomegalovirus enhances HIV-1 infection in CD34+ progenitor cells

TitleLatent human cytomegalovirus enhances HIV-1 infection in CD34+ progenitor cells
Authors
Issue Date2017
PublisherAmerican Society of Hematology. The Journal's web site is located at http://www.bloodadvances.org/
Citation
Blood Advances, 2017, v. 1, p. 306-318 How to Cite?
AbstractIndividuals who have been preinfected by human cytomegalovirus (HCMV) are more prone to AIDS disease progression after subsequent HIV-1 infection but the underlying mechanism remains elusive. HCMV is a ubiquitous DNA virus that commonly establishes lifelong latent infection in CD34+ progenitor cells, where latency-specific HCMV genes may modulate host restriction to HIV-1 infection. To test this hypothesis, we studied progenitor cells that are known to resist replicative HIV-1 infection because of the intrinsic expression of host restriction factors. Interestingly, in primary CD34+ cells undergoing latent HCMV infection, an enhanced level of HIV-1 proviral DNA and replication was observed as measured by digital polymerase chain reaction, quantitative polymerase chain reaction, and Gag expression, and confirmed using dual-reporter pseudovirus encoding X4- or R5-tropic envelope and T-cell transfer. This phenomenon may be partially explained by the upregulation of HIV-1 entry coreceptors, including chemokine receptors CXCR4 and CCR5, but not of the primary receptor CD4. Furthermore, latent HCMV infection downregulated the expression of HIV-1 restriction factors SAMHD1, APOBEC3G, tetherin, and Mx2 in CD34+ progenitor cells, which may confer to enhanced HIV-1 infection. However, this enhancement was abrogated when ultraviolet-inactivated HCMV was used for comparison, suggesting that expression of latent HCMV genes is essential for this effect. Importantly, HCMV gB and HIV-1 p24 can be detected in the same cell by immunofluorescence and flow cytometry; therefore, the establishment of HCMV latency in CD34+ cells likely leads to host cell gene modulation that favors HIV-1 infection.
Persistent Identifierhttp://hdl.handle.net/10722/239563

 

DC FieldValueLanguage
dc.contributor.authorCheung, KLA-
dc.contributor.authorHuang, Y-
dc.contributor.authorKwok, HY-
dc.contributor.authorChen, M-
dc.contributor.authorChen, Z-
dc.date.accessioned2017-03-21T09:15:52Z-
dc.date.available2017-03-21T09:15:52Z-
dc.date.issued2017-
dc.identifier.citationBlood Advances, 2017, v. 1, p. 306-318-
dc.identifier.urihttp://hdl.handle.net/10722/239563-
dc.description.abstractIndividuals who have been preinfected by human cytomegalovirus (HCMV) are more prone to AIDS disease progression after subsequent HIV-1 infection but the underlying mechanism remains elusive. HCMV is a ubiquitous DNA virus that commonly establishes lifelong latent infection in CD34+ progenitor cells, where latency-specific HCMV genes may modulate host restriction to HIV-1 infection. To test this hypothesis, we studied progenitor cells that are known to resist replicative HIV-1 infection because of the intrinsic expression of host restriction factors. Interestingly, in primary CD34+ cells undergoing latent HCMV infection, an enhanced level of HIV-1 proviral DNA and replication was observed as measured by digital polymerase chain reaction, quantitative polymerase chain reaction, and Gag expression, and confirmed using dual-reporter pseudovirus encoding X4- or R5-tropic envelope and T-cell transfer. This phenomenon may be partially explained by the upregulation of HIV-1 entry coreceptors, including chemokine receptors CXCR4 and CCR5, but not of the primary receptor CD4. Furthermore, latent HCMV infection downregulated the expression of HIV-1 restriction factors SAMHD1, APOBEC3G, tetherin, and Mx2 in CD34+ progenitor cells, which may confer to enhanced HIV-1 infection. However, this enhancement was abrogated when ultraviolet-inactivated HCMV was used for comparison, suggesting that expression of latent HCMV genes is essential for this effect. Importantly, HCMV gB and HIV-1 p24 can be detected in the same cell by immunofluorescence and flow cytometry; therefore, the establishment of HCMV latency in CD34+ cells likely leads to host cell gene modulation that favors HIV-1 infection.-
dc.languageeng-
dc.publisherAmerican Society of Hematology. The Journal's web site is located at http://www.bloodadvances.org/-
dc.relation.ispartofBlood Advances-
dc.rightsThis research was originally published in The Hematologist: ASH News and Reports. Author(s). Title. The Hematologist: ASH News and Reports. Year;Vol,Issue:pp-pp. © the American Society of Hematology.-
dc.titleLatent human cytomegalovirus enhances HIV-1 infection in CD34+ progenitor cells-
dc.typeArticle-
dc.identifier.emailCheung, KLA: allenc@hku.hk-
dc.identifier.emailHuang, Y: yrhuang@hku.hk-
dc.identifier.emailKwok, HY: hauyeek@hku.hk-
dc.identifier.emailChen, M: jiange@hkucc.hku.hk-
dc.identifier.emailChen, Z: zchenai@hku.hk-
dc.identifier.authorityChen, Z=rp00243-
dc.identifier.doi10.1182/bloodadvances.2016000638-
dc.identifier.hkuros271557-
dc.identifier.volume1-
dc.identifier.spage306-
dc.identifier.epage318-
dc.publisher.placeUnited States-

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