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JournalISSN: 1570-162X

Current HIV Research 

Bentham Science Publishers
About: Current HIV Research is an academic journal published by Bentham Science Publishers. The journal publishes majorly in the area(s): Population & Medicine. It has an ISSN identifier of 1570-162X. Over the lifetime, 1112 publications have been published receiving 21792 citations.


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Journal ArticleDOI
TL;DR: Cell populations of the monocyte-macrophage lineage, which originate in the bone marrow, are of particular importance in HIV-1 persistence due to their ability to cross the blood-brain barrier and spread HIV- 1 infection in the immunoprivileged central nervous system (CNS).
Abstract: A major obstacle in human immunodeficiency virus type 1 (HIV-1) eradication is the ability of the virus to remain latent in a subpopulation of the cells it infects. Latently infected cells can escape the viral immune response and persist for long periods of time, despite the presence of successful highly active antiretroviral therapy (HAART). Given the appropriate stimulus, latently infected cells can reactivate and start producing infectious virions. The susceptibility of these cell populations to HIV-1, their life span, their proliferative capacity, and their ability to periodically produce infectious virus subsequent to alterations in cellular physiology and/or immunologic controls are critical issues which determine the contribution of these cells to viral persistence. Memory CD4+ T cells due to the long life span, which may be several years, and their ability to reactivate upon encounter with their cognate antigen or other stimulation, are considered a critical reservoir for maintenance of latent HIV-1 proviral DNA. Cells of the monocyte-macrophage lineage, which originate in the bone marrow (BM), are of particular importance in HIV-1 persistence due to their ability to cross the blood-brain barrier (BBB) and spread HIV-1 infection in the immunoprivileged central nervous system (CNS). Hematopoietic progenitor cells (HPCs) are also a potential HIV-1 reservoir, as several studies have shown that CD34+ HPCs carrying proviral DNA can be found in vivo in a subpopulation of HIV-1-infected patients. The ability of HPCs to proliferate and potentially generate clonal populations of infected cells of the monocyte-macrophage lineage may be crucial in HIV-1 dissemination. The contribution of these and other cell populations in HIV-1 persistence, as well as the possible strategies to eliminate latently infected cells are critically examined in this review.

325 citations

Journal ArticleDOI
TL;DR: It is demonstrated that LL-37 inhibits HIV-1 replication in PBMC, including primary CD4(+) T cells, and the HIV- 1 inhibitory effect was shown to be independent of FPRL-1 signalling.
Abstract: The antimicrobial peptide LL-37 is the only cathelicidin that has been described in humans. LL-37 exerts chemotactic, immunomodulatory and angiogenic effects; activities that are mediated through binding to the formyl peptide receptor like (FPRL)-1 receptor. Agonistic ligation of FPRL-1 can also induce down-regulation of HIV-1 chemokine receptors and reduce susceptibility to HIV-1 infection in vitro. Therefore, we have evaluated the capacity of LL-37 to inhibit HIV-1 infection in vitro. Here we demonstrate that LL-37 inhibits HIV-1 replication in PBMC, including primary CD4(+) T cells. This inhibition was readily reproduced using various HIV-1 isolates without detectable changes in the target cell expression of HIV-1 chemokine receptors. Accordingly, the HIV-1 inhibitory effect was shown to be independent of FPRL-1 signalling. Given the epithelial expression of LL-37, it may contribute to the local protection against HIV-1 infection.

