Human immunodeficiency virus (HIV) is a sexually transmitted infection that currently affects approximately 1.2 million people in the US, one in five of whom are unaware of their infection [1]. As of December 2012, an estimated 33.5 million people were infected with HIV worldwide, and there is little to no indication that incidence rates are decreasing [2]. Classically, HIV infection is defined as a progressive loss of CD4+ T lymphocytes, leading to the inability to mount an immune response against opportunistic infections and, ultimately, death [3]. Infection with HIV can lead to multiple physiological effects aside from immunosuppression, including neurological complications in later stages of the infection such as HIV-associated dementia [4••, 5]. Infection of the brain caused by the retrovirus associated with HIV infection, HIV-1, is commonly referred to as neuroAIDS and can develop into a chronic neurological disorder known as HIV-1-associated dementia (HAD) or various stages of neurocognitive impairments known as HIV-1-associated neurocognitive disorders (HAND). Attention deficits, impaired short-term memory, compromised fine motor skills, tremors, and slowness of movements have all been associated with HAD, while symptoms of HAND can range from undetectable impairment to encephalitis and dementia [6••].
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HIV infection occurs when glycoproteins found on the HIV-1 retrovirus envelope (commonly gp120) interact with cell surface markers on immune cells, allowing for fusion of the viral and host membranes and the subsequent release of the viral core into the host immune cell. In the central nervous system (CNS), the surface markers implicated in the progression of HIV infection via interaction with HIV-1 glycoprotein interaction include CD4+ T lymphocytes, monocytes, macrophages, and microglia [3]. The extracellular interactions of gp120 lead to a variety of intracellular signaling mechanisms, including activation of transcription factors, such as the nuclear factor kappa-light-chain-enhancer of activated B cells, NF-κB, which signals the release of pro-inflammatory cytokines and chemokines [7, 8]. An influx of inflammatory cytokines and chemokines generated by an HIV-infected immune cell increases activation and ultimately infection of neighboring immune cells [7]. Oxidative stress, secretion of neurotoxins (including quinolinic acid and arachidonic acid metabolites), and release of HIV proteins such as transcriptional transactivator (Tat) often accompany HIV infection as well [9, 10••].
Several illicit drugs are also known to cause neuronal dysfunctions that can lead to neurocognitive deficiencies, and use of these substances can accelerate neurotoxin release [10••]. For example, methamphetamine (METH) elicits neurotoxicity by binding to the dopamine transporter (DAT) and reversing its function. In other words, METH forces the DAT to abandon its normal physiological function as a reuptake transporter for synaptic dopamine (DA), and instead causes it to release excess DA into the synapse [11, 12]. This reversal elicits persistent changes in striatal DAT expression [12]. Once METH is in the nerve terminal, it reverses the vesicular monoamine transporter (VMAT), forcing DA to be released from synaptic vesicles and generating a large pool of cytosolic DA for DAT to transport into the synapse [11, 13]. As with DAT, persistent changes in VMAT expression are also observed [14]. Additionally, METH drastically reduces concentrations of the DA precursor tyrosine hydroxylase (TH), further depleting DA stores in the striatum. However, the neurotoxic effects of METH extend beyond the dopaminergic system. One major downstream effect of METH use is glutamate excitotoxicity, as evidenced by the upregulation of both AMPA and NMDA receptors in the hippocampus following high-dose METH use [15]. In addition to dopaminergic and glutamatergic toxicities, METH can generate reactive oxygen and nitrogen species, via oxidation/metabolism of DA and increased nitric oxide synthase activity [16, 17, 18].
Because psychoactive drugs of abuse and HIV both have CNS toxic effects, comorbidity is a concern. Many behavioral risk factors result in the propagation of HIV, but injection drug use is the second most common behavior directly associated with HIV transmission in the US [4••]. Injection drug use directly accounted for one-third of the total number of acquired immunodeficiency syndrome (AIDS) cases in the US through 2002, and the National Institute on Drug Abuse (NIDA) also acknowledges that drug abuse (regardless of route of administration) can interfere with sexual judgment, indirectly leading to HIV transmission through sexual intercourse [19]. Thus, drug abuse can propagate HIV infection, both directly and indirectly. Not only can drugs of abuse potentiate the effects of HIV infection, but the reverse appears to be true as well, as evidence suggests HIV infection can increase preference and sensitivity to certain drugs of abuse, thus implying the relationship between HIV and drug abuse is symbiotic.
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