Neurobiology of HIV, psychiatric and substance abuse comorbidity research: Workshop report

Viral infections can cause persistent and progressive changes in emotional and cognitive functions. The viral-induced imbalances in neuronal network functioning may precipitate or accentuate psychiatric conditions in vulnerable individuals, in part, as a function of the host response to proinflammatory cytokines resulting from infection or brain injury. Research indicates that the mediators of psychiatric illnesses and HIV-neuropathogenesis utilize similar brain structures, neurocircuitry and receptor systems. The genetic, cellular and molecular mechanisms contributing to HIV neuropathogenesis and its late stage clinical correlate, HIV-associated-dementia (HAD), are active areas of neuroAIDS research. The study of HIV in the context of psychiatric comorbidities and comorbid pathogenesis is in a fledgling stage despite epidemiological studies suggesting that >60% of HIV infected individuals will suffer from at least one major psychiatric disorder during the course of infection. Depression is the primary comorbid disorder but anxiety and substance abuse disorders are also considerable in certain HIV+ populations. Certain substances of abuse and the biological mediators of psychiatric illnesses reportedly interact in the brain and presumptively worsen HIV-related neuropathogenesis and survival measures. A panel of experts discussed approaches for studying the neuroscience of HIV and psychiatric comorbidity at a basic, mechanistic level since they co-exist in high proportion in the human population. Recommended approaches ranged from improving human consent forms and maximizing the value of repository resources to novel research designs and identifying human and animal endophenotypes.