210 citations

Journal ArticleDOI
TL;DR: It is found that YMSM were more likely to have heard about PrEP if they were older, more educated, were residentially unstable in the prior 30 days, had insurance, or reported having at least one sexually transmitted infection in their lifetime.
Abstract: Pre-exposure prophylaxis (PrEP) has the potential to help reduce new HIV infections among young men who have sex with men (YMSM). Using a cross-sectional survey of YMSM (N=1,507; ages 18-24), we gauged YMSM's PrEP awareness and PrEP-related beliefs regarding side effects, accessibility, and affordability. Overall, 27% of the sample had heard about PrEP; 1% reported ever using PrEP prior to sex. In a multivariate logistic regression, we found that YMSM were more likely to have heard about PrEP if they were older, more educated, were residentially unstable in the prior 30 days, had insurance, or reported having at least one sexually transmitted infection in their lifetime. We found no differences by race/ethnicity, history of incarceration, or recent sexual risk behavior. In multivariate linear regression models, Black and Latino YMSM were more likely than Whites to state they would not use PrEP because of side effect concerns. YMSM were more likely to indicate that they would not be able to afford PrEP if they did not have insurance or if they had a prior sexually transmitted infection, PrEP rollout may be hindered due to lack of awareness, as well as perceived barriers regarding its use. We propose strategies to maximize equity in PrEP awareness and access if it is to be scaled up among YMSM.

198 citations

Journal ArticleDOI
TL;DR: A review of the current in vitro models of restricted HIV-1 replication in astrocytes, and an analysis of the available evidence supporting a role for infected cells in the pathogenesis of HIV-associated dementia is provided in this paper.
Abstract: Astrocytes are the most numerous cell type in the brain, and their physiological roles are essential for normal brain function. Studies of post-mortem brain tissue samples from individuals with AIDS have revealed that a small proportion of astrocytes are infected by HIV-1 which is linked to the development of HIVassociated dementia (HIVD), a frequent clinical manifestation of HIV-1 disease affecting up to 20% of infected adults. However, astrocyte infection by HIV-1 in vivo is generally non-productive, and can only be readily detected by sensitive techniques that detect HIV-1 RNA or proviral DNA. Similarly, primary astrocyte cultures and astrocytic cell lines can be permissive to infection by HIV-1 strains, but are refractory to efficient HIV-1 expression. In efforts to delineate the molecular mechanisms underlying the restricted infection, several studies have demonstrated that efficient HIV-1 replication is blocked in astrocytes at different steps of the virus life cycle, including virus entry, reverse transcription, nucleocytoplasmic HIV-1 RNA transport, translation of viral RNA, and maturation of progeny virions. However, the relative importance of each of these possible replication blocks in restricting HIV-1 replication in astrocytes is unclear. Moreover, how restricted astrocyte infection contributes to the development of HIVD is unknown. This review surveys the current in vitro models of restricted HIV-1 replication in astrocytes, and provides an analysis of the available evidence supporting a role for astrocyte infection in the pathogenesis of HIVD. A greater understanding of the fate of HIV-1 in astrocytes may assist in the identification of viral reservoirs in the central nervous system, novel therapies for the treatment of HIVD, and also novel strategies to suppress HIV-1 replication in CD4+ cells of the immune system.

192 citations

Journal ArticleDOI
TL;DR: HIV-1 TAR RNA is the binding site of the viral protein Tat, the trans-activator of the HIV-1 LTR, which has a highly folded stem-bulge-loop structure, which also binds cellular proteins to form ribonucleoprotein complexes.
Abstract: HIV-1 TAR RNA is the binding site of the viral protein Tat, the trans-activator of the HIV-1 LTR. It is present at the 5' end of all HIV-1 spliced and unspliced mRNAs in the nucleus as well as in the cytoplasm. It has a highly folded stem-bulge-loop structure, which also binds cellular proteins to form ribonucleoprotein complexes. The Tat-Cyclin T1-CDK9 complex is the main component in the trans-activation of HIV-1 and its affinity for TAR is regulated through Tat acetylation by histone acetyl transferases. Recent studies show that this complex is able to recruit other cellular partners to mediate efficient transcriptional elongation. TRBP, PKR and La bind directly to the TAR RNA structure and influence translation of HIV-1 in either positive or negative manners. Some mutations in TAR RNA severely impair HIV-1 trans-activation, translation and viral production, showing its functional importance. The overexpression or suppression of several TAR RNA- binding proteins has a strong impact on viral replication pointing out their major role in the viral life cycle. TAR RNA has been the target of drug development to inhibit viral replication. Recent data using small molecules or RNA-based technologies show that acting on the TAR RNA or on its viral and cellular binding factors effectively decreases virion production.

181 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
202344
2022102
202136
202054
201955
201822