作者: James Williams , Sarah Fidler , John Frater
DOI: 10.5772/22942
关键词:
摘要: HIV induces persistent infection and, despite improvements in mortality and morbidity conferred by Highly Active Antiretroviral Therapy (HAART), there is currently no cure [1]. The immune system controls only partially, plasma proviral DNA can be detected from acute primary to end-stage AIDS [2]. More than 99% of replication has been demonstrated activated infected CD4+ T-cells [3]. These are the very cells that instrumental clearance virus through host’s adaptive response. Gradually, throughout course infection, repeated rounds T cell lead an overall marked decrease total number [4] this linked clinical manifestations disease [5]. HIV-1 replicates rapidly patients, with a virion half-life less 6 hours [6], 1-2 days proliferating [7] [8] [9], corresponding short-lived population produces most major problem eradication lies existence pool latently cells. Retroviral latency occurs when provirus infects integrates into genomic its target cell, but transcriptionally silent [10]. able persistently produce infectious virions activated, even patients on highly active antiretroviral therapy potential source rebounded after HAART treatment interrupted There myriad tissue types which integrate, it at these sites long-term preservation replication-competent occur [11]. Infectious within reservoirs longer half life where viral [12]. reservoir estimated 43.9 months during three years HAART, [13] 44.2 whilst seven [14]. Thus, had take possibly as long 60 eradicate using alone [13]. In other studies , optimal suppression was little [15] [16].