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To prevent the development of ATL among carriers, it is important to control HTLV-1-infected cells in infected individuals. Therefore, the establishment of novel therapies with drugs specifically targeting infected cells is urgently required. This study aimed to develop a potential therapy by generating recombinant vesicular stomatitis viruses (rVSVs) that lack an envelope glycoprotein G and instead encode an HTLV-1 receptor with human glucose transporter 1 (GLUT1), neuropilin 1 (NRP1), or heparan sulfate proteoglycans (HSPGs), including syndecan 1 (SDC1), designated VSV\u0394G-GL, VSV\u0394G-NP, or VSV\u0394G-SD, respectively. In an attempt to enhance the infectivity of rVSV against HTLV-1-infected cells, we also constructed rVSVs with a combination of two or three receptor genes, designated VSV\u0394G-GLN and VSV\u0394G-GLNS, respectively. The present study demonstrates VSV\u0394G-GL, VSV\u0394G-NP, VSV\u0394G-GLN, and VSV\u0394G-GLNS have tropism for HTLV-1 envelope (Env)-expressing cells. Notably, the inoculation of VSV\u0394G-GL or VSV\u0394G-NP significantly eliminated HTLV-1-infected cells under the culture conditions. Furthermore, in an HTLV-1-infected humanized mouse model, VSV\u0394G-NP was capable of efficiently preventing HTLV-1-induced leukocytosis in the periphery and eliminating HTLV-1-infected Env-expressing cells in the lymphoid tissues. In summary, an rVSV engineered to express HTLV-1 primary receptor, especially human NRP1, may represent a drug candidate that has potential for the development of unique virotherapy against HTLV-1<jats:italic>de novo<\/jats:italic>infection.<\/jats:p><jats:p><jats:bold>IMPORTANCE<\/jats:bold>Although several anti-ATL therapies are currently available, ATL is still frequently resistant to therapeutic approaches, and its prognosis remains poor. Control of HTLV-1<jats:italic>de novo<\/jats:italic>infection or expansion of HTLV-1-infected cells in the carrier holds considerable promise for the prevention of ATL development. In this study, we developed rVSVs that specifically target and kill HTLV-1 Env-expressing cells (not ATL cells, which generally do not express Env<jats:italic>in vivo<\/jats:italic>) through replacement of the G gene with HTLV-1 receptor gene(s) in the VSV genome. Notably, an rVSV engineered to express human NRP1 controlled the number of HTLV-1-infected Env-expressing cells<jats:italic>in vitro<\/jats:italic>and<jats:italic>in vivo<\/jats:italic>, suggesting the present approach may be a promising candidate for novel anti-HTLV-1 virotherapy in HTLV-1 carriers, including as a prophylactic treatment against the development of ATL.<\/jats:p>","DOI":"10.1128\/jvi.01885-17","type":"journal-article","created":{"date-parts":[[2017,12,6]],"date-time":"2017-12-06T16:20:34Z","timestamp":1512577234000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":8,"title":["Control of Human T-Cell Leukemia Virus Type 1 (HTLV-1) Infection by Eliminating Envelope Protein-Positive Cells with Recombinant Vesicular Stomatitis Viruses Encoding HTLV-1 Primary Receptor"],"prefix":"10.1128","volume":"92","author":[{"given":"Kenta","family":"Tezuka","sequence":"first","affiliation":[{"name":"Department of Safety Research on Blood and Biological Products, National Institute of Infectious Diseases, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0038-699X","authenticated-orcid":false,"given":"Kazu","family":"Okuma","sequence":"additional","affiliation":[{"name":"Department of Safety Research on Blood and Biological Products, National Institute of Infectious Diseases, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3064-5219","authenticated-orcid":false,"given":"Madoka","family":"Kuramitsu","sequence":"additional","affiliation":[{"name":"Department of Safety Research on Blood and Biological Products, National Institute of Infectious Diseases, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sahoko","family":"Matsuoka","sequence":"additional","affiliation":[{"name":"Department of Safety Research on Blood and Biological Products, National Institute of Infectious Diseases, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Reiko","family":"Tanaka","sequence":"additional","affiliation":[{"name":"Department of Immunology, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuetsu","family":"Tanaka","sequence":"additional","affiliation":[{"name":"Department of Immunology, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isao","family":"Hamaguchi","sequence":"additional","affiliation":[{"name":"Department of Safety Research on Blood and Biological Products, National Institute of Infectious Diseases, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.78.10.6476"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.77.12.7415"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.antiviral.2016.10.015"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/ijc.2910430618"},{"key":"e_1_3_3_6_2","first-page":"481","article-title":"Oral transmission of human T-cell leukemia virus type-I into a common marmoset (Callithrix jacchus) as an experimental model for milk-borne transmission","volume":"76","author":"Yamanouchi K","year":"1985","unstructured":"Yamanouchi K, Kinoshita K, Moriuchi R, Katamine S, Amagasaki T, Ikeda S, Ichimaru M, Miyamoto T, Hino S. 1985. 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