ArticleRetrovirology2011
Tat RNA silencing suppressor activity contributes to perturbation of lymphocyte miRNA by HIV-1.
Article in Retrovirology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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30 citing papers in PubMed, 55 citations in OpenAlex.
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- MicroRNA-29 family expression and its relation to antiviral immune response and viro-immunological markers in HIV-1-infected patients.BMC infectious diseases · 2015Article
- MicroRNAs Expressed during Viral Infection: Biomarker Potential and Therapeutic Considerations.Biomarker insights · 2015Review
- Non-coding RNAs and HIV: viral manipulation of host dark matter to shape the cellular environment.Frontiers in genetics · 2015Review
- HIV-1 Vpr redirects host ubiquitination pathway.Journal of virology · 2014Article
- Role of microRNA modulation in the interferon-α/ribavirin suppression of HIV-1 in vivo.PloS one · 2014Article
- HIV-1 transcription and latency: an update.Retrovirology · 2013Review
- Hepatitis C Virus and HIV Type 1 Co-Infection.Infectious disease reports · 2013Review
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- Cellular RNA helicases and HIV-1: insights from genome-wide, proteomic, and molecular studies.Virus research · 2013Review
- HLA-G/C, miRNAs, and their role in HIV infection and replication.BioMed research international · 2013Review
- Host restriction factors in retroviral infection: promises in virus-host interaction.Retrovirology · 2012Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMicroRNA (miRNA)-mediated RNA silencing is integral to virtually every cellular process including cell cycle progression and response to virus infection. The interplay between RNA silencing and HIV-1 is multifaceted, and accumulating evidence posits a strike-counterstrike interface that alters the cellular environment to favor virus replication. For instance, miRNA-mediated RNA silencing of HIV-1 translation is antagonized by HIV-1 Tat RNA silencing suppressor activity. The activity of HIV-1 accessory proteins Vpr/Vif delays cell cycle progression, which is a process prominently modulated by miRNA. The expression profile of cellular miRNA is altered by HIV-1 infection in both cultured cells and clinical samples. The open question stands of what, if any, is the contribution of Tat RNA silencing suppressor activity or Vpr/Vif activity to the perturbation of cellular miRNA by HIV-1.
resultsHerein, we compared the perturbation of miRNA expression profiles of lymphocytes infected with HIV-1(NL4-3) or derivative strains that are deficient in Tat RNA silencing suppressor activity (Tat K51A substitution) or ablated of the vpr/vif open reading frames. Microarrays recapitulated the perturbation of the cellular miRNA profile by HIV-1 infection. The miRNA expression trends overlapped ~50% with published microarray results on clinical samples from HIV-1 infected patients. Moreover, the number of miRNA perturbed by HIV-1 was largely similar despite ablation of Tat RSS activity and Vpr/Vif; however, the Tat RSS mutation lessened HIV-1 downregulation of twenty-two miRNAs.
conclusionsOur study identified miRNA expression changes attributable to Tat RSS activity in HIV-1(NL4-3). The results accomplish a necessary step in the process to understand the interface of HIV-1 with host RNA silencing activity. The overlap in miRNA expression trends observed between HIV-1 infected CEMx174 lymphocytes and primary cells supports the utility of cultured lymphocytes as a tractable model to investigate interplay between HIV-1 and host RNA silencing. The subset of miRNA determined to be perturbed by Tat RSS in HIV-1 infection provides a focal point to define the gene networks that shape the cellular environment for HIV-1 replication.
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