Transforming growth factor-beta1 and interferon-alpha in the AIDS dementiacomplex (ADC): possible relationship with cerebral viral load?

Mechanisms involved in the pathogenesis of the AIDS-dementia complex are st ill unclear. The dichotomy between a small number of HIV-infected cells in the brain and their marked dysfunction could be related to a cellular ampli fication and/or activation of cerebral viral load by several cytokines, Thi s link between cytokines and viral load could play a role in the generation of the clinical dementia syndrome. We have studied cerebral levels of tran sforming growth factor-beta1 and interferon-alpha, both in the mild and sev ere AIDS-dementia complex and also compared these cytokines with HIV RNA lo ad in patients with different degrees of dementia, Our data indicate that p roduction of different cytokines characterized the expression of clinical d ementia, In the mild AIDS-dementia complex, there was a significant inverse correlation between interferon-alpha and transforming factor-beta1 (r = -0 .743; p < 0.001), and HIV-RNA was present in inverse proportion to transfor ming growth beta1 (r = -0.751; p < 0.001), In patients with severe AIDS-dem entia, transforming factor-beta1 was undetectable, while interferon-alpha l evel were higher than in mild AIDS dementia and correlated, positively to c erebral HIV-RNA, No significant difference was evident between these cytoki nes in the serum of ADC patients and in the control samples, Our study sugg ests that a relationship is possible between productive HIV infection in th e cerebral nervous system and a heterogenous and different expression of th e immune response via a complex interaction of cytokines with a differentia l modulation of the dementia phenotype.