{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T14:16:25Z","timestamp":1768313785589,"version":"3.49.0"},"reference-count":136,"publisher":"MDPI AG","issue":"4","license":[{"start":{"date-parts":[[2018,3,29]],"date-time":"2018-03-29T00:00:00Z","timestamp":1522281600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Viruses"],"abstract":"<jats:p>Jan Svoboda studied aspects of viral latency, in particular with respect to disease induction by avian RNA tumor viruses, which were later renamed as part of the extended retrovirus family. The course of retroviral pathogenesis is intrinsically linked to their unique property of integrating the DNA copy of the retroviral genome into that of the host cell, thus forming the provirus. Retroviral latency has recently become of major clinical interest to allow a better understanding of why we can effectively block the human immunodeficiency virus type 1 (HIV-1) in infected individuals with antiviral drugs, yet never reach a cure. We will discuss HIV-1 latency and its direct consequence\u2014the formation of long-lasting HIV-1 reservoirs. We next focus on one of the most explored strategies in tackling HIV-1 reservoirs\u2014the \u201cshock and kill\u201d strategy\u2014which describes the broadly explored pharmacological way of kicking the latent provirus, with subsequent killing of the virus-producing cell by the immune system. We furthermore present how the clustered regularly interspaced palindromic repeats (CRISPR) and associated protein (Cas) system can be harnessed to reach the same objective by reactivating HIV-1 gene expression from latency. We will review the benefits and drawbacks of these different cure strategies.<\/jats:p>","DOI":"10.3390\/v10040157","type":"journal-article","created":{"date-parts":[[2018,3,29]],"date-time":"2018-03-29T12:51:56Z","timestamp":1522327916000},"page":"157","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Tackling HIV Persistence: Pharmacological versus CRISPR-Based Shock Strategies"],"prefix":"10.3390","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8192-1351","authenticated-orcid":false,"given":"Gilles","family":"Darcis","sequence":"first","affiliation":[{"name":"Laboratory of Experimental Virology, Department of Medical Microbiology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands"},{"name":"Infectious Diseases Department, Li\u00e8ge University Hospital, 4000 Liege, Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Atze","family":"Das","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Virology, Department of Medical Microbiology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ben","family":"Berkhout","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Virology, Department of Medical Microbiology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2018,3,29]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"183","DOI":"10.1038\/387183a0","article-title":"Quantification of latent tissue reservoirs and total body viral load in HIV-1 infection","volume":"387","author":"Chun","year":"1997","journal-title":"Nature"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"1284","DOI":"10.1038\/nm1295-1284","article-title":"In vivo fate of HIV-1-infected T cells: Quantitative analysis of the transition to stable latency","volume":"1","author":"Chun","year":"1995","journal-title":"Nat. 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