HIV-1 infection and alcohol abuse: Neurocognitive impairment, mechanisms of neurodegeneration and therapeutic interventions

Persidsky, Yuri; Ho, Wen‐Zhe; Ramirez, Servio H.; Potula, Raghava; Abood, Mary E.; Unterwald, Ellen M.; Tuma, Ronald F.

doi:10.1016/j.bbi.2011.03.001

Cited by 102 publications

(65 citation statements)

References 138 publications

(173 reference statements)

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“…First, it can result in negative health outcomes, either directly or because of interactions with antiretroviral medications. Among HIV-positive individuals, heavy alcohol use has been found to be associated with decreased cluster of differentiation 4 (CD4) cell counts or nonsuppression of HIV viral load (Baum et al, 2010;Hahn and Samet, 2010;Samet et al, 2007;Shacham et al, 2011), increased neurodegeneration or memory impairment (Fama et al, 2009(Fama et al, , 2011Persidsky et al, 2011), decreased health-related quality of life (Uphold et al, 2007), and increased mortality from various causes (Bonacini, 2011;Braithwaite et al, 2007;Katcher et al, 2010). Likewise, crystal methamphetamine use among HIV-positive individuals has been found to be associated with decreased CD4 cell counts or nonsuppression of HIV viral load (Fairbairn et al, 2011;King et al, 2009;Toussi et al, 2009), neurode-generation or memory impairment (Scott et al, 2007), and resistance to antiretroviral medications (Cachay et al, 2007;Colfax et al, 2007).…”

Section: H IV Continues To Disproportionately Affect Men Who Have Sexmentioning

confidence: 99%

Risk Behaviors Among HIV-Positive Gay and Bisexual Men at Party-Oriented Vacations

Fisher

Ramchand

Bana

et al. 2013

J. Stud. Alcohol Drugs

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ABSTRACT. Objective: This study examined substance use (intended and actual), unprotected sex, and HIV disclosure practices (disclosure and questioning) among HIV-positive men who have sex with men (MSM) at two party-oriented vacations, where substance use and sexual risk may be heightened. Method: A random sample of 489 MSM attending one of two party-oriented vacations participated in PartyIntents, a short-term longitudinal survey. Nearly half (47%) completed a follow-up assessment at the event or online for up to 2 weeks after the event. We examined rates of baseline intentions to use substances, actual substance use, and unprotected intercourse among HIV-positive men in attendance. Rates among HIV-negative men were estimated for comparison. Multiple logistic regression was used to assess the impact of illegal drug use and HIV status on unprotected anal intercourse (UAI). Results: HIV-positive attendees (17%) were signifi cantly more likely than HIV-negative attendees to use nitrite inhalants (or "poppers") (24.3% vs. 10.7%). HIVpositive attendees were also signifi cantly more likely to have insertive UAI (64.3% vs. 34.1%) and receptive UAI (68.8% vs. 22.2%). Multivariate models showed associations between HIV status and illegal drug use with UAI (for HIV status, odds ratio [OR] = 4.5, p = .001; for any illegal drug use, OR = 16.4, p < .001). There was no evidence that the infl uence of drug use moderated risk by HIV status. Rates of HIV disclosure and questioning did not differ by HIV status. Conclusions: HIV-positive men attending these events engaged in higher rates of illegal drug use and sexual risk than HIV-negative men. Prevention campaigns targeting MSM at high-risk events should include messages geared toward HIVpositive men. (J. Stud. Alcohol Drugs, 74, 158-167, 2013)

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Section: H IV Continues To Disproportionately Affect Men Who Have Sexmentioning

confidence: 99%

Risk Behaviors Among HIV-Positive Gay and Bisexual Men at Party-Oriented Vacations

Fisher

Ramchand

Bana

et al. 2013

J. Stud. Alcohol Drugs

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“…Anti-inflammatory interventions dampening monocyte activation and diminishing their migratory potential could be neuroprotective and prevent other organ injury in HIV infection. 16 In summary, the work of Nowlin et al 3 provides key new data on the development of SIVE, potentially guiding new treatment approaches for HANDdnamely, prevention of monocyte CNS infiltration in HIV-1 infection.…”

