MicroRNAs and HIV-1: Complex Interactions

Klase, Zachary; Houzet, Laurent; Jeang, Kuan‐Teh

doi:10.1074/jbc.r112.415448

Cited by 60 publications

(72 citation statements)

References 100 publications

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“…Upregulation of CXCR4 and TRAF6, through different pathways, promotes HIV-1 entry and replication in activated CD4 þ T lymphocytes. During viral infection, the expression of miRNAs that target viral sequences or host genes that influence the course of viral replication and pathogenesis may be altered (Houzet and Jeang, 2011;Klase et al, 2012). Here we found that miR-146a is expressed in human primary resting CD4 þ T lymphocytes, downregulated during their activation, but its influence on HIV-1 replication should be further investigated.…”

Section: Discussionmentioning

confidence: 70%

“…miRNAs are small non-coding RNA involved in posttranscriptional gene regulation that participates in RNA interference (RNAi)-mediated gene silencing (Bartel, 2009). RNAi activity is involved in many eukaryotic cellular processes and the deregulated expression of miRNAs and other RNAi components has been described in cancers, metabolic disorders, and infectious diseases (Triboulet et al, 2007;Bivalkar-Mehla et al, 2011;Yeung and Jeang, 2011;Klase et al, 2012). These miRNAs represent a new generation biomarkers for diagnostics and prognostics and, given their stability in vivo (Yeung and Jeang, 2011), new tools to control specific target in disease, including AIDS (Klase et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

“…The role of viral-encoded miRNAs derived from viral genomes (Pfeffer et al, 2004) in virus replication and virus-host interaction is currently under investigation (Ouellet et al, 2013;Zhang et al, 2014), as well as the role of cellular miRNAs in the regulation of HIV-1 viral replication (Lecellier et al, 2005;Huang et al, 2007) and in the complex interactions with HIV-1 (Klase et al, 2012). miRNA 146a (miR-146a) is considered as a crucial modulator of differentiation and function of cells of the innate and adaptive immunity, acting as a negative feedback regulator of the innate immune response by targeting two adapter proteins, TRAF6 (Tumor necrosis factor receptor -associated factor 6) and IRAK1(IL-1 receptorassociated kinase 1), acting in pro-inflammatory signaling (Taganov et al, 2006;Hou et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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miR-146a controls CXCR4 expression in a pathway that involves PLZF and can be used to inhibit HIV-1 infection of CD4+ T lymphocytes

et al. 2015

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MicroRNA miR-146a and PLZF are reported as major players in the control of hematopoiesis, immune function and cancer. PLZF is described as a miR-146a repressor, whereas CXCR4 and TRAF6 were identified as miR-146a direct targets in different cell types. CXCR4 is a co-receptor of CD4 molecule that facilitates HIV-1 entry into T lymphocytes and myeloid cells, whereas TRAF6 is involved in immune response. Thus, the role of miR-146a in HIV-1 infection is currently being thoroughly investigated. In this study, we found that PLZF mediates suppression of miR-146a to control increases of CXCR4 and TRAF6 protein levels in human primary CD4(+) T lymphocytes. We show that miR-146a upregulation by AMD3100 treatment or PLZF silencing, decreases CXCR4 protein expression and prevents HIV-1 infection of leukemic monocytic cell line and CD4(+) T lymphocytes. Our findings improve the prospects of developing new therapeutic strategies to prevent HIV-1 entry via CXCR4 by using the PLZF/miR-146a axis.

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Section: Discussionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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miR-146a controls CXCR4 expression in a pathway that involves PLZF and can be used to inhibit HIV-1 infection of CD4+ T lymphocytes

et al. 2015

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“…72 This finding is very intriguing as it represents a major deviation from the usual norm that host miRNAs generally repress viral replication. 80 …”

Section: Micrornas: Introduction and A Brief Historymentioning

confidence: 99%

MicroRNAs

2013

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The discovery of microRNAs (miRNAs) in 1993 followed by developments and discoveries in small RNA biology have redefined the biological landscape by significantly altering the longstanding dogmas that defined gene regulation. These small RNAs play a significant role in modulation of an array of physiological and pathological processes ranging from embryonic development to neoplastic progression. Unique miRNA signatures of various inherited, metabolic, infectious, and neoplastic diseases have added a new dimension to the studies that look at their pathogenesis and highlight their potential to be reliable biomarkers. Also, altering miRNA functionality and the development of novel in vivo delivery systems to achieve targeted modulation of specific miRNA function are being actively pursued as novel approaches for therapeutic intervention in many diseases. Here we review the current body of knowledge on the role of miRNAs in development and disease and discuss future implications.

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“…[1][2][3][4] In general, miRNAs affect HIV-1 infection by either directly binding to viral RNA or targeting the cellular factors that are related to HIV-1 survival. 1 For example, Huang et al 2 showed that five miRNAs (miRs-28, -125b, -150, -223, and -382) could suppress HIV-1 replication by binding to 3¢-UTR of HIV-1 RNA. Enrichment of these miRNAs in resting CD4 + T cells was suggested to be pivotal in HIV-1 latency, and thus, the manipulation of these miRNAs could be an effective approach for anti-HIV-1 therapy.…”

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confidence: 99%

Short Communication: HIV-1 Infection Suppresses Circulating Viral Restriction microRNAs

Zhou

Lee

Wang

et al. 2016

AIDS Research and Human Retroviruses

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MicroRNAs (miRNAs) participate in host innate immunity against HIV-1 infection. We examined the impact of HIV-1 infection on viral restriction miRNAs in plasma of HIV-1-infected subjects. HIV-1-infected subjects had significantly lower plasma levels of HIV-1 restriction miRNAs , and -382) than control subjects. Further in vitro studies showed that HIV-1 infection of macrophages suppressed production of the extracellular miRs-29b, -125b, and -223. These data demonstrate the compelling evidence that HIV-1 infection impairs host innate immunity by inhibiting antiviral miRNAs, which provide a possible mechanism for HIV-1 persistence in the host.

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MicroRNAs and HIV-1: Complex Interactions

Cited by 60 publications

References 100 publications

miR-146a controls CXCR4 expression in a pathway that involves PLZF and can be used to inhibit HIV-1 infection of CD4+ T lymphocytes

miR-146a controls CXCR4 expression in a pathway that involves PLZF and can be used to inhibit HIV-1 infection of CD4+ T lymphocytes

MicroRNAs

Short Communication: HIV-1 Infection Suppresses Circulating Viral Restriction microRNAs

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