---
title: "Defective HIV-1 Proviral Transcription Drives Interferon Responses in Myeloid Cells"
id: "pubmed-42573264"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42573264"
content_type: "clinical_feed_article"
specialty: "Infectious Disease"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42573264/"
doi: "10.1128/jvi.00552-26"
published_at: "2026-09-22T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Defective HIV-1 Proviral Transcription Drives Interferon Responses in Myeloid Cells
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42573264
- **Specialty:** [Infectious Disease](https://medichelpline.com/clinical-feed/infectious-disease.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42573264/)
- **DOI:** [10.1128/jvi.00552-26](https://doi.org/10.1128%2Fjvi.00552-26)
- **Published At:** 2026-09-22T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- The study examines how transcription from **defective HIV-1 proviruses** can trigger innate immune responses in myeloid cells and potentially contribute to chronic inflammation in people with HIV (PWH). - The authors previously identified an intragenic promoter inside the HIV-1 **env** gene that drives expression of aberrant viral RNAs; serum levels of these transcripts correlated with inflammatory cytokines in PWH. - To test effects of defective proviruses, CRISPR-Cas9 was used to inactivate the 5' long terminal repeat (LTR) promoter/enhancer, creating proviruses unable to produce full-length viral transcripts from the canonical LTR. - Cells harboring the 5' LTR deletion produced significantly higher levels of the chemokines **IP-10** and **IL-8** in monocytic cell lines and in primary monocyte-derived macrophages in vitro. - Transcripts originating from the intragenic **env** promoter were shown to be capped and polyadenylated, indicating they are processed like conventional mRNAs. - Induction of **IP-10** by these transcripts depended on the cytosolic RNA-sensing pathway components **MDA5** and **MAVS**, whereas DNA sensor **cGAS** and RNA sensor **RIG-I** were not required. - The authors propose that ongoing expression from defective proviruses contributes to chronic type I interferon pathway activation and systemic inflammation in PWH despite ART-mediated viral suppression. - The work underscores the biological importance of the large pool of defective proviruses in the persistent inflammatory phenotype observed in treated HIV-1 infection and suggests mechanistic links to innate immune sensing in myeloid cells.
## Clinical Analysis & Structured Key Points
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Epub 2026 Aug 10. # Intragenic transcription from defective HIV proviruses triggers interferon responses in myeloid cells [Jonathan M Kilroy](https://pubmed.ncbi.nlm.nih.gov/?term=Kilroy+JM&cauthor_id=42573264)[#](https://pubmed.ncbi.nlm.nih.gov/42573264/#full-view-equal-contrib-explanation "Contributed equally")[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#full-view-affiliation-1 "Department of Virology, Immunology, and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA."), [Aparna A Deokar](https://pubmed.ncbi.nlm.nih.gov/?term=Deokar+AA&cauthor_id=42573264)[#](https://pubmed.ncbi.nlm.nih.gov/42573264/#full-view-equal-contrib-explanation "Contributed equally")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#full-view-affiliation-2 "Department of Biology, Boston University, Boston, Massachusetts, USA."), [Samantha Patalano](https://pubmed.ncbi.nlm.nih.gov/?term=Patalano+S&cauthor_id=42573264)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#full-view-affiliation-2 "Department of Biology, Boston University, Boston, Massachusetts, USA."), [Juan I Fuxman Bass](https://pubmed.ncbi.nlm.nih.gov/?term=Fuxman+Bass+JI&cauthor_id=42573264)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#full-view-affiliation-2 "Department of Biology, Boston University, Boston, Massachusetts, USA."), [Manish Sagar](https://pubmed.ncbi.nlm.nih.gov/?term=Sagar+M&cauthor_id=42573264)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#full-view-affiliation-1 "Department of Virology, Immunology, and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#full-view-affiliation-3 "Boston Medical Center, Department of Medicine, Section of Infectious Diseases, Boston, Massachusetts, USA."), [Suryaram Gummuluru](https://pubmed.ncbi.nlm.nih.gov/?term=Gummuluru+S&cauthor_id=42573264)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#full-view-affiliation-1 "Department of Virology, Immunology, and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA."), [Andrew J