{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T18:32:24Z","timestamp":1789756344617,"version":"4.0.1"},"reference-count":57,"publisher":"MDPI AG","issue":"1","license":[{"start":{"date-parts":[[2013,12,30]],"date-time":"2013-12-30T00:00:00Z","timestamp":1388361600000},"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>Human immunodeficiency virus type 1 (HIV-1) infection of target cells requires CD4 and a co-receptor, predominantly the chemokine receptor CCR5. CCR5-delta32 homozygosity results in a truncated protein providing natural protection against  HIV infection\u2014this without detrimental effects to the host\u2014and transplantation of  CCR5-delta32 stem cells in a patient with HIV (\u201cBerlin patient\u201d) achieved viral eradication. As a more feasible approach gene-modification strategies are being developed to engineer cellular resistance to HIV using autologous cells. We have developed a dual therapeutic anti-HIV lentiviral vector (LVsh5\/C46) that down-regulates CCR5 and inhibits HIV-1 fusion via cell surface expression of the gp41-derived peptide, C46. This construct, effective against multiple strains of both R5- and X4-tropic HIV-1, is being tested in Phase I\/II trials by engineering HIV-resistant hematopoietic cells.<\/jats:p>","DOI":"10.3390\/v6010054","type":"journal-article","created":{"date-parts":[[2013,12,30]],"date-time":"2013-12-30T12:08:05Z","timestamp":1388405285000},"page":"54-68","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["CCR5 as a Natural and Modulated Target for Inhibition of HIV"],"prefix":"10.3390","volume":"6","author":[{"given":"Bryan","family":"Burke","sequence":"first","affiliation":[{"name":"Calimmune, Inc., Los Angeles, California, CA 90024, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maureen","family":"Boyd","sequence":"additional","affiliation":[{"name":"Calimmune, Inc., Los Angeles, California, CA 90024, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helen","family":"Impey","sequence":"additional","affiliation":[{"name":"Calimmune, Inc., Los Angeles, California, CA 90024, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Louis","family":"Breton","sequence":"additional","affiliation":[{"name":"Calimmune, Inc., Los Angeles, California, CA 90024, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey","family":"Bartlett","sequence":"additional","affiliation":[{"name":"Calimmune, Inc., Los Angeles, California, CA 90024, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Geoff","family":"Symonds","sequence":"additional","affiliation":[{"name":"Calimmune, Inc., Los Angeles, California, CA 90024, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gero","family":"H\u00fctter","sequence":"additional","affiliation":[{"name":"Institute of Transfusion Medicine and Immunology, Medical Faculty Mannheim,  Heidelberg University, German Red Cross Blood Service Baden-W\u00fcrttemberg-Hessen,  68167 Mannheim, Germany"},{"name":"Cellex GmbH, 01307 Dresden, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2013,12,30]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"367","DOI":"10.1016\/S0092-8674(00)80110-5","article-title":"Homozygous defect in HIV-1 coreceptor accounts for resistance of some multiply-exposed individuals to HIV-1 infection","volume":"86","author":"Liu","year":"1996","journal-title":"Cell"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"692","DOI":"10.1056\/NEJMoa0802905","article-title":"Long-term control of HIV by CCR5 Delta32\/Delta32 stem-cell transplantation","volume":"360","author":"Nowak","year":"2009","journal-title":"N. 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