Role of the CTCF binding site in Human T-Cell Leukemia Virus-1 pathogenesis.

During HTLV-1 infection, the virus integrates into the host cell genome as a provirus with a single CCCTC binding protein (CTCF) binding site (vCTCF-BS), which acts as an insulator between transcriptionally active and inactive regions. Previous studies have shown that the vCTCF-BS is important for m...

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Main Authors: Ancy Joseph, Xiaogang Cheng, John Harding, Jacob Al-Saleem, Patrick Green, Malachi Griffith, Deborah Veis, Daniel A Rauch, Lee Ratner
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2025-06-01
Series:PLoS Pathogens
Online Access:https://doi.org/10.1371/journal.ppat.1012293
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author Ancy Joseph
Xiaogang Cheng
John Harding
Jacob Al-Saleem
Patrick Green
Malachi Griffith
Deborah Veis
Daniel A Rauch
Lee Ratner
author_facet Ancy Joseph
Xiaogang Cheng
John Harding
Jacob Al-Saleem
Patrick Green
Malachi Griffith
Deborah Veis
Daniel A Rauch
Lee Ratner
author_sort Ancy Joseph
collection DOAJ
description During HTLV-1 infection, the virus integrates into the host cell genome as a provirus with a single CCCTC binding protein (CTCF) binding site (vCTCF-BS), which acts as an insulator between transcriptionally active and inactive regions. Previous studies have shown that the vCTCF-BS is important for maintenance of chromatin structure, regulation of viral expression, and DNA and histone methylation. Here, we show that the vCTCF-BS also regulates viral infection and pathogenesis in vivo in a humanized (Hu) mouse model of adult T-cell leukemia/lymphoma. Three cell lines were used to initiate infection of the Hu-mice, i) HTLV-1-WT which carries an intact HTLV-1 provirus genome, ii) HTLV-1-CTCF, which contains a provirus with a mutated vCTCF-BS which abolishes CTCF binding, and a stop codon immediately upstream of the mutated vCTCF-BS which deletes the last 23 amino acids of the p12 gene, and iii) HTLV-1-p12stop that contains the intact vCTCF-BS, but retains the same stop codon in p12 as in the HTLV-1-CTCF cell line. Hu-mice were infected with mitomycin-treated or irradiated HTLV-1 producing cell lines. There was a delay in pathogenicity when Hu-mice were infected with the HTLV-1-CTCF virus compared to mice infected with either HTLV-1-p12 stop or HTLV-1-WT virus. Proviral load (PVL), spleen weights, and CD4 T cell counts were significantly lower in HTLV-1-CTCF infected mice compared to HTLV-1-p12stop infected mice. Furthermore, we found a direct correlation between the PVL in peripheral blood and death of HTLV-1-CTCF infected mice. In cell lines, we found that the vCTCF-BS regulates Tax expression in a time-dependent manner. The scRNAseq analysis of splenocytes from infected mice suggests that the vCTCF-BS plays an important role in activation and expansion of T lymphocytes in vivo. Overall, these findings indicate that the vCTCF-BS regulates Tax expression, proviral load, and HTLV pathogenicity in vivo.
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spelling doaj-art-af66c8fd7e3d4ff4ac0ccf8eee084d512025-08-20T03:22:03ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742025-06-01216e101229310.1371/journal.ppat.1012293Role of the CTCF binding site in Human T-Cell Leukemia Virus-1 pathogenesis.Ancy JosephXiaogang ChengJohn HardingJacob Al-SaleemPatrick GreenMalachi GriffithDeborah VeisDaniel A RauchLee RatnerDuring HTLV-1 infection, the virus integrates into the host cell genome as a provirus with a single CCCTC binding protein (CTCF) binding site (vCTCF-BS), which acts as an insulator between transcriptionally active and inactive regions. Previous studies have shown that the vCTCF-BS is important for maintenance of chromatin structure, regulation of viral expression, and DNA and histone methylation. Here, we show that the vCTCF-BS also regulates viral infection and pathogenesis in vivo in a humanized (Hu) mouse model of adult T-cell leukemia/lymphoma. Three cell lines were used to initiate infection of the Hu-mice, i) HTLV-1-WT which carries an intact HTLV-1 provirus genome, ii) HTLV-1-CTCF, which contains a provirus with a mutated vCTCF-BS which abolishes CTCF binding, and a stop codon immediately upstream of the mutated vCTCF-BS which deletes the last 23 amino acids of the p12 gene, and iii) HTLV-1-p12stop that contains the intact vCTCF-BS, but retains the same stop codon in p12 as in the HTLV-1-CTCF cell line. Hu-mice were infected with mitomycin-treated or irradiated HTLV-1 producing cell lines. There was a delay in pathogenicity when Hu-mice were infected with the HTLV-1-CTCF virus compared to mice infected with either HTLV-1-p12 stop or HTLV-1-WT virus. Proviral load (PVL), spleen weights, and CD4 T cell counts were significantly lower in HTLV-1-CTCF infected mice compared to HTLV-1-p12stop infected mice. Furthermore, we found a direct correlation between the PVL in peripheral blood and death of HTLV-1-CTCF infected mice. In cell lines, we found that the vCTCF-BS regulates Tax expression in a time-dependent manner. The scRNAseq analysis of splenocytes from infected mice suggests that the vCTCF-BS plays an important role in activation and expansion of T lymphocytes in vivo. Overall, these findings indicate that the vCTCF-BS regulates Tax expression, proviral load, and HTLV pathogenicity in vivo.https://doi.org/10.1371/journal.ppat.1012293
spellingShingle Ancy Joseph
Xiaogang Cheng
John Harding
Jacob Al-Saleem
Patrick Green
Malachi Griffith
Deborah Veis
Daniel A Rauch
Lee Ratner
Role of the CTCF binding site in Human T-Cell Leukemia Virus-1 pathogenesis.
PLoS Pathogens
title Role of the CTCF binding site in Human T-Cell Leukemia Virus-1 pathogenesis.
title_full Role of the CTCF binding site in Human T-Cell Leukemia Virus-1 pathogenesis.
title_fullStr Role of the CTCF binding site in Human T-Cell Leukemia Virus-1 pathogenesis.
title_full_unstemmed Role of the CTCF binding site in Human T-Cell Leukemia Virus-1 pathogenesis.
title_short Role of the CTCF binding site in Human T-Cell Leukemia Virus-1 pathogenesis.
title_sort role of the ctcf binding site in human t cell leukemia virus 1 pathogenesis
url https://doi.org/10.1371/journal.ppat.1012293
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