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CD4+ T cells "have it in them" to restrict HIV-1

Feb 25, 2014 3:51:08 PM / by Maria

hiv_CD4+Independent publication uses purified CD4+ T cells and peripheral blood mononuclear cells (PBMCs) supplied by HemaCare to identify how quiescent CD4+ T cells counteract HIV-1

The human immunodeficiency virus (HIV) responsible for causing the acquired immunodeficiency syndrome (AIDS) derails the immune system by invading CD4+ T cells (also known as helper T cells), replicating in high numbers within these cells and ultimately destroying them, leading to low levels of CD4+ T cells. A patient with low levels of CD4+ T cells is prone to a diverse range of infections.

Given the impact of HIV infection on human health, there is a continuous and intense search for ways to combat the virus. A recent study by Liu et al., offers insight into one such mechanism [1]. The authors investigate as to why HIV-1 is efficient in attacking only activated CD4+ T cells (proliferative) and not quiescent (non-proliferative) CD4+ T cells. This type of T cell typically progresses from quiescent to activated state upon exposure to mitogens and cytokines. This study for the first time defines the molecular mechanisms behind HIV-1 invasion of activated CD4+ T cells. Using  purified CD4+ T cells and peripheral blood mononuclear cells (PBMCs) supplied by HemaCare the researchers identified that monocyte chemotactic protein-induced protein 1 (MCPIP1) is involved in HIV-1 restriction.

So what is MCPIP1?

MCPIP1 is known to be a critical regulator of the inflammatory response and immune homeostasis, is routinely expressed by the quiescent CD4+ T cells.  Liu et al., specifically found that MCPIP1 also has RNase activity, and this action degrades HIV1, a RNA virus. These results were further validated with use of MCPIP1 mutations that abolish RNase activity and could not restrict HIV1 replication. Intriguingly, the expression of MCPIP1 is decreased in CD4+ T cells activated by mitogens such as phytohemagglutinin and IL-2.  Activated CD4+ T cells thus lose the ability to degrade HIV1. However, treatment of quiescent CD4+ T cells with MG132, a proteosomal inhibitor, prevents MCPIP1 degradation even upon T cell activation. In such a condition, activated CD4+ T cells could degrade HIV1, implicating a critical role for MCPIP1 in control of HIV1. While MALT1 protease is thought to degrade MCPIP1 in activated CD4+ T cells, finer details of regulation are unknown.  

We are excited to read how HemaCare cells have helped further studies on MCPIP1 regulation in CD4+ T cells  and potentially aid in research to develop effective therapy against HIV1 infection. Try HemaCare’s purified CD4+ T cells and PBMCs yourself!




[1] Shufeng Liu, Chao Qiu, Ruidong Miao, Jianhua Zhou, Aram Lee, Baoming Liu, Sandra N. Lester, Weihui Fu, Lingyan Zhu, Linxia Zhang, Jianqing Xu, Daping Fan, Kui Li, Mingui Fu, and Tianyi Wang. MCPIP1 restricts HIV infection and is rapidly degraded in activated CD4+ T cells. PNAS 2013 110 (47) 19083-19088; November 2013


Topics: HIV, Independent validation, PBMCs, T Cells


Written by Maria

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