{"title":"CRISPR-Cas9 Gene Editing Permanently Eliminates HIV-1 DNA","authors":"Alex, R. Gonçalves","doi":"10.15406/jhvrv.2017.05.00177","DOIUrl":null,"url":null,"abstract":"Submit Manuscript | http://medcraveonline.com condition as a situation where the host’s genome was invaded, manipulated and exploited by a viral intruder. By the end of 2016, there were 36.9 million HIV-infected individuals living around the world and 19.5 million people were accessing antiretroviral therapy (UNAIDS 2017). We can typically treat patients with antiretroviral therapies and other symptomatic treatments or we can develop new ways to prevent the HIV infection with the development of new vaccines. However, while different vaccines are being tested with various degrees of success, there is still no evidence vaccination will be the best choice due to the HIV infection strategy. Therefore, while scientists keep testing and designing new vaccines against HIV/AIDS, recent advances in personalized medicine can be a game changer. Scientists are evaluating a new CRISPR-Cas9 strategy to achieve a permanent cure for HIV infection. There have been different approaches to treat HIV/ AIDS but there are several reasons preventing scientists from finding a viable cure for the HIV infection, for example, the HIV virus plasticity and its ability to remain in a latent state in hidden HIV reservoirs away from the host immune defense system [1]. A hallmark of the AIDS pathogenesis is the progressive depletion of CD4+ T-cell populations in association with an impaired immunity response [2]. It is that immune response weakening and the inability to initiate an effective cellular immune response against HIV that increases the susceptibility to opportunistic and often deadly infections. An updated list of opportunistic diseases and recommended responses is prepared yearly by the Centers for Disease Control and Prevention, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America [3]. Recent studies identified a new CD4 T-cell HIV reservoir marker that might pave the way for the development of new HIV treatments [4, 5]. CD32a+ lymphocytes can be used to identify the elusive HIV-1 reservoir. That finding may lead to novel insights that will allow the specific targeting and elimination of this resistant HIV reservoir. Establishing CD32a+ as a marker to identify those quiescent HIV cells is the perfect target to unleash the most recent genetic engineering tool that allows the modification of the hosts’ genome, the CRISPR-Cas9 method. The CRISPR-Cas9 gene editing complex is an elegant tool from the Streptococcus pyogenes [6]. The Cas9 nuclease protein uses a guide RNA sequence to cut DNA at a complementary site making this process the ideal mechanism to direct a precise genetic deletion and modification of the genome.","PeriodicalId":92670,"journal":{"name":"Journal of human virology & retrovirology","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2017-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of human virology & retrovirology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15406/jhvrv.2017.05.00177","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Submit Manuscript | http://medcraveonline.com condition as a situation where the host’s genome was invaded, manipulated and exploited by a viral intruder. By the end of 2016, there were 36.9 million HIV-infected individuals living around the world and 19.5 million people were accessing antiretroviral therapy (UNAIDS 2017). We can typically treat patients with antiretroviral therapies and other symptomatic treatments or we can develop new ways to prevent the HIV infection with the development of new vaccines. However, while different vaccines are being tested with various degrees of success, there is still no evidence vaccination will be the best choice due to the HIV infection strategy. Therefore, while scientists keep testing and designing new vaccines against HIV/AIDS, recent advances in personalized medicine can be a game changer. Scientists are evaluating a new CRISPR-Cas9 strategy to achieve a permanent cure for HIV infection. There have been different approaches to treat HIV/ AIDS but there are several reasons preventing scientists from finding a viable cure for the HIV infection, for example, the HIV virus plasticity and its ability to remain in a latent state in hidden HIV reservoirs away from the host immune defense system [1]. A hallmark of the AIDS pathogenesis is the progressive depletion of CD4+ T-cell populations in association with an impaired immunity response [2]. It is that immune response weakening and the inability to initiate an effective cellular immune response against HIV that increases the susceptibility to opportunistic and often deadly infections. An updated list of opportunistic diseases and recommended responses is prepared yearly by the Centers for Disease Control and Prevention, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America [3]. Recent studies identified a new CD4 T-cell HIV reservoir marker that might pave the way for the development of new HIV treatments [4, 5]. CD32a+ lymphocytes can be used to identify the elusive HIV-1 reservoir. That finding may lead to novel insights that will allow the specific targeting and elimination of this resistant HIV reservoir. Establishing CD32a+ as a marker to identify those quiescent HIV cells is the perfect target to unleash the most recent genetic engineering tool that allows the modification of the hosts’ genome, the CRISPR-Cas9 method. The CRISPR-Cas9 gene editing complex is an elegant tool from the Streptococcus pyogenes [6]. The Cas9 nuclease protein uses a guide RNA sequence to cut DNA at a complementary site making this process the ideal mechanism to direct a precise genetic deletion and modification of the genome.