LAUSR

Despite the advent of combined antiretroviral therapy and the consequent effective control of HIV RNA in both the serum and CSF, many HIV-positive patients still develop HIV-associated brain disease, including cognitive impairment. It has been suggested that inflammation continues in the brain, despite undetectable viral loads, and that this inflammation is responsible for the gradually accruing cognitive deficits evident in many treated HIV patients. One of the hypotheses regarding the mechanism of chronic immune activation in treated HIV patients relates to the concept of microbial translocation: the passage of gut flora into the bloodstream due to early CD4 T cell depletion in the gastrointestinal tract in the first few weeks of HIV infection, causing a breach in the mucosal immune system. The consequent presence of microbes in the systemic circulation (without overt bacteraemia) is postulated to be causative in the subsequent chronic inflammatory state in treated HIV patients. This cross-sectional, case–control study explored the presence of microglial activation in cognitively healthy HIV-positive patients on suppressive antiretroviral therapy, correlating this with brain structure and function, peripheral chemokines and markers of microbial translocation. Twelve treated HIV patients and ten controls underwent [11C]PBR28 PET CT scans, volumetric and diffusion MR imaging, cognitive testing, measurement of CSF chemokines and HIV RNA, as well as PCR of plasma ribosomal 16s rRNA (a marker of microbial translocation). Introduction