Henderson](https://pubmed.ncbi.nlm.nih.gov/?term=Henderson+AJ&cauthor_id=42573264)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#full-view-affiliation-1 "Department of Virology, Immunology, and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#full-view-affiliation-3 "Boston Medical Center, Department of Medicine, Section of Infectious Diseases, Boston, Massachusetts, USA.") Affiliations Expand ### Affiliations * 1 Department of Virology, Immunology, and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA. * 2 Department of Biology, Boston University, Boston, Massachusetts, USA. * 3 Boston Medical Center, Department of Medicine, Section of Infectious Diseases, Boston, Massachusetts, USA. # Contributed equally. * PMID: **42573264** * DOI: [ 10.1128/jvi.00552-26 ](https://doi.org/10.1128/jvi.00552-26) Item in Clipboard # Intragenic transcription from defective HIV proviruses triggers interferon responses in myeloid cells Jonathan M Kilroy et al. J Virol. 2026. Show details Display options Display options Format Abstract PubMed PMID J Virol Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22J+Virol%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22J+Virol%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42573264/) . 2026 Sep 22;100(9):e0055226. doi: 10.1128/jvi.00552-26. Epub 2026 Aug 10. ### Authors [Jonathan M Kilroy](https://pubmed.ncbi.nlm.nih.gov/?term=Kilroy+JM&cauthor_id=42573264)[#](https://pubmed.ncbi.nlm.nih.gov/42573264/#short-view-equal-contrib-explanation "Contributed equally")[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#short-view-affiliation-1 "Department of Virology, Immunology, and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA."), [Aparna A Deokar](https://pubmed.ncbi.nlm.nih.gov/?term=Deokar+AA&cauthor_id=42573264)[#](https://pubmed.ncbi.nlm.nih.gov/42573264/#short-view-equal-contrib-explanation "Contributed equally")[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#short-view-affiliation-2 "Department of Biology, Boston University, Boston, Massachusetts, USA."), [Samantha Patalano](https://pubmed.ncbi.nlm.nih.gov/?term=Patalano+S&cauthor_id=42573264)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#short-view-affiliation-2 "Department of Biology, Boston University, Boston, Massachusetts, USA."), [Juan I Fuxman Bass](https://pubmed.ncbi.nlm.nih.gov/?term=Fuxman+Bass+JI&cauthor_id=42573264)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#short-view-affiliation-2 "Department of Biology, Boston University, Boston, Massachusetts, USA."), [Manish Sagar](https://pubmed.ncbi.nlm.nih.gov/?term=Sagar+M&cauthor_id=42573264)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#short-view-affiliation-1 "Department of Virology, Immunology, and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#short-view-affiliation-3 "Boston Medical Center, Department of Medicine, Section of Infectious Diseases, Boston, Massachusetts, USA."), [Suryaram Gummuluru](https://pubmed.ncbi.nlm.nih.gov/?term=Gummuluru+S&cauthor_id=42573264)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#short-view-affiliation-1 "Department of Virology, Immunology, and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA."), [Andrew J Henderson](https://pubmed.ncbi.nlm.nih.gov/?term=Henderson+AJ&cauthor_id=42573264)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#short-view-affiliation-1 "Department of Virology, Immunology, and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42573264/#short-view-affiliation-3 "Boston Medical Center, Department of Medicine, Section of Infectious Diseases, Boston, Massachusetts, USA.") ### Affiliations * 1 Department of Virology, Immunology, and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, USA. * 2 Department of Biology, Boston University, Boston, Massachusetts, USA. * 3 Boston Medical Center, Department of Medicine, Section of Infectious Diseases, Boston, Massachusetts, USA. # Contributed equally. * PMID: **42573264** * DOI: [ 10.1128/jvi.00552-26 ](https://doi.org/10.1128/jvi.00552-26) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract The persistent HIV-1 reservoir includes a subset of cells harboring transcriptionally repressed latent HIV-1 that contributes to rebound upon antiretroviral treatment (ART) interruption. However, the majority of the reservoir consists of defective proviral genomes with mutations that prevent production of HIV-1 virions. People with HIV (PWH), even with suppression of viremia, demonstrate comorbidities of the central nervous system, heart, gut, and general aging-associated inflammation. Previously, we identified a transcriptionally active element within the envelope gene (_env_) of HIV-1, which mediates the expression