Pathogenesis of HIV-associated pain

While life expectancy and the overall well-being of individuals infected with the human immunodeficiency virus (HIV) have markedly improved during the post–combination antiretroviral therapy (cART) era, the prevalence of chronic pain remains a significant neurological concern. The intricate interplay of cellular and molecular factors within pain processing pathways, encompassing both peripheral and central neuropathology, appears to underlie the development of HIV-associated chronic pain. Nevertheless, the precise mechanisms responsible for this phenomenon remain enigmatic. This chapter provides an overview of our present comprehension of this intricate subject. Initially, we outline the neuropathological aspects related to pain within the neural circuits of both HIV patients and relevant animal models. Subsequently, we explore potential contributing factors that might be responsible for the emergence of this condition. Lastly, we discuss the mechanisms by which neurons and glial cells, along with other nonneuronal elements, mediate these pathogenic processes. The advancement in mechanistic understanding holds the promise of identifying novel cellular and molecular targets for the development of effective therapeutic strategies to alleviate the burden of HIV-associated pain.