Association of aflatoxin B1 levels with mean CD4 cell count and uptake of ART among HIV infected patients: A prospective study

Academic Article


  • Background Aflatoxin suppresses cellular immunity and accentuates HIV-associated changes in T- cell phenotypes and B- cells. Objective This prospective study was conducted to examine the association of aflatoxin levels with CD4 T-cell count and antiretroviral therapy uptake over time. Methods Sociodemographic and food data were collected from antiretroviral therapy na├»ve HIVinfected patients. CD4+ counts were collected from participants' medical records. Plasma samples were tested for aflatoxin B1 albumin adducts, hepatitis B surface antigen, and HIV viral load. Participants were separated into high and low aflatoxin groups based on the median aflatoxin B1 albumin adduct level of 10.4 pg/ml for data analysis. Results Participants with high aflatoxin B1 albumin adduct levels had lower mean CD4 at baseline and at each follow-up period. Adjusted multivariable logistic regression analysis showed that higher baseline aflatoxin B1 adduct levels were associated with statistically significant lower CD4 counts (est = -66.5, p = 0.043). Not starting ART and low/middle socioeconomic status were associated with higher CD4 counts (est = 152.2, p<0.001) and (est = 86.3, p = 0.027), respectively. Conclusion Consistent correlations of higher aflatoxin B1 adduct levels with lower CD4 over time indicate that there is an independent early and prolonged effect of aflatoxin on CD4 even with the initiation of antiretroviral therapy. The prospective study design, evaluation of baseline and follow-up measures, extensive control for potential confounders, and utilization of objective measures of aflatoxin exposure and CD4 count provide compelling evidence for a strong epidemiologic association that deserves careful attention in HIV care and treatment programs.
  • Authors

    Published In

  • PLoS One  Journal
  • Digital Object Identifier (doi)

    Author List

  • Jolly PE; Akinyemiju TF; Sakhuja S; Sheth R
  • Volume

  • 17
  • Issue

  • 1 January