What we are learning on HTLV-1 pathogenesis from animal models
Open accessAbstract
Isolated and identified more than 30 years ago, human T cell leukemia virus type 1 (HTLV-1) is the etiological agent of adult T cell leukemia/lymphoma, an aggressive lymphoproliferative disease of activated CD4(+) T cells, and other inflammatory disorders such as HTLV-1-associated myelopathy/tropical spastic paraparesis. A variety of animal models have contributed to the fundamental knowledge of HTLV-1 transmission, pathogenesis, and to the design of novel therapies to treat HTLV-1-associated diseases. Small animal models (rabbits, rats, and mice) as well as large animal models (monkeys) have been utilized to significantly advance characterization of the viral proteins and of virus-infected cells in the early steps of infection, as well as in the development of leukemogenic and immunopathogenic processes. Over the past two decades, the creation of new immunocompromised mouse strains that are robustly reconstituted with a functional human immune system (HIS) after being transplanted with human tissues or progenitor cells has revolutionized the in vivo investigation of viral infection and pathogenesis. Recent observations obtained in HTLV-1-infected humanized HIS mice that develop lymphomas provide the opportunity to study the evolution of the proviral clonality in human T cells present in different lymphoid organs. Current progress in the improvement of those humanized models will favor the testing of drugs and the development of targeted therapies against HTLV-1-associated diseases.
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Humanised models provide a more robust recapitulation of the disease microenvironment and immune responses; however, infection is short term, and the lack of a functional adaptive immune system does not capture the persistence of HTLV-1 infection.
“Whilst they do provide a more robust recapitulation of the disease microenvironment and immune responses; infection is short term, and the lack of a functional adaptive immune system does not capture the persistence of HTLV-1 infection [149].”
From Current State of Therapeutics for HTLV-1 (2024) · cites this paper as [149]
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Experimental — accuracy not yet measuredAnimal models can provide information about HTLV-1 replication and virus-associated disease progression.
“Some mechanisms of HTLV-1 replication and virus-associated disease progression can be learnt from animal models [44,122,136,137].”
From HIV-1 and HTLV-1 Transmission Modes: Mechanisms and Importance for Virus Spread (2022) · cites this paper as [136]
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Cited by
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HIV-1 and HTLV-1 Transmission Modes: Mechanisms and Importance for Virus Spread
Kalinichenko, S., Komkov, D., & Mazurov, D. (2022) · Viruses · doi:10.3390/v14010152 · Cited by 68 · see citing works
“Some mechanisms of HTLV-1 replication and virus-associated disease progression can be learnt from animal models [44,122,136,137].”
BackgroundCurrent State of Therapeutics for HTLV-1
Wang, T. T., Hirons, A., Doerflinger, M., Morris, K. V., Ledger, S., Purcell, D. F. J., Kelleher, A. D., & Ahlenstiel, C. L. (2024) · Viruses · doi:10.3390/v16101616 · Cited by 22 · see citing works
“Overexpression of Hbz was observed to prevent Tax-induced NF-κ B and PRC2 activation, shedding light on the co-modulatory interplay of Tax and Hbz [157].”
Background
- Authors
- Dodon, M. D., Villaudy, J., Gazzolo, L., Haines, R., & Lairmore, M.
- Affiliations
- École Normale Supérieure de Lyon (FR)
- The Ohio State University (US)
- University of California, Davis (US)
- Venue
- Frontiers in Microbiology
- Publisher
- Frontiers Media SA
- Published
- 2012
- Volume
- 3
- Pages
- 320-320
- ISSN
- 1664-302X (ISSN-L)
- PMC
- PMC3431546
- OpenAlex
- W2128736639
- Cited by
- 23
- References
- 0
- Citations by year
- 2024: 1 · 2023: 1 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 1 · 2016: 3 · 2015: 3 · 2014: 3 · 2013: 1
- FWCI
- 0.98
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Microbiology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- European Commission (2005-018704, LSHC-CT-2005-018704)
- Institut National de la Santé et de la Recherche Médicale
- Fondation de France
- Institut National Du Cancer
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and Retrovirus Studies
- Health Sciences › Medicine › Oncology › Viral-associated cancers and disorders
- Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
- Keywords
- HTLV-1, adult T-cell leukemia/lymphoma, HTLV-1-associated myelopathy/tropical spastic paraparesis, viral pathogenesis, animal models, humanized mice, immunodeficient mice, virus transmission, immunopathogenesis, leukemogenesis, drug testing
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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