HIV-1 exploits LBPA-dependent intraepithelial trafficking for productive infection of human intestinal mucosa.

The gastrointestinal tract is a prominent portal of entry for HIV-1 during sexual or perinatal transmission, as well as a major site of HIV-1 persistence and replication. Elucidation of underlying mechanisms of intestinal HIV-1 infection are thus needed for the advancement of HIV-1 curative therapie...

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Main Authors: Anusca G Rader, Alexandra P M Cloherty, Kharishma S Patel, Dima D A Almandawi, Dasja Pajkrt, Katja C Wolthers, Adithya Sridhar, Sterre van Piggelen, Liselotte E Baaij, Renée R C E Schreurs, Carla M S Ribeiro
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2024-12-01
Series:PLoS Pathogens
Online Access:https://doi.org/10.1371/journal.ppat.1012714
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author Anusca G Rader
Alexandra P M Cloherty
Kharishma S Patel
Dima D A Almandawi
Dasja Pajkrt
Katja C Wolthers
Adithya Sridhar
Sterre van Piggelen
Liselotte E Baaij
Renée R C E Schreurs
Carla M S Ribeiro
author_facet Anusca G Rader
Alexandra P M Cloherty
Kharishma S Patel
Dima D A Almandawi
Dasja Pajkrt
Katja C Wolthers
Adithya Sridhar
Sterre van Piggelen
Liselotte E Baaij
Renée R C E Schreurs
Carla M S Ribeiro
author_sort Anusca G Rader
collection DOAJ
description The gastrointestinal tract is a prominent portal of entry for HIV-1 during sexual or perinatal transmission, as well as a major site of HIV-1 persistence and replication. Elucidation of underlying mechanisms of intestinal HIV-1 infection are thus needed for the advancement of HIV-1 curative therapies. Here, we present a human 2D intestinal immuno-organoid system to model HIV-1 disease that recapitulates tissue compartmentalization and epithelial-immune cellular interactions. Our data demonstrate that apical exposure of intestinal epithelium to HIV-1 results in viral internalization, with subsequent basolateral shedding of replication-competent viruses, in a manner that is impervious to antiretroviral treatment. Incorporation of subepithelial dendritic cells resulted in HIV-1 luminal sampling and amplification of residual viral replication of lab-adapted and transmitted-founder (T/F) HIV-1 variants. Markedly, intraepithelial viral capture ensued an altered distribution of specialized endosomal pathways alongside durable sequestration of infectious HIV-1 within lysobisphosphatidic acid (LPBA)-rich vesicles. Therapeutic neutralization of LBPA-dependent trafficking limited productive HIV-1 infection, and thereby demonstrated the pivotal role of intraepithelial multivesicular endosomes as niches for virulent HIV-1 within the intestinal mucosa. Our study showcases the application of primary human 2D immune-competent organoid cultures in uncovering mechanisms of intestinal HIV-1 disease as well as a platform for preclinical antiviral drug discovery.
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spelling doaj-art-c3eabf9638324a299f8b346ecaf98c7c2025-08-20T02:45:00ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742024-12-012012e101271410.1371/journal.ppat.1012714HIV-1 exploits LBPA-dependent intraepithelial trafficking for productive infection of human intestinal mucosa.Anusca G RaderAlexandra P M ClohertyKharishma S PatelDima D A AlmandawiDasja PajkrtKatja C WolthersAdithya SridharSterre van PiggelenLiselotte E BaaijRenée R C E SchreursCarla M S RibeiroThe gastrointestinal tract is a prominent portal of entry for HIV-1 during sexual or perinatal transmission, as well as a major site of HIV-1 persistence and replication. Elucidation of underlying mechanisms of intestinal HIV-1 infection are thus needed for the advancement of HIV-1 curative therapies. Here, we present a human 2D intestinal immuno-organoid system to model HIV-1 disease that recapitulates tissue compartmentalization and epithelial-immune cellular interactions. Our data demonstrate that apical exposure of intestinal epithelium to HIV-1 results in viral internalization, with subsequent basolateral shedding of replication-competent viruses, in a manner that is impervious to antiretroviral treatment. Incorporation of subepithelial dendritic cells resulted in HIV-1 luminal sampling and amplification of residual viral replication of lab-adapted and transmitted-founder (T/F) HIV-1 variants. Markedly, intraepithelial viral capture ensued an altered distribution of specialized endosomal pathways alongside durable sequestration of infectious HIV-1 within lysobisphosphatidic acid (LPBA)-rich vesicles. Therapeutic neutralization of LBPA-dependent trafficking limited productive HIV-1 infection, and thereby demonstrated the pivotal role of intraepithelial multivesicular endosomes as niches for virulent HIV-1 within the intestinal mucosa. Our study showcases the application of primary human 2D immune-competent organoid cultures in uncovering mechanisms of intestinal HIV-1 disease as well as a platform for preclinical antiviral drug discovery.https://doi.org/10.1371/journal.ppat.1012714
spellingShingle Anusca G Rader
Alexandra P M Cloherty
Kharishma S Patel
Dima D A Almandawi
Dasja Pajkrt
Katja C Wolthers
Adithya Sridhar
Sterre van Piggelen
Liselotte E Baaij
Renée R C E Schreurs
Carla M S Ribeiro
HIV-1 exploits LBPA-dependent intraepithelial trafficking for productive infection of human intestinal mucosa.
PLoS Pathogens
title HIV-1 exploits LBPA-dependent intraepithelial trafficking for productive infection of human intestinal mucosa.
title_full HIV-1 exploits LBPA-dependent intraepithelial trafficking for productive infection of human intestinal mucosa.
title_fullStr HIV-1 exploits LBPA-dependent intraepithelial trafficking for productive infection of human intestinal mucosa.
title_full_unstemmed HIV-1 exploits LBPA-dependent intraepithelial trafficking for productive infection of human intestinal mucosa.
title_short HIV-1 exploits LBPA-dependent intraepithelial trafficking for productive infection of human intestinal mucosa.
title_sort hiv 1 exploits lbpa dependent intraepithelial trafficking for productive infection of human intestinal mucosa
url https://doi.org/10.1371/journal.ppat.1012714
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