MiRNA-103 downmodulates CCR5 expression reducing human immunodeficiency virus type-1 entry and impacting latency establishment in CD4+ T cells

Bellini, Nicolas; Lodge, Robert; Pham, Tram N. Q.; Jain, Jaspreet; Murooka, Thomas T.; Herschhorn, Alon; Bernard, Nicole F.; Routy, Jean‐Pierre; Tremblay, Cécile; Cohen, Éric A.

doi:10.1016/j.isci.2022.105234

Cited by 7 publications

(4 citation statements)

References 72 publications

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“…This effect was mitigated by depleting p53 in cells using siRNA- mediated silencing of p53 . Inhibition of p53 expression leads to an increase in pol II levels associated with the HIV-1 genome sequences, transcripts elongation, and amplified viral replication [ 58 , 59 ]. Other studies have also found that the N-terminal acidic structural domain of p53 can combine directly with TATA-box binding protein subunit of the universal transcription factor TFIID.…”

Section: Hiv-associated Factors That Can Be Inhibited By P53mentioning

confidence: 99%

HIV-1-related factors interact with p53 to influence cellular processes

Liu,

Guo,

et al. 2023

AIDS Res Ther

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Human immunodeficiency virus type 1 (HIV-1) is the primary epidemic strain in China. Its genome contains two regulatory genes (tat and rev), three structural genes (gag, pol, and env), and four accessory genes (nef, vpr, vpu, and vif). Long terminal repeats (LTRs) in thegenome regulate integration, duplication, and expression of viral gene. The permissibility of HIV-1 infection hinges on the host cell cycle status. HIV-1 replicates by exploiting various cellular processes via upregulation or downregulation of specific cellular proteins that also control viral pathogenesis. For example, HIV-1 regulates the life cycle of p53, which in turn contributes significantly to HIV-1 pathogenesis. In this article, we review the interaction between HIV-1-associated factors and p53, providing information on their regulatory and molecular mechanisms, hinting possible directions for further research.

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Section: Hiv-associated Factors That Can Be Inhibited By P53mentioning

confidence: 99%

HIV-1-related factors interact with p53 to influence cellular processes

Liu,

Guo,

et al. 2023

AIDS Res Ther

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“…Hundreds of eukaryotic cellular miRNAs found to function as post-transcriptional regulators of viral genes have been identified [ 8 , 10 ]. Some of these host cell miRNAs play a role in interfering with the establishment of latent HIV-1 infection [ 11 , 12 ], while others promote cell activation and HIV-1 latency [ 13 , 14 ]. Interestingly, HIV-1-infected cells differentially express cellular miRNAs depending on whether the virus is productive or latent [ 15 ], thereby marking them as possible candidates for biomarkers of disease progression [ 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

The Role of HIV-1-Encoded microRNAs in Viral Replication

Carmi,

Gotlieb,

Shemer-Avni

et al. 2024

Microorganisms

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microRNAs (miRNAs) are small non-coding RNAs (sncRNAs) that play an important role in the life cycle of human viruses. We sought to characterize human immunodeficiency virus 1 (HIV-1)-encoded miRNAs and determine their role in viral replication. Initially, a bioinformatic analysis was used to predict HIV-1-encoded miRNAs. Next, a representative number of these predicted sequences were verified using a miRNA microarray chip, reverse transcription PCR (RT-PCR), and the deep sequencing of RNA extracted from HIV-1-infected cells. Eight HIV-1-encoded sncRNA sequences conforming to the criteria that define miRNAs were identified in HIV-1-infected immortalized T cells and human primary CD4+ lymphocytes; five of the eight sequences have not been previously reported. Deep sequencing validated the presence of these virus-encoded miRNA sequences and uncovered large numbers of atypical sncRNA sequences, lacking characteristics of conventional miRNAs. We named these sequences small RNAs (smRNAs). The overexpression of four candidate HIV-1-encoded miRNAs and silencing of two smRNAs significantly increased HIV-1 viral replication. Our study uncovered novel HIV-1-encoded sncRNAs that, upon deregulated expression, alter viral titers in HIV-1-infected cells, suggesting that miRNAs and smRNAs play an important role in regulating viral replication. Future studies may reveal the function of HIV-1-encoded sncRNAs and their possible implications for diagnosis and treatment.

