The effects of alcohol abuse on HIV disease progression have not been definitively established. A prospective, 30-month, longitudinal study of 231 HIV⁺ adults included history of alcohol and illicit drug use, adherence to antiretroviral therapy (ART), CD4⁺ cell count, and HIV viral load every 6 months. Frequent alcohol users (two or more drinks daily) were 2.91 times (95% CI: 1.23–6.85, p = 0.015) more likely to present a decline of CD4 to ≤200 cells/μl, independent of baseline CD4⁺ cell count and HIV viral load, antiretroviral use over time, time since HIV diagnosis, age, and gender. Frequent alcohol users who were not on ART also increased their risk for CD4 cell decline to ≤200 cells/mm³ (HR = 7.76: 95% CI: 1.2–49.2, p = 0.03). Combined frequent alcohol use with crack-cocaine showed a significant risk of CD4⁺ cell decline (HR = 3.57: 95% CI: 1.24–10.31, p = 0.018). Frequent alcohol intake was associated with higher viral load over time (β = 0.259, p = 0.038). This significance was maintained in those receiving ART (β = 0.384, p = 0.0457), but not in those without ART. Frequent alcohol intake and the combination of frequent alcohol and crack-cocaine accelerate HIV disease progression. The effect of alcohol on CD4⁺ cell decline appears to be independent of ART, through a direct action on CD4 cells, although alcohol and substance abuse may lead to unmeasured behaviors that promote HIV disease progression. The effect of alcohol abuse on viral load, however, appears to be through reduced adherence to ART.

Background: HIV infection is prevalent among substance abusers. The effects of specific illicit drugs on HIV disease progression have not been established. We evaluated the relationship between substances of abuse and HIV disease progression in a cohort of HIV-1-positive active drug users. Methods: A prospective, 30-month, longitudinal study was conducted on 222 HIV-1 seropositive drug users in Miami, FL. History of illicit drug, alcohol, and medication use, CD4⁺ cell count, and viral load were performed every 6 months. Results: Crack-cocaine users were 2.14 times [95% confidence interval (CI): 1.08 to 4.25, P = 0.029] more likely to present a decline of CD4 to ≤200 cells/mL, independent of antiretroviral use. Viral load over 30 months was significantly higher in crack users (β = 0.315, P = 0.037) independent of highly active antiretroviral therapy (HAART) over time. The only multidrug combination that significantly increased the risk of disease progression was crack cocaine with marijuana (hazard ratio = 2.42; 95% CI: 1.042 to 5.617, P = 0.04). Of those on HAART, a significantly lower proportion of crack-cocaine users versus nonusers had controlled viral load (P < 0.001), suggesting lower medication adherence, whereas crack-cocaine users not on HAART showed a greater risk for HIV disease progression than nonusers (hazard ratio = 3.946; 95% CI: 1.049 to 14.85, P = 0.042). Conclusions: Crack-cocaine use facilitates HIV disease progression by reducing adherence in those on HAART and by accelerating disease progression independently of HAART.

Botswana, in sub-Saharan Africa, reports one of the highest rates of human immunodeficiency virus (HIV) infection in the world, with an estimated 23.4% of individuals aged 15 to 49 years having HIV infection in 2011.¹ Moreover, HIV subtype C, the subtype most prevalent in Botswana, has been associated with more prolonged early viremia and a higher set point than other HIV subtypes, with more adverse health consequences.^2,3

Background. Adequate zinc is critical for immune function; however, zinc deficiency occurs in 150% of human immunodeficiency virus (HIV)-infected adu

Viral infections have afflicted human health and despite great advancements in scientific knowledge and technologies, continue to affect our society today. The current coronavirus (COVID-19) pandemic has put a spotlight on the need to review the evidence on the impact of nutritional strategies to maintain a healthy immune system, particularly in instances where there are limited therapeutic treatments. Selenium, an essential trace element in humans, has a long history of lowering the occurrence and severity of viral infections. Much of the benefits derived from selenium are due to its incorporation into selenocysteine, an important component of proteins known as selenoproteins. Viral infections are associated with an increase in reactive oxygen species and may result in oxidative stress. Studies suggest that selenium deficiency alters immune response and viral infection by increasing oxidative stress and the rate of mutations in the viral genome, leading to an increase in pathogenicity and damage to the host. This review examines viral infections, including the novel SARS-CoV-2, in the context of selenium, in order to inform potential nutritional strategies to maintain a healthy immune system.

Zinc deficiency is the most prevalent micronutrient abnormality seen in human immunodeficiency virus (HIV) infection. Low levels of plasma zinc predi