LENTIVIRAL INFECTION, IMMUNE-RESPONSE PEPTIDES AND SLEEP

The aberrant sleep documented in subjects with human immunodeficiency virus (HIV) infection is uniquely important because of the contributio n this poor quality sleep makes to the fatigue, disability, and eventu al unemployment that befalls these patients. Especially given this imp ortance in clinical care, the research on the prominent sleep changes described in HIV infection remains modest in quantity. The chronic asy mptomatic stage of HIV infection is associated with the most intriguin g and singular sleep structure changes. Especially robust is the incre ase in slow wave sleep, particularly in latter portions of the sleep p eriod. This finding is rare in other primary or secondary sleep disord ers. The sleep structure alterations are among the most replicable of several pathophysiological sequelae in the brain associated with early HIV infection. It is unlikely that these sleep architecture changes a re psychosocial in etiology, and they occur before medical pathology i s evident. They are not associated with stress, anxiety, or depression . Evidence is accumulating to support a role for the somnogenic immune peptides tumor necrosis factor (TNF)alpha and interleukin (IL-1 beta) in the sleep changes and fatigue commonly seen in HIV infection. Thes e peptides are elevated in the blood of HIV-infected individuals, and are somnogenic in clinical use and animal models. The peripheral produ ction of these peptides may also have a role in the regulation of norm al sleep physiology. The lentivirus family contains both HIV and the f eline immunodeficiency virus (FIV). The use of the FIV model of HIV in fection may provide a way to further investigate the mechanism of a ne urotropic, neurotoxic virus initiating the immune acute phase response and affecting sleep. Neurotropic lentivirus infection is a microbiolo gical probe facilitating neuroimmune investigation.