{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T01:44:29Z","timestamp":1792028669100,"version":"4.4.0"},"reference-count":88,"publisher":"MDPI AG","issue":"8","license":[{"start":{"date-parts":[[2011,8,8]],"date-time":"2011-08-08T00:00:00Z","timestamp":1312761600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Viruses"],"abstract":"<jats:p>Innate immunity plays a critical role in the host response to a viral infection. The innate response has two main functions. First, it triggers effector mechanisms that restrict the infection. Second, it primes development of the adaptive response, which completes the elimination of the pathogen or of infected cells. In vivo, HTLV-1 infects T lymphocytes that participate in adaptive immunity but also monocytes and dendritic cells that are major players in innate immunity. Herein, we will review the interplay between HTLV-1 and innate immunity. Particular emphasis is put on HTLV-1-induced alteration of type-I interferon (IFN-I) function. In vitro, the viral Tax protein plays a significant role in the alteration of IFN synthesis and signaling. Despite this, IFN-I\/AZT treatment of Adult T\u2011cell Leukemia\/Lymphoma (ATLL) patients leads to complete remission. We will discuss a model in which exogenous IFN-I could act both on the microenvironment of the T-cells to protect them from infection, and also on infected cells when combined with other drugs that lead to Tax down-regulation\/degradation.<\/jats:p>","DOI":"10.3390\/v3081374","type":"journal-article","created":{"date-parts":[[2011,8,9]],"date-time":"2011-08-09T05:28:55Z","timestamp":1312867735000},"page":"1374-1394","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["HTLV-1 and Innate Immunity"],"prefix":"10.3390","volume":"3","author":[{"given":"Chlo\u00e9","family":"Journo","sequence":"first","affiliation":[{"name":"Retroviral Oncogenesis Laboratory, INSERM-U758 Human Virology, 69364 Lyon cedex 07, France"},{"name":"Ecole Normale Sup\u00e9rieure de Lyon, 69364 Lyon cedex 07, France"},{"name":"IFR 128 Biosciences Lyon-Gerland, 69364 Lyon cedex 07, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renaud","family":"Mahieux","sequence":"additional","affiliation":[{"name":"Retroviral Oncogenesis Laboratory, INSERM-U758 Human Virology, 69364 Lyon cedex 07, France"},{"name":"Ecole Normale Sup\u00e9rieure de Lyon, 69364 Lyon cedex 07, France"},{"name":"IFR 128 Biosciences Lyon-Gerland, 69364 Lyon cedex 07, France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2011,8,8]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"268","DOI":"10.1098\/rspb.1957.0049","article-title":"Virus interference. 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