Ified as key factors that maintain T cell quiescence . Loss of
Ified as key factors that maintain T cell quiescence . Loss of expression of any of the above proteins resulted in aberrant T cell proliferation, cellular damage due to higher metabolism, and cell death. CD4+ T cell quiescence and its effect on HIV infection has been a topic of intense investigation as early studies indicated that they are resistant to HIV infection. As a result a strong interest was developed to identify cellular factors that mediate this block and can potentially be the* Correspondence: [email protected] 1 Department of Medicine, Division of Hematology-Oncology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA Full list of author information is available at the end of the articlebasis for effective therapeutic approaches against HIV. None of the factors regulating T cell quiescence have been implicated in influencing HIV infection. In this review, we will discuss the steps of the viral life cycle inhibited in quiescent CD4+ T cells, the factors involved and the impact these studies have in understanding HIV infection in quiescent T cells as well as the development of better targets against the virus.HIV replication is defective in quiescent CD4+ T cellsFor the past two decades, the infection of quiescent CD4 T cells by HIV has been an area of intense investigation. Unlike other retroviruses, HIV replication is not dependent on cell cycle. Nevertheless, HIV and other lentiviruses more efficiently infect non-dividing cells and establish a latent infection [21-23]. While early reports supported the notion that only pre-activated T cells can be infected by HIV [24-26], subsequent studies showed that quiescent T cells could be infected by the virus [27-30]. Yet, key differences arose relating to the degree and levels of infection efficiency. On the one hand it was shown that HIV viral entry and initiation of reverse transcription were not affected. However, completion of reverse transcription was Lasalocid (sodium) chemical information inefficient resulting in the accumulation of labile, intermediate viral cDNA species [28,29]. Rescue of infection was?2013 Zack et al.; licensee BioMed Central Ltd. This is an Open Access article distributed PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27735993 under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Zack et al. Retrovirology 2013, 10:37 http://www.retrovirology.com/content/10/1/Page 2 ofpossible with stimulation but it was temporally sensitive as production of viral progeny decreased at later reactivation timepoints [29]. Additional work focusing on the CD25- (non-activated) and CD25+ (activated) T cell populations lent more support to the notion that quiescent T cells are resistant to HIV infection [31-33]. In the absence of any stimulation, HIV infection of CD25- T cells failed while that of CD25+ was successful. Furthermore, when total human peripheral blood monocytes were infected, the CD25- population did carry viral cDNA suggesting either bystander activation of the non-activated population or more efficient infection via cell-cell contact. Finally, Tang and colleagues further supported the above observations PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27488460 by demonstrating that infection of quiescent cells with HIV did not result in the production of virus [34]. On the other hand, other studies showed that HIV infection of quiescent T cells could be productive. More specifically, they demonstrated that the viral cDNA wa.
