Anti-HIV Factors: Targeting Each Step of HIV's Replication Cycle

Colomer-Lluch, Marta; Gollahon, Lauren; Serra-Moreno, Ruth

doi:10.2174/1570162x14999160224094621

Cited by 13 publications

(7 citation statements)

References 87 publications

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“…None of these variants were associated with HIV-1 plasma RNA set point among HIV-1 seroconverters ( S11 Table ), indicating that the associations we have found are unlikely to act through altered viral replication with these gene products functioning as intracellular viral restriction factors [ 38 ].…”

Section: Resultsmentioning

confidence: 99%

Whole genome sequencing of extreme phenotypes identifies variants in CD101 and UBE2V1 associated with increased risk of sexually acquired HIV-1

et al. 2017

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Host genetic variation modifying HIV-1 acquisition risk can inform development of HIV-1 prevention strategies. However, associations between rare or intermediate-frequency variants and HIV-1 acquisition are not well studied. We tested for the association between variation in genic regions and extreme HIV-1 acquisition phenotypes in 100 sub-Saharan Africans with whole genome sequencing data. Missense variants in immunoglobulin-like regions of CD101 and, among women, one missense/5’ UTR variant in UBE2V1, were associated with increased HIV-1 acquisition risk (p = 1.9x10-4 and p = 3.7x10-3, respectively, for replication). Both of these genes are known to impact host inflammatory pathways. Effect sizes increased with exposure to HIV-1 after adjusting for the independent effect of increasing exposure on acquisition risk.Trial registration: ClinicalTrials.gov NCT00194519; NCT00557245

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Section: Resultsmentioning

confidence: 99%

Whole genome sequencing of extreme phenotypes identifies variants in CD101 and UBE2V1 associated with increased risk of sexually acquired HIV-1

et al. 2017

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“…Both species-specific and cell-specific tropism of viruses may be due to differences in availability of specific virus receptors on the surface of cells that are required for binding and entry. However, host factors that restrict virus replication after successful entry-many of which are expressed in response to interferon-have been identified for many RNA viruses (7,8).…”

Section: Why Are Neurons Susceptible To Zika Virus?mentioning

confidence: 99%

Why are neurons susceptible to Zika virus?

Griffin

2017

Science

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“…NF-κB has a complex role in HIV-1 replication and pathogenesis. ISGs exert numerous effector functions and may target almost every step of the retroviral replication cycle ( Kluge et al, 2015 ; Colomer-Lluch et al, 2016 ). Thus, their induction by NF-κB transcription factors might have beneficial effects for the host by suppressing HIV-1 replication.…”

Section: Introductionmentioning

confidence: 99%

Primate Lentiviruses Modulate NF-κB Activity by Multiple Mechanisms to Fine-Tune Viral and Cellular Gene Expression

Heusinger

Kirchhoff

2017

Front. Microbiol.

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The transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) plays a complex role during the replication of primate lentiviruses. On the one hand, NF-κB is essential for induction of efficient proviral gene expression. On the other hand, this transcription factor contributes to the innate immune response and induces expression of numerous cellular antiviral genes. Recent data suggest that primate lentiviruses cope with this challenge by boosting NF-κB activity early during the replication cycle to initiate Tat-driven viral transcription and suppressing it at later stages to minimize antiviral gene expression. Human and simian immunodeficiency viruses (HIV and SIV, respectively) initially exploit their accessory Nef protein to increase the responsiveness of infected CD4+ T cells to stimulation. Increased NF-κB activity initiates Tat expression and productive replication. These events happen quickly after infection since Nef is rapidly expressed at high levels. Later during infection, Nef proteins of HIV-2 and most SIVs exert a very different effect: by down-modulating the CD3 receptor, an essential factor for T cell receptor (TCR) signaling, they prevent stimulation of CD4+ T cells via antigen-presenting cells and hence suppress further induction of NF-κB and an effective antiviral immune response. Efficient LTR-driven viral transcription is maintained because it is largely independent of NF-κB in the presence of Tat. In contrast, human immunodeficiency virus type 1 (HIV-1) and its simian precursors have lost the CD3 down-modulation function of Nef and use the late viral protein U (Vpu) to inhibit NF-κB activity by suppressing its nuclear translocation. In this review, we discuss how HIV-1 and other primate lentiviruses might balance viral and antiviral gene expression through a tight temporal regulation of NF-κB activity throughout their replication cycle.

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Anti-HIV Factors: Targeting Each Step of HIV's Replication Cycle

Cited by 13 publications

References 87 publications

Whole genome sequencing of extreme phenotypes identifies variants in CD101 and UBE2V1 associated with increased risk of sexually acquired HIV-1

Whole genome sequencing of extreme phenotypes identifies variants in CD101 and UBE2V1 associated with increased risk of sexually acquired HIV-1

Why are neurons susceptible to Zika virus?

Primate Lentiviruses Modulate NF-κB Activity by Multiple Mechanisms to Fine-Tune Viral and Cellular Gene Expression

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