ArticleAIDS research and human retroviruses2013
Reduced basal transcriptional activity of central nervous system-derived HIV type 1 long terminal repeats.
Article in AIDS research and human retroviruses, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- HIV Promoters Isolated from Brain and Peripheral Tissue of Virally Suppressed PWH Are Phylogenetically and Functionally Similar.International journal of molecular sciences · 2026Article
- Genetic variation of the HIV-1 subtype C transmitted/founder viruses long terminal repeat elements and the impact on transcription activation potential and clinical disease outcomes.PLoS pathogens · 2023Article
- Shock and kill within the CNS: A promising HIV eradication approach?Journal of leukocyte biology · 2022Review
- Balance between Retroviral Latency and Transcription: Based on HIV Model.Pathogens (Basel, Switzerland) · 2020Review
- Impact of Myeloid Reservoirs in HIV Cure Trials.Current HIV/AIDS reports · 2019Review
- HIV-1 and Compromised Adult Neurogenesis: Emerging Evidence for a New Paradigm of HAND PersistenceAIDS reviews · 2019Review
- Variation in cell-associated unspliced HIV RNA on antiretroviral therapy is associated with the circadian regulator brain-and-muscle-ARNT-like-1.AIDS (London, England) · 2018Observational
- Contrasting effect of the latency-reversing agents bryostatin-1 and JQ1 on astrocyte-mediated neuroinflammation and brain neutrophil invasion.Journal of neuroinflammation · 2017Article
- Toxicity and in vitro activity of HIV-1 latency-reversing agents in primary CNS cells.Journal of neurovirology · 2016Article
- Strategies to target non-T-cell HIV reservoirs.Current opinion in HIV and AIDS · 2016Review
- CNS-specific regulatory elements in brain-derived HIV-1 strains affect responses to latency-reversing agents with implications for cure strategies.Molecular psychiatry · 2016Article
- Targeting the Brain Reservoirs: Toward an HIV Cure.Frontiers in immunology · 2016Review
- Progress and challenges in the use of latent HIV-1 reactivating agents.Acta pharmacologica Sinica · 2015Review
- HIV-1 transcriptional regulation in the central nervous system and implications for HIV cure research.Journal of neurovirology · 2015Review
- Is the central nervous system a reservoir of HIV-1?Current opinion in HIV and AIDS · 2014Review
- Treatment of HIV in the CNS: effects of antiretroviral therapy and the promise of non-antiretroviral therapeutics.Current HIV/AIDS reports · 2014Article
- Article
- HIV and neurocognitive dysfunction.Current HIV/AIDS reports · 2013Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
New evidence indicates that astrocytes of the central nervous system (CNS) are extensively infected with human immunodeficiency virus type 1 (HIV-1) in vivo. Although no new virus is produced, this nonproductive or restricted infection contributes to the pathogenesis of HIV-associated dementia (HAD) and compromises virus eradication strategies. The HIV-1 long terminal repeat (LTR) plays a critical role in regulating virus production from infected cells. Here, we determined whether LTRs derived from CNS and non-CNS compartments are genetically and functionally distinct and contribute to the restricted nature of astrocyte infection. CNS- and/or non-CNS-derived LTRs (n=82) were cloned from primary HIV-1 viruses isolated from autopsy tissues of seven patients who died with HAD. Phylogenetic analysis showed interpatient and intrapatient clustering of LTR nucleotide sequences. Functional analysis showed reduced basal transcriptional activity of CNS-derived LTRs in both astrocytes and T cells compared to that of non-CNS-derived LTRs. However, LTRs were heterogeneous in their responsiveness to activation by Tat. Therefore, using a relatively large, independent panel of primary HIV-1 LTRs derived from clinically well-characterized subjects, we show that LTRs segregate CNS- from non-CNS-derived tissues both genetically and functionally. The reduced basal transcriptional activity of LTRs derived from the CNS may contribute to the restricted HIV-1 infection of astrocytes and latent infection within the CNS. These findings have significance for understanding the molecular basis of HIV-1 persistence within cellular reservoirs of the CNS that need to be considered for strategies aimed at eradicating HIV-1.
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Registered trials
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