of aberrant HIV-1 RNAs. We hypothesize that spurious expression of defective proviruses contributes to the general inflammation that drives these comorbidities. We observed correlations between levels of inflammatory cytokines in serum of PWH and levels of HIV-1 transcripts from this intragenic promoter. To investigate the impact of defective proviruses, we employed CRISPR-Cas9 to render the 5' long terminal repeat (LTR), which acts as the enhancer and promoter for proviral transcription, non-functional. HIV-1-infected cells harboring this deletion produce significantly higher levels of IP-10 and IL-8 _in vitro_ in both monocytic cell lines and primary monocyte-derived macrophages. Transcripts generated from the _env_ promoter include a 5' cap and polyA tail, and the induction of IP-10 expression was dependent on the cytosolic innate immune sensing pathway components MDA5 and MAVS and not cGAS and RIG-I. We propose that defective HIV proviruses contribute to chronic inflammation in PWH through an MDA5-dependent induction of type I interferon pathways.**IMPORTANCE** People with HIV-1 are at higher risk of developing age-associated comorbidities and immune exhaustion even when receiving antiviral treatments and having no detectable viremia. Transcription and translation have been documented from latent and defective proviruses, but their impact on inflammation associated with chronic HIV-1 infection remains poorly understood. The significance of this work is in identifying a role for defective HIV-1 proviruses and correlating their transcription in triggering a type I interferon response. These results highlight the importance of the persistent defective HIV-1 proviruses and understanding their impact on driving chronic inflammation to inform future strategies to assure people with HIV-1 healthy living and aging. **Keywords:** HIV-1; defective proviruses; inflammation; transcription. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement The authors declare no conflict of interest. ## Update of * [ Intragenic Transcription from Defective HIV Proviruses Triggers Interferon Responses in Myeloid Cells. ](https://pubmed.ncbi.nlm.nih.gov/41993403/) Kilroy J, Deokar A, Patalano S, Bass JF, Sagar M, Gummuluru S, Henderson AJ. Kilroy J, et al. bioRxiv [Preprint]. 2026 Apr 7:2026.04.06.716685. doi: 10.64898/2026.04.06.716685. bioRxiv. 2026. Update in: [J Virol. 2026 Sep 22;100(9):e0055226. doi: 10.1128/jvi.00552-26.](https://pubmed.ncbi.nlm.nih.gov/42573264/) PMID: 41993403 Free PMC article. Updated. Preprint. ## Similar articles * [ Intragenic Transcription from Defective HIV Proviruses Triggers Interferon Responses in Myeloid Cells. ](https://pubmed.ncbi.nlm.nih.gov/41993403/) Kilroy J, Deokar A, Patalano S, Bass JF, Sagar M, Gummuluru S, Henderson AJ.Kilroy J, et al.bioRxiv [Preprint]. 2026 Apr 7:2026.04.06.716685. doi: 10.64898/2026.04.06.716685.bioRxiv. 2026.Update in: [J Virol. 2026 Sep 22;100(9):e0055226. doi: 10.1128/jvi.00552-26.](https://pubmed.ncbi.nlm.nih.gov/42573264/)PMID: 41993403Free PMC article.Updated.Preprint. * [ Intragenic proviral elements support transcription of defective HIV-1 proviruses. ](https://pubmed.ncbi.nlm.nih.gov/34962974/) Kuniholm J, Armstrong E, Bernabe B, Coote C, Berenson A, Patalano SD, Olson A, He X, Lin NH, Fuxman Bass JI, Henderson AJ.Kuniholm J, et al.PLoS Pathog. 2021 Dec 28;17(12):e1009982. doi: 10.1371/journal.ppat.1009982. eCollection 2021 Dec.PLoS Pathog. 2021.PMID: 34962974Free PMC article. * [ Defective HIV-1 genomes and their potential impact on HIV pathogenesis. ](https://pubmed.ncbi.nlm.nih.gov/35764966/) Kuniholm J, Coote C, Henderson AJ.Kuniholm J, et al.Retrovirology. 2022 Jun 28;19(1):13. doi: 10.1186/s12977-022-00601-8.Retrovirology. 2022.PMID: 35764966Free PMC article.Review. * [ Non-suppressible HIV viremia sustained by clonally expanded CD4+ T cells harboring a genomically defective provirus with an immune-evasive protein expression profile. ](https://pubmed.ncbi.nlm.nih.gov/41910264/) Omondi FH, Sang Y, Dong W, Mwimanzi F, Cheung PK, Barad E, Derza Z, Anderson K, Shahid A, Mysak V, Lima VD, Hull M, Brumme CJ, Harris M, Montaner JSG, Guillemi S, Brockman MA, Brumme ZL.Omondi FH, et al.mBio. 2026 May 13;17(5):e0390925. doi: 10.1128/mbio.03909-25. Epub 2026 Mar 30.mBio. 2026.PMID: 41910264Free PMC article. * [ Chronic HIV Transcription, Translation, and Persistent Inflammation. ](https://pubmed.ncbi.nlm.nih.gov/38793632/) Kilroy JM, Leal AA, Henderson AJ.Kilroy JM, et al.Viruses. 2024 May 9;16(5):751. doi: 10.3390/v16050751.Viruses. 2024.PMID: 38793632Free PMC article.Review. 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