Status of selected nutrients and progression of human immunodeficiency virus type 1 infection.

Published

Journal Article

BACKGROUND: Immune function is highly dependent on nutritional status because the large mass and high rate of cellular turnover of the immune system make it a major user of nutrients. Furthermore, nutrient requirements may be increased during acute and chronic infections, including HIV-1 infection. OBJECTIVE: The current study was designed to assess relations among HIV-1 progression and 11 nutritional and demographic variables. DