Researchers show that early ART initiation limits #HIV1 clonal expansion and reservoir formation, while #AIDS-stage initiation promotes monoclonal dominance and persistence, highlighting benefits of early treatment.
#STTT #OpenAccess: doi.org/10.1038/s413...
#virology #ViiVHealthcare #steatoticliverdisease #Dovato #2drugHIVregimens #3drugHIVregimens #PASODOBLEstudy #HIV1 #HIV #Biktarvy #ConferenceonRetrovirusesandOpportunisticInfections2026 #HIVinnovation #metabolichealthoutcome #longtermHIVtreatment
zurl.co/ESlts
Left: Virion-associated Vpr proteins induce epigenetic remodeling. Representative fluorescence microscopy images of DDR activation in HeLa and differentiated THP1 cells infected with Vpr or control viruses pre-treated with raltegravir or combination zidovudine/etravirine (n = 50 cells). For these experiments, the mCherry reporter is expressed from the viral promoter instead of being driven by CMV. This allows for tracking infection kinetics in real time to assess DDR activation from virion-associated Vpr. Right: Electrostatic surface potential of a Vpr-DCAF1 co-complex. Surfaces associated with hyperactive or DDR-deficient Vpr mutants are colored in blue and red, respectively.
HIV-1 induces #DNADamageResponse via Vpr, but does this affect the viral cycle? This study shows that Vpr-driven #DNA damage promotes epigenetic remodeling & transcriptional programs to enhance #HIV1 transcription & latency reactivation, with therapeutic potential @plosbiology.org 🧪 plos.io/4c9wVhe
Left: Virion-associated Vpr proteins induce epigenetic remodeling. Representative fluorescence microscopy images of DDR activation in HeLa and differentiated THP1 cells infected with Vpr or control viruses pre-treated with raltegravir or combination zidovudine/etravirine (n = 50 cells). For these experiments, the mCherry reporter is expressed from the viral promoter instead of being driven by CMV. This allows for tracking infection kinetics in real time to assess DDR activation from virion-associated Vpr. Right: Electrostatic surface potential of a Vpr-DCAF1 co-complex. Surfaces associated with hyperactive or DDR-deficient Vpr mutants are colored in blue and red, respectively.
HIV-1 induces #DNADamageResponse via Vpr, but does this affect the viral cycle? This study shows that Vpr-driven #DNA damage promotes epigenetic remodeling & transcriptional programs to enhance #HIV1 transcription & latency reactivation, with therapeutic potential @plosbiology.org 🧪 plos.io/4c9wVhe
Left: Virion-associated Vpr proteins induce epigenetic remodeling. Representative fluorescence microscopy images of DDR activation in HeLa and differentiated THP1 cells infected with Vpr or control viruses pre-treated with raltegravir or combination zidovudine/etravirine (n = 50 cells). For these experiments, the mCherry reporter is expressed from the viral promoter instead of being driven by CMV. This allows for tracking infection kinetics in real time to assess DDR activation from virion-associated Vpr. Right: Electrostatic surface potential of a Vpr-DCAF1 co-complex. Surfaces associated with hyperactive or DDR-deficient Vpr mutants are colored in blue and red, respectively.
HIV-1 induces #DNADamageResponse via Vpr, but does this affect the viral cycle? This study shows that Vpr-driven #DNA damage promotes epigenetic remodeling & transcriptional programs to enhance #HIV1 transcription & latency reactivation, with therapeutic potential @plosbiology.org 🧪 plos.io/4c9wVhe
[Publication Vol 56 - N°1] The first issue of 2026 of "Infectious Diseases Now" is now available.
➡️ www.sciencedirect.com/journal/infe...
#IDsky #Articles #InfectiousDiseases #HumanMetapneumovirus #TickBorneEncephalitis #HumanParainfluenzaVirus #Tuberculosis #HIV1 #AI #Vaccination
This #STTT study identified that retinol-bound holo-RBP4 strongly reactivates #HIV1 in various latently infected T-cell lines via the activation of the canonical NF-κB, JAK/STAT5, and JNK signaling pathways.
