Abstract
Drug abuse is a common comorbidity in people infected with HIV. HIV-infected individuals who abuse drugs are a key population who frequently experience suboptimal outcomes along the HIV continuum of care. A modest proportion of HIV-infected individuals develop HIV-associated neurocognitive issues, the severity of which further increases with drug abuse. Moreover, the tendency of the virus to go into latency in certain cellular reservoirs again complicates the elimination of HIV and HIV-associated illnesses. Antiretroviral therapy (ART) successfully decreased the overall viral load in infected people, yet it does not effectively eliminate the virus from all latent reservoirs. Although ART increased the life expectancy of infected individuals, it showed inconsistent improvement in CNS functioning, thus decreasing the quality of life. Research efforts have been dedicated to identifying common mechanisms through which HIV and drug abuse lead to neurotoxicity and CNS dysfunction. Therefore, in order to develop an effective treatment regimen to treat neurocognitive and related symptoms in HIV-infected patients, it is crucial to understand the involved mechanisms of neurotoxicity. Eventually, those mechanisms could lead the way to design and develop novel therapeutic strategies addressing both CNS HIV reservoir and illicit drug use by HIV patients.
Highlights
If not treated, the human immunodeficiency virus (HIV) infection can result in the development of acquired immune deficiency syndrome (AIDS)
The main objective of this review is to explore the mechanisms through which HIV infection and various drugs of abuse contribute to neurotoxicity that manifests as HIVassociated neurocognitive disorder (HAND)
Enzymatic and non-enzymatic metabolism of dopamine and/or related substances may result in the production of free radicals; drugs of abuse that act via the dopaminergic system, such as amphetamine, amphetamine derivatives, cocaine, 3,4-methylenedioxymethamphetamine (MDMA), and opioids, have all been reported to generate oxidative stress through similar mechanisms [127,128]
Summary
The human immunodeficiency virus (HIV) infection can result in the development of acquired immune deficiency syndrome (AIDS). To make ART more effective, research efforts have been diverted to identify the mechanisms through which latent HIV can be reactivated before being targeted by antiretrovirals [9,10,11,12,13]. Latency reversal agents such as romidepsin, JQ-1, and panobinostat have effectively reactivated the peripheral latent viral reservoir. The main objective of this review is to explore the mechanisms through which HIV infection and various drugs of abuse contribute to neurotoxicity that manifests as HAND. We will discuss the possible outcome of certain ART regimens in contributing to HAND, especially in those HIV-infected people who use drugs (PWUDs)
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