HTLV-1 p13 Protein Hijacks Macrophage Polarization and Promotes T-Cell Recruitment

The human T-cell leukemia type-1 (HTLV-1) retrovirus establishes chronic life-long infection in a fraction of infected individuals associated with severe pathological conditions. Although the mechanism driving disease development is not fully understood, current evidence indicates the essential func...

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Main Authors: Ramona Moles, Maria Omsland, Cynthia A. Pise-Masison, Jeffrey J. Subleski, Daniel W. McVicar, Sarkis Sarkis, Anna Gutowska, Luca Schifanella, Melvin Doster, Robyn Washington-Parks, Vincenzo Ciminale, Genoveffa Franchini
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Language:English
Published: MDPI AG 2025-03-01
Series:Viruses
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Online Access:https://www.mdpi.com/1999-4915/17/4/471
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author Ramona Moles
Maria Omsland
Cynthia A. Pise-Masison
Jeffrey J. Subleski
Daniel W. McVicar
Sarkis Sarkis
Anna Gutowska
Luca Schifanella
Melvin Doster
Robyn Washington-Parks
Vincenzo Ciminale
Genoveffa Franchini
author_facet Ramona Moles
Maria Omsland
Cynthia A. Pise-Masison
Jeffrey J. Subleski
Daniel W. McVicar
Sarkis Sarkis
Anna Gutowska
Luca Schifanella
Melvin Doster
Robyn Washington-Parks
Vincenzo Ciminale
Genoveffa Franchini
author_sort Ramona Moles
collection DOAJ
description The human T-cell leukemia type-1 (HTLV-1) retrovirus establishes chronic life-long infection in a fraction of infected individuals associated with severe pathological conditions. Although the mechanism driving disease development is not fully understood, current evidence indicates the essential functions of viral regulatory proteins. Among these, the p13 protein has previously been shown to localize to the inner mitochondrial membrane in T cells, altering mitochondrial biology and T-cell function. While CD4<sup>+</sup> T cells are the primary cell target of HTLV-1 infection, genomic viral DNA has also been detected in monocytes, macrophages, and dendritic cells, which orchestrate innate and adaptive immunity and play a critical role in protecting against virus-induce diseases by establishing the appropriate balance of pro and anti-inflammatory responses. Given the central role of mitochondria in monocyte differentiation, we investigated the effect of p13 in monocytes/macrophages and found that by localizing to mitochondria, p13 affects mitochondrial respiration. Moreover, we demonstrate that p13 expression affects macrophage polarization to favor the recruitment of CD4<sup>+</sup> T cells, the primary target of the virus, potentially facilitating the spread of viral infection and the development of disease.
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spelling doaj-art-47bf4cccdef3457ab2962ba9f0b4cf002025-08-20T03:13:33ZengMDPI AGViruses1999-49152025-03-0117447110.3390/v17040471HTLV-1 p13 Protein Hijacks Macrophage Polarization and Promotes T-Cell RecruitmentRamona Moles0Maria Omsland1Cynthia A. Pise-Masison2Jeffrey J. Subleski3Daniel W. McVicar4Sarkis Sarkis5Anna Gutowska6Luca Schifanella7Melvin Doster8Robyn Washington-Parks9Vincenzo Ciminale10Genoveffa Franchini11Animal Models and Retroviral Vaccines Section, Vaccine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USAAnimal Models and Retroviral Vaccines Section, Vaccine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USAAnimal Models and Retroviral Vaccines Section, Vaccine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USACancer and Innovation Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USACancer and Innovation Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USAAnimal Models and Retroviral Vaccines Section, Vaccine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USAAnimal Models and Retroviral Vaccines Section, Vaccine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USAAnimal Models and Retroviral Vaccines Section, Vaccine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USAAnimal Models and Retroviral Vaccines Section, Vaccine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USAAnimal Models and Retroviral Vaccines Section, Vaccine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USADepartment of Surgery, Oncology and Gastroenterology, University of Padua, 35122 Padua, ItalyAnimal Models and Retroviral Vaccines Section, Vaccine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USAThe human T-cell leukemia type-1 (HTLV-1) retrovirus establishes chronic life-long infection in a fraction of infected individuals associated with severe pathological conditions. Although the mechanism driving disease development is not fully understood, current evidence indicates the essential functions of viral regulatory proteins. Among these, the p13 protein has previously been shown to localize to the inner mitochondrial membrane in T cells, altering mitochondrial biology and T-cell function. While CD4<sup>+</sup> T cells are the primary cell target of HTLV-1 infection, genomic viral DNA has also been detected in monocytes, macrophages, and dendritic cells, which orchestrate innate and adaptive immunity and play a critical role in protecting against virus-induce diseases by establishing the appropriate balance of pro and anti-inflammatory responses. Given the central role of mitochondria in monocyte differentiation, we investigated the effect of p13 in monocytes/macrophages and found that by localizing to mitochondria, p13 affects mitochondrial respiration. Moreover, we demonstrate that p13 expression affects macrophage polarization to favor the recruitment of CD4<sup>+</sup> T cells, the primary target of the virus, potentially facilitating the spread of viral infection and the development of disease.https://www.mdpi.com/1999-4915/17/4/471HTLV-1p13viral proteinmitochondriamonocytesmacrophages
spellingShingle Ramona Moles
Maria Omsland
Cynthia A. Pise-Masison
Jeffrey J. Subleski
Daniel W. McVicar
Sarkis Sarkis
Anna Gutowska
Luca Schifanella
Melvin Doster
Robyn Washington-Parks
Vincenzo Ciminale
Genoveffa Franchini
HTLV-1 p13 Protein Hijacks Macrophage Polarization and Promotes T-Cell Recruitment
Viruses
HTLV-1
p13
viral protein
mitochondria
monocytes
macrophages
title HTLV-1 p13 Protein Hijacks Macrophage Polarization and Promotes T-Cell Recruitment
title_full HTLV-1 p13 Protein Hijacks Macrophage Polarization and Promotes T-Cell Recruitment
title_fullStr HTLV-1 p13 Protein Hijacks Macrophage Polarization and Promotes T-Cell Recruitment
title_full_unstemmed HTLV-1 p13 Protein Hijacks Macrophage Polarization and Promotes T-Cell Recruitment
title_short HTLV-1 p13 Protein Hijacks Macrophage Polarization and Promotes T-Cell Recruitment
title_sort htlv 1 p13 protein hijacks macrophage polarization and promotes t cell recruitment
topic HTLV-1
p13
viral protein
mitochondria
monocytes
macrophages
url https://www.mdpi.com/1999-4915/17/4/471
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