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“…Movements of these elements outward lead to Env transitions to an open conformation that exposes the gp120 co-receptor binding region and exposes/forms the gp41 heptad repeat 1 coil on the Env surface ( 5 , 8 , 9 ). Subsequent binding to CCR5 or CXCR4 co-receptor facilitates further steps during viral entry that culminates in gp41-mediated fusion of the viral and cellular membranes ( 10 – 13 ).…”

Section: Introductionmentioning

confidence: 99%

Alternative substitutions of N332 in HIV-1 _AD8 gp120 differentially affect envelope glycoprotein function and viral sensitivity to broadly neutralizing antibodies targeting the V3-glycan

Jeffy,

Parthasarathy,

Ahmed

et al. 2024

mBio

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The envelope glycoprotein (Env) trimer on the surface of human immunodeficiency virus type I (HIV-1) mediates viral entry into host CD4 + T cells and is the sole target of neutralizing antibodies. Broadly neutralizing antibodies (bnAbs) that target gp120 V3-glycan of HIV-1 Env trimer are potent and block the entry of diverse HIV-1 strains. Most V3-glycan bnAbs interact, to a different extent, with a glycan attached to N332, but Asn at this position is not absolutely conserved or required for HIV-1 entry based on the prevalence of N332 in different circulating HIV-1 strains from diverse clades. Here, we studied the effects of amino acid changes at position 332 of HIV-1 AD8 Envs on HIV-1 sensitivity to antibodies, cold exposure, and soluble CD4. We further investigated how these changes affect Env function and HIV-1 infectivity in vitro . Our results suggest robust tolerability of HIV-1 AD8 Env N332 to changes, with specific changes that resulted in extended exposure of gp120 V3 loop, which is typically concealed in most primary HIV-1 isolates. Viral evolution leading to Asn at position 332 of HIV AD8 Envs is supported by the selection advantage of high levels of cell–cell fusion, transmission, and infectivity with high levels of cell surface expression and slightly higher gp120 shedding than most N332 variants. Thus, tolerance of HIV-1 AD8 Envs to different amino acids at position 332 provides increased flexibility to respond to changing conditions/environments and evade the immune system. Modeling studies of the distance between N332 glycan and specific bnAbs were in agreement with N332 glycan dependency on bnAb neutralization. Overall, our studies provide insights into the contribution of specific amino acids at position 332 to Env antigenicity, stability on ice, and conformational states. IMPORTANCE Glycan attached to amino acid asparagine at position 332 of HIV-1 envelope glycoproteins is a main target of a subset of broadly neutralizing antibodies that block HIV-1 infection. Here, we defined the contribution of different amino acids at this position to Env antigenicity, stability on ice, and conformational states.

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MiRNA-103 downmodulates CCR5 expression reducing human immunodeficiency virus type-1 entry and impacting latency establishment in CD4+ T cells

Cited by 7 publications

References 72 publications

HIV-1-related factors interact with p53 to influence cellular processes

HIV-1-related factors interact with p53 to influence cellular processes

The Role of HIV-1-Encoded microRNAs in Viral Replication

Alternative substitutions of N332 in HIV-1 _AD8 gp120 differentially affect envelope glycoprotein function and viral sensitivity to broadly neutralizing antibodies targeting the V3-glycan

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MiRNA-103 downmodulates CCR5 expression reducing human immunodeficiency virus type-1 entry and impacting latency establishment in CD4+ T cells

Cited by 7 publications

References 72 publications

HIV-1-related factors interact with p53 to influence cellular processes

HIV-1-related factors interact with p53 to influence cellular processes

The Role of HIV-1-Encoded microRNAs in Viral Replication

Alternative substitutions of N332 in HIV-1 AD8 gp120 differentially affect envelope glycoprotein function and viral sensitivity to broadly neutralizing antibodies targeting the V3-glycan

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Alternative substitutions of N332 in HIV-1 _AD8 gp120 differentially affect envelope glycoprotein function and viral sensitivity to broadly neutralizing antibodies targeting the V3-glycan