The institution of highly active antiretroviral therapy for the treatment of HIV has led to viral suppression but HIV is not eliminated and persists in reservoirs and viral rebound almost always occurs when therapy is interrupted. It has been demonstrated in numerous published papers that inflammation is reduced on initiation of therapy but still persists in viral suppressed patients . This relationship of viral latency and chronic inflammation has not been well defined. There are numerous causes of chronic inflammation that includes microbial translocation co-infection with other viruses ie CMV ,and persistent virus. This presentation will highlight our current understanding of this complex relationship of persistent virus and inflammation by reviewing studies on this relationship in subjects on ARV and following ARV intensification. The discussion will review studies where therapeutic interruption has been used to evaluate the relation of baseline inflammation and viral rebound. The critical question in this field is what happens to viral persistence in tissue. There will be discussions on measures of the virus in critical tissue sites that include gastrointestinal tract, lymph nodes and adipose tissue and the related inflammatory responses. The talk will conclude with potential therapeutic approaches that target inflammatory responses and how they impact viral persistence.