Transcriptional Reprogramming during Effector-to-Memory Transition Renders CD4 + T Cells Permissive for Latent HIV-1 Infection.

Autor:	Shan L; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA., Deng K; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, 510080, China., Gao H; Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong, 510080, China., Xing S; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA., Capoferri AA; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA., Durand CM; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA., Rabi SA; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA., Laird GM; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA., Kim M; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA., Hosmane NN; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA., Yang HC; National Taiwan University Hospital, Taipei 100, Taiwan., Zhang H; Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA., Margolick JB; Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA., Li L; Department of Infectious Diseases, Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510060, China., Cai W; Department of Infectious Diseases, Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510060, China., Ke R; Department of Mathematics, North Carolina State University, Raleigh, NC 27695, USA., Flavell RA; Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA; Howard Hughes Medical Institute, Yale University, New Haven, CT 06520, USA., Siliciano JD; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA., Siliciano RF; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Howard Hughes Medical Institute, Johns Hopkins University, Baltimore, MD 21205, USA. Electronic address: rsiliciano@jhmi.edu.
Jazyk:	angličtina
Zdroj:	Immunity [Immunity] 2017 Oct 17; Vol. 47 (4), pp. 766-775.e3.
DOI:	10.1016/j.immuni.2017.09.014
Abstrakt:	The latent reservoir for HIV-1 in resting memory CD4 + T cells is the major barrier to curing HIV-1 infection. Studies of HIV-1 latency have focused on regulation of viral gene expression in cells in which latent infection is established. However, it remains unclear how infection initially becomes latent. Here we described a unique set of properties of CD4 + T cells undergoing effector-to-memory transition including temporary upregulation of CCR5 expression and rapid downregulation of cellular gene transcription. These cells allowed completion of steps in the HIV-1 life cycle through integration but suppressed HIV-1 gene transcription, thus allowing the establishment of latency. CD4 + T cells in this stage were substantially more permissive for HIV-1 latent infection than other CD4 + T cells. Establishment of latent HIV-1 infection in CD4 + T could be inhibited by viral-specific CD8 + T cells, a result with implications for elimination of latent HIV-1 infection by T cell-based vaccines. (Copyright © 2017. Published by Elsevier Inc.)
Databáze:	MEDLINE
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