Human immunodeficiency virus 1
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1256474 | ENA |
REPOSITORIES: ENA
Similar Datasets
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Project description:Human T-leukemia virus 1 (HTLV-1) is an oncogenic retrovirus with no available curative therapy. In-vitro data suggests HTLV-1 may be susceptible to certain HIV-1 antiretroviral compounds but their value, if any, in the context of a clinically-relevant transmission model is unknown. We addressed this knowledge gap by investigating the efficacy of the anti-retroviral compounds, tenofovir and dolutegravir, in preventing HTLV-1 transmission and infection in a humanised mouse model of HTLV-1 subtype c (HTLV-1c) infection, the first of its kind. Characterisation of this model revealed that HTLV-1c and HTLV-1 subtype a (HTLV-1a) showed subtle differences in natural history of disease but not as striking as the differences observed clinically, indicating additional host and environmental contributors to human disease. Single cell RNA sequencing of CD4+ T cell VDJ transcripts revealed poly- and oligoclonal expansion of HTLV-1c-infected CD4+ T cells. We show that tenofovir significantly reduces HTLV-1 transmission in vivo at clinically relevant doses when administered as pre-exposure prophylaxis. Further, tenofovir and dolutegravir combination significantly attenuates viral spread and disease progression during early infection. Our data support the use of tenofovir and dolutegravir against HTLV-1 transmission and early infection. Routine use of these drugs as effective prophylactic agents against HIV-1 infection will facilitate their rapid translation to HTLV-1 clinical trials.
2025-12-31 | GSE157492 | GEO
Project description:Increased morbidity and fetal growth restriction are reported in uninfected children born to human immunodeficiency virus type 1 (HIV-1)–infected women treated with antiretroviral (ARV) therapy. Viruses and/or pharmacological interventions such as ARVs can induce metabolic stress, skewing the cell’s immune response and restricting (cell) growth. Novel metabolomic techniques provided the opportunity to investigate the impact of fetal HIV-1 and combination ARV therapy (cART) exposure on the infants’ immune metabolome. Peroxidized lipids, generated by reactive oxygen species, were increased in cART/HIV-1–exposed infants, indicating altered mitochondrial functioning. The lipid metabolism was further dysregulated with increased triglyceride species and a subsequent decrease in phospholipids in cART/HIV-1–exposed infants compared to control infants. Proinflammatory immune mediators, lysophospholipids as well as cytokines such as CXCL10 and CCL3, were increased whereas anti-inflammatory metabolites from the cytochrome P450 pathway were reduced in cART/HIV-1–exposed infants. Taken together, these data demonstrate that the fetal metabolism is impacted by maternal factors (cART and HIV-1) and skews physiological immune responses toward inflammation in the newborn infant.
2018-06-06 | MTBLS449 | MetaboLights
Project description:Although HIV-1 integration sites are considered to favor active transcription units in the human genome, high-resolution analysis of individual HIV-1 integration sites have shown that the virus can integrate in a variety of host genomic locations, including non-genic regions, challenging the traditional understanding of HIV-1 integration site selection. Here, we showed that HIV-1 targets R-loops, a genomic structure made up of DNA–RNA hybrids, for integration. HIV-1 initiates the formation of R-loops in both genic and non-genic regions of the host genome and preferentially integrates into regions of HIV-1-induced R-loops. Using a cell model that can independently control transcriptional activity and R-loop formation, we demonstrated that the presence of R-loops, regardless of transcriptional activity, directs HIV-1 integration targeting sites. We also found that HIV-1 integrase proteins bind to the host genomic R-loops. These findings provide fundamental insights into the mechanisms of retroviral integration and the new strategies of antiretroviral therapy against HIV-1 latent infection.
2024-11-05 | GSE281025 | GEO
Project description:Although HIV-1 integration sites are considered to favor active transcription units in the human genome, high-resolution analysis of individual HIV-1 integration sites have shown that the virus can integrate in a variety of host genomic locations, including non-genic regions, challenging the traditional understanding of HIV-1 integration site selection. Here, we showed that HIV-1 targets R-loops, a genomic structure made up of DNA–RNA hybrids, for integration. HIV-1 initiates the formation of R-loops in both genic and non-genic regions of the host genome and preferentially integrates into regions of HIV-1-induced R-loops. Using a cell model that can independently control transcriptional activity and R-loop formation, we demonstrated that the presence of R-loops, regardless of transcriptional activity, directs HIV-1 integration targeting sites. We also found that HIV-1 integrase proteins bind to the host genomic R-loops. These findings provide fundamental insights into the mechanisms of retroviral integration and the new strategies of antiretroviral therapy against HIV-1 latent infection.
2024-11-05 | GSE281027 | GEO
Project description:Although HIV-1 integration sites are considered to favor active transcription units in the human genome, high-resolution analysis of individual HIV-1 integration sites have shown that the virus can integrate in a variety of host genomic locations, including non-genic regions, challenging the traditional understanding of HIV-1 integration site selection. Here, we showed that HIV-1 targets R-loops, a genomic structure made up of DNA–RNA hybrids, for integration. HIV-1 initiates the formation of R-loops in both genic and non-genic regions of the host genome and preferentially integrates into regions of HIV-1-induced R-loops. Using a cell model that can independently control transcriptional activity and R-loop formation, we demonstrated that the presence of R-loops, regardless of transcriptional activity, directs HIV-1 integration targeting sites. We also found that HIV-1 integrase proteins bind to the host genomic R-loops. These findings provide fundamental insights into the mechanisms of retroviral integration and the new strategies of antiretroviral therapy against HIV-1 latent infection.
2024-11-05 | GSE281026 | GEO