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The abuse of methamphetamine (MA) has increased in the United States over the past 15 years and is associated with considerable negative social, psychological, and health effects, including symptoms of depression. Infection with the hepatitis C virus (HCV), which is independently associated with increased risk of depression, is common among MA users, possibly due to high rates of transmission risk behaviors in this cohort (eg, injection drug use). Given the prevalence of depression among HCV-infected individuals and MA users separately, the current study aimed to determine whether HCV infection and MA dependence are associated with additive effects on depression. Focused psychiatric evaluations were conducted on 39 individuals with both MA dependence and HCV infection (MA + HCV +), 57 persons with only MA dependence (MA + HCV -), and a comparison sample of 46 participants with neither risk factor (MA - HCV -). Consistent with prior research, greater self-reported symptoms of depression were observed in the MA + groups relative to MA - HCV - participants; however, there was no evidence to suggest an additive effect of HCV infection. Surprisingly, the prevalence of current and lifetime diagnoses of Major Depressive Disorder (MDD) did not differ across the study groups. Results from this study suggest that HCV infection does not confer an additive effect on the severity of depressive symptoms or the prevalence of major depression in persons with MA dependence. [ABSTRACT FROM AUTHOR]

The 2021 Conference on Retroviruses and Opportunistic Infections (CROI) featured a timely review of the neurologic complications of COVID-19 as well as new research findings on mechanisms by which SARS-CoV-2 may affect the brain. CROI included new and important findings about the neurologic complications of HIV-1, human polyomavirus 2 (also known as JC Virus), and cryptococcus. New long-term analyses of cognition in people with HIV-1 identified that cognitive decline over time is associated with multimorbidity, particularly diabetes, chronic lung disease, and vascular disease risk conditions. These conditions are associated with aging, and the question of whether people with HIV are at risk for premature aging was addressed by several reports. New findings from large analyses of resting state networks also provided valuable information on the structural and functional networks that are affected by HIV-1 infection and cognitive impairment. Several reports addressed changes after initiating or switching antiretroviral therapy (ART). Findings that will improve understanding of the biologic mechanisms of brain injury in people with HIV were also presented and included evidence that host (eg, myeloid activation, inflammation, and endothelial activation) and viral (eg, transcriptional activity and compartmentalization) factors adversely affect brain health. Other research focused on adjunctive therapies to treat HIV-1 and its complications in the central nervous system. This summary will review these and other findings in greater detail and identify key gaps and opportunities for researchers and clinicians.

Objective: To investigate the effect of hepatitis C virus (HCV) on neurocognitive performance in chronically HIV-infected patients enrolled in the CNS HIV Antiretroviral Therapy Effects Research (CHARTER) study., Methods: A total of 1,582 participants in CHARTER who were tested for HCV antibody underwent neurocognitive testing; serum HCV RNA was available for 346 seropositive patients. Neurocognitive performance was compared in 408 HCV-seropositive and 1,174 HCV-seronegative participants and in a subset of 160 seropositive and 707 seronegative participants without serious comorbid neurologic conditions that might impair neurocognitive performance, using linear regression and taking into account HIV-associated and demographic factors (including IV drug use) and liver function., Results: Neurocognitive performance characterized by global deficit scores and the proportion of individuals who were impaired were the same in the HCV-seropositive and HCV-seronegative groups. In univariable analyses in the entire sample, only verbal domain scores showed small statistically different superior performance in the HCV+ group that was not evident in multivariable analysis. In the subgroup without significant comorbidities, scores in all 7 domains of neurocognitive functioning did not differ by HCV serostatus. Among the HCV-seropositive participants, there was no association between neurocognitive performance and serum HCV RNA concentration., Conclusion: In HIV-infected patients, HCV coinfection does not contribute to neurocognitive impairment, at least in the absence of substantial HCV-associated liver damage, which was not evident in our cohort., (© 2014 American Academy of Neurology.)