#OpenAccess: doi.org/10.1038/s413...
A schematic diagram showing two models of HIV-1 infection. Left panel (HIV-1 latency model): Under HIV-1 infection, upregulated RBM39 promotes m⁶A methylation of Tat RNA. This modification is recognized by YTHDC1, which subsequently recruits the RNA helicase DDX5 to degrade m⁶A-methylated Tat RNA. As a result, Tat RNA fails to undergo splicing and translation into functional Tat protein, thereby preventing activation of the HIV-1 LTR promoter and maintaining viral latency. Right panel (HIV-1 reactivation model): Treatment with indisulam induces degradation of RBM39. This abolishes the recognition of Tat RNA by YTHDC1 and its degradation by DDX5. Consequently, Tat RNA is efficiently translated into Tat protein, which activates the HIV-1 LTR promoter, leading to HIV-1 reactivation.
Latent HIV-1 resists current #reactivation therapies, hindering viral eradication. This study identifies #RNAbindingProtein RBM39 as a scaffold assembling an m⁶A-dependent RNA decay complex that degrades Tat transcripts, enforcing & maintaining #HIV1 latency @plosbiology.org 🧪 plos.io/4nRrHsO
A schematic diagram showing two models of HIV-1 infection. Left panel (HIV-1 latency model): Under HIV-1 infection, upregulated RBM39 promotes m⁶A methylation of Tat RNA. This modification is recognized by YTHDC1, which subsequently recruits the RNA helicase DDX5 to degrade m⁶A-methylated Tat RNA. As a result, Tat RNA fails to undergo splicing and translation into functional Tat protein, thereby preventing activation of the HIV-1 LTR promoter and maintaining viral latency. Right panel (HIV-1 reactivation model): Treatment with indisulam induces degradation of RBM39. This abolishes the recognition of Tat RNA by YTHDC1 and its degradation by DDX5. Consequently, Tat RNA is efficiently translated into Tat protein, which activates the HIV-1 LTR promoter, leading to HIV-1 reactivation.
Latent HIV-1 resists current #reactivation therapies, hindering viral eradication. This study identifies #RNAbindingProtein RBM39 as a scaffold assembling an m⁶A-dependent RNA decay complex that degrades Tat transcripts, enforcing & maintaining #HIV1 latency @plosbiology.org 🧪 plos.io/4nRrHsO
A schematic diagram showing two models of HIV-1 infection. Left panel (HIV-1 latency model): Under HIV-1 infection, upregulated RBM39 promotes m⁶A methylation of Tat RNA. This modification is recognized by YTHDC1, which subsequently recruits the RNA helicase DDX5 to degrade m⁶A-methylated Tat RNA. As a result, Tat RNA fails to undergo splicing and translation into functional Tat protein, thereby preventing activation of the HIV-1 LTR promoter and maintaining viral latency. Right panel (HIV-1 reactivation model): Treatment with indisulam induces degradation of RBM39. This abolishes the recognition of Tat RNA by YTHDC1 and its degradation by DDX5. Consequently, Tat RNA is efficiently translated into Tat protein, which activates the HIV-1 LTR promoter, leading to HIV-1 reactivation.
Latent HIV-1 resists current #reactivation therapies, hindering viral eradication. This study identifies #RNAbindingProtein RBM39 as a scaffold assembling an m⁶A-dependent RNA decay complex that degrades Tat transcripts, enforcing & maintaining #HIV1 latency @plosbiology.org 🧪 plos.io/4nRrHsO
[Publication] The article "LncRNA NEAT1 rs3825071 polymorphisms associated with HIV-1 infection in the Hulunbuir population of China" is now available.
www.sciencedirect.com/science/arti...
#IDsky #NEAT1 #Rs3825071 #Polymorphisms #HIV1 #HulunbuirPopulation
Systematic screening of a hemofiltrate-derived #PeptideLibrary identified that retinol-bound holo-RBP4 strongly reactivates latent #HIV1 in various T cell lines via activating the canonical NF-κB pathway, JAK/STAT5 & JNK signaling. #medsky
#STTT #OpenAccess: doi.org/10.1038/s413...