Section: Discussionmentioning

confidence: 99%

“…When differentiated into long-living tissue macrophages, these cells become a virus reservoir that is difficult (if not impossible) to eradicate. 16 This is especially true for CNS macrophages protected by the bloodbrain barrier that is poorly penetrable by antiretroviral drugs.…”

Section: Commentarymentioning

confidence: 99%

“…The underlying causes of HAND (the complication most feared by infected individuals) are believed to be associated with chronic neuroinflammatory responses, 15 the generation of proinflammatory factors by activated macrophages and microglia, and persistent injury of the bloodbrain barrier. 16 Virus appears in the CNS weeks after HIV infection and coincides with the appearance of inflammatory molecules in the cerebrospinal fluid. 17 Virus then resides in the perivascular monocytes/macrophages that are infected in the periphery.…”

Section: Future Directionsmentioning

confidence: 99%

“…16 Prolonged activation of perivascular macrophages and microglia in the CNS contributes to HIV-1 neuroinflammation and is associated with neurodegeneration and neurocognitive impairment. 16 Although host-specific differences exist between HIV and SIV infection, the macaque model provides a more relevant model for human disease as compared to other models (like humanized mouse models where infectious HIV-1 is used), 19 which do not allow studies of macrophage turnover in the natural host, limiting their utility for studies performed by Nowlin et al 3 Findings by Nowlin et al 3 also emphasize that development of SIVE is a late event in the infection process, secondary to the loss of immune function and lack of virus suppression in the periphery. 18 Monocytes (particularly more mature CD16 þ monocytes) 20 can be infected with HIV.…”

Section: Commentarymentioning

confidence: 99%

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Insights into End-Organ Injury in HIV Infection

Persidsky

2015

The American Journal of Pathology

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Neurocognitive impairment (collectively named as HIV1eassociated neurocognitive disorders or HAND) is highly prevalent in HIV-1einfected patients, including those receiving antiretroviral therapy (ART).1 Monocyte and macrophage infiltration in the brain is associated with HAND development 2 ; however, precise timing and dynamics of this infiltration remain debatable. Researchers recapitulate HIV infection in nonhuman primates (macaque model) by infecting with SIV. For the first time, by using SIV-infected animals that developed SIV encephalitis (SIVE), Nowlin et al 3 studied monocyte-to-macrophage turnover in the central nervous system (CNS) under physiological conditions. 4 Study DesignNeuropathologic features of SIVE recapitulate signs of HIV encephalitis, 4 a morphological correlate of cognitive decline. Nowlin et al 3 used straightforward multilabel immunohistochemical approaches to assess macrophage populations and their turnover in the choroid plexus, meninges, perivascular space, and parenchymal lesions (when present in animals with SIVE). The method also allowed comparison of the rates of turnover in early acute inflammation and in the later inflammation as the animals developed AIDS and CNS lesions. They used a cuttingedge combination of bromodeoxyuridine (BrdU)elabeled macrophage precursors in bone marrow (that can potentially traffic to the brain) to detect macrophage populations and the serial injection of dextran dyes intercisternally to determine the macrophage populations (early or late) contributing to lesion formation as well as to identify the infected cells in the CNS. Study OutcomeThe findings of Nowlin et al 3 are of great interest to CNS macrophage biologists as well as immunologists studying acute and chronic inflammation. Early during SIV infection, Nowlin et al 3 reported most cells to be MAC387 þ recently recruited monocytes/macrophages. As expected, most of these cells were detected in the meninges and the choroid plexus (which appeared to have trafficking kinetics similar to the blood than to the CNS compartments). Consistent with the observations from the bone marrow during inflammation, most BrdU þ cells were also MAC387 þ . During the late stages of inflammation, Nowlin et al 3 found macrophage accumulation primarily in the perivascular space and in SIVE lesions, not in the meninges and choroid plexus. It is likely that the meninges and choroid plexus have cells trafficking through them in late stages of inflammation, thereby decreasing accumulation. Interestingly, most cells in the SIVE lesion (>80%) were present in the CNS before lesion development, suggesting Supported by NIH research grants AA015913 and MH65151.

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