Cargando…

Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets

The human T-cell leukemia virus type 1 (HTLV-1) is the only known human oncogenic retrovirus. HTLV-1 can cause a type of cancer called adult T-cell leukemia/lymphoma (ATL). The virus is transmitted through the body fluids of infected individuals, primarily breast milk, blood, and semen. At least 5–1...

Descripción completa

Detalles Bibliográficos
Autores principales: Marino-Merlo, Francesca, Grelli, Sandro, Mastino, Antonio, Lai, Michele, Ferrari, Paola, Nicolini, Andrea, Pistello, Mauro, Macchi, Beatrice
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10572738/
https://www.ncbi.nlm.nih.gov/pubmed/37834255
http://dx.doi.org/10.3390/ijms241914807
_version_ 1785120302863220736
author Marino-Merlo, Francesca
Grelli, Sandro
Mastino, Antonio
Lai, Michele
Ferrari, Paola
Nicolini, Andrea
Pistello, Mauro
Macchi, Beatrice
author_facet Marino-Merlo, Francesca
Grelli, Sandro
Mastino, Antonio
Lai, Michele
Ferrari, Paola
Nicolini, Andrea
Pistello, Mauro
Macchi, Beatrice
author_sort Marino-Merlo, Francesca
collection PubMed
description The human T-cell leukemia virus type 1 (HTLV-1) is the only known human oncogenic retrovirus. HTLV-1 can cause a type of cancer called adult T-cell leukemia/lymphoma (ATL). The virus is transmitted through the body fluids of infected individuals, primarily breast milk, blood, and semen. At least 5–10 million people in the world are infected with HTLV-1. In addition to ATL, HTLV-1 infection can also cause HTLV-I-associated myelopathy (HAM/TSP). ATL is characterized by a low viral expression and poor prognosis. The oncogenic mechanism triggered by HTLV-1 is extremely complex and the molecular pathways are not fully understood. However, viral regulatory proteins Tax and HTLV-1 bZIP factor (HBZ) have been shown to play key roles in the transformation of HTLV-1-infected T cells. Moreover, several studies have shown that the final fate of HTLV-1-infected transformed Tcell clones is the result of a complex interplay of HTLV-1 oncogenic protein expression with cellular transcription factors that subvert the cell cycle and disrupt regulated cell death, thereby exerting their transforming effects. This review provides updated information on the mechanisms underlying the transforming action of HTLV-1 and highlights potential therapeutic targets to combat ATL.
format Online
Article
Text
id pubmed-10572738
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-105727382023-10-14 Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets Marino-Merlo, Francesca Grelli, Sandro Mastino, Antonio Lai, Michele Ferrari, Paola Nicolini, Andrea Pistello, Mauro Macchi, Beatrice Int J Mol Sci Review The human T-cell leukemia virus type 1 (HTLV-1) is the only known human oncogenic retrovirus. HTLV-1 can cause a type of cancer called adult T-cell leukemia/lymphoma (ATL). The virus is transmitted through the body fluids of infected individuals, primarily breast milk, blood, and semen. At least 5–10 million people in the world are infected with HTLV-1. In addition to ATL, HTLV-1 infection can also cause HTLV-I-associated myelopathy (HAM/TSP). ATL is characterized by a low viral expression and poor prognosis. The oncogenic mechanism triggered by HTLV-1 is extremely complex and the molecular pathways are not fully understood. However, viral regulatory proteins Tax and HTLV-1 bZIP factor (HBZ) have been shown to play key roles in the transformation of HTLV-1-infected T cells. Moreover, several studies have shown that the final fate of HTLV-1-infected transformed Tcell clones is the result of a complex interplay of HTLV-1 oncogenic protein expression with cellular transcription factors that subvert the cell cycle and disrupt regulated cell death, thereby exerting their transforming effects. This review provides updated information on the mechanisms underlying the transforming action of HTLV-1 and highlights potential therapeutic targets to combat ATL. MDPI 2023-09-30 /pmc/articles/PMC10572738/ /pubmed/37834255 http://dx.doi.org/10.3390/ijms241914807 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Marino-Merlo, Francesca
Grelli, Sandro
Mastino, Antonio
Lai, Michele
Ferrari, Paola
Nicolini, Andrea
Pistello, Mauro
Macchi, Beatrice
Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets
title Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets
title_full Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets
title_fullStr Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets
title_full_unstemmed Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets
title_short Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets
title_sort human t-cell leukemia virus type 1 oncogenesis between active expression and latency: a possible source for the development of therapeutic targets
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10572738/
https://www.ncbi.nlm.nih.gov/pubmed/37834255
http://dx.doi.org/10.3390/ijms241914807
work_keys_str_mv AT marinomerlofrancesca humantcellleukemiavirustype1oncogenesisbetweenactiveexpressionandlatencyapossiblesourceforthedevelopmentoftherapeutictargets
AT grellisandro humantcellleukemiavirustype1oncogenesisbetweenactiveexpressionandlatencyapossiblesourceforthedevelopmentoftherapeutictargets
AT mastinoantonio humantcellleukemiavirustype1oncogenesisbetweenactiveexpressionandlatencyapossiblesourceforthedevelopmentoftherapeutictargets
AT laimichele humantcellleukemiavirustype1oncogenesisbetweenactiveexpressionandlatencyapossiblesourceforthedevelopmentoftherapeutictargets
AT ferraripaola humantcellleukemiavirustype1oncogenesisbetweenactiveexpressionandlatencyapossiblesourceforthedevelopmentoftherapeutictargets
AT nicoliniandrea humantcellleukemiavirustype1oncogenesisbetweenactiveexpressionandlatencyapossiblesourceforthedevelopmentoftherapeutictargets
AT pistellomauro humantcellleukemiavirustype1oncogenesisbetweenactiveexpressionandlatencyapossiblesourceforthedevelopmentoftherapeutictargets
AT macchibeatrice humantcellleukemiavirustype1oncogenesisbetweenactiveexpressionandlatencyapossiblesourceforthedevelopmentoftherapeutictargets