Left: Immunofluorescence analysis of PMA-differentiated THP-1 parental (control) macrophages infected with Lai∆envGFP/G (WT, M10, or WT in the presence of RT inhibitor (EFV), MOI 1), and stained with anti-dsRNA (J2) antibody. The establishment of productive HIV-1 infection in THP1/PMA macrophages was visualized by GFP expression, and nucleus is stained with DAPI. The white arrowheads indicate positive staining of dsRNA puncta. Scale bar represents 5 μm. Right: Schematic of the diversity of cytosolic HIV-1 icRNA sensing and innate immune activation pathways in myeloid cells. Image was created in BioRender. Jalloh, S. (2025)
Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @plosbiology.org 🧪 plos.io/45VTGBR
Left: Immunofluorescence analysis of PMA-differentiated THP-1 parental (control) macrophages infected with Lai∆envGFP/G (WT, M10, or WT in the presence of RT inhibitor (EFV), MOI 1), and stained with anti-dsRNA (J2) antibody. The establishment of productive HIV-1 infection in THP1/PMA macrophages was visualized by GFP expression, and nucleus is stained with DAPI. The white arrowheads indicate positive staining of dsRNA puncta. Scale bar represents 5 μm. Right: Schematic of the diversity of cytosolic HIV-1 icRNA sensing and innate immune activation pathways in myeloid cells. Image was created in BioRender. Jalloh, S. (2025)
Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @plosbiology.org 🧪 plos.io/45VTGBR
Left: Immunofluorescence analysis of PMA-differentiated THP-1 parental (control) macrophages infected with Lai∆envGFP/G (WT, M10, or WT in the presence of RT inhibitor (EFV), MOI 1), and stained with anti-dsRNA (J2) antibody. The establishment of productive HIV-1 infection in THP1/PMA macrophages was visualized by GFP expression, and nucleus is stained with DAPI. The white arrowheads indicate positive staining of dsRNA puncta. Scale bar represents 5 μm. Right: Schematic of the diversity of cytosolic HIV-1 icRNA sensing and innate immune activation pathways in myeloid cells. Image was created in BioRender.
Even with #antiretroviral therapy, HIV-1 can still cause persistent inflammation in macrophages. This study shows that intron-containing #HIV1 RNA (icRNA) activates NLRP1 #inflammasome & induces IL-1β secretion in myeloid cells, independent of RIG-I-like receptors @plosbiology.org 🧪 plos.io/45VTGBR
Test
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Dr. Amir Ardeshir and a team in Dr.
@mamartins83.bsky.social
's lab at
@wertheimufscripps.bsky.social
used AAV vectors to generate #HIV1 immunity in infant rhesus macaques!
Article: https://go.nature.com/4lwHts2
Episode with discussion: https://bit.ly/4mIESvZ
Beautiful work! RRE binds CRM1. Wow! 😊
#HIV1 #Rev #RRE #CRM1 #Exportin1 #Ran
www.cell.com/molecular-ce...
Dr. Amir Ardeshir and a team in Dr. @mamartins83.bsky.social's lab at @wertheimufscripps.bsky.social used AAV vectors to generate #HIV1 immunity in infant rhesus macaques!
Article: https://go.nature.com/4lwHts2
Episode with discussion: https://bit.ly/4mIESvZ
#CRISPR snipped #HIV Out Of #Human #Immune Cells. It Stayed Gone!
#Scientists used CRISPR/#Cas9 #GeneEditing to delete #HIV1 #DNA from #Tcells
Unlike #treatments that only #suppress the #virus, this removes HIV’s #genetic code from the immune system! #Science #Biology #Health
x.com/i/grok/share...
Novel antiviral protein SAMD9L blocks HIV-1 and other lentiviruses 🔬🧬✨ www.news-medical.net/news/2024070... #HIV #Research #Antiviral #SAMD9L #HIV1 #VirusInhibition #CellularImmunity #Interferon #Lentiviruses #ViralTranslation #Biomedical @plos.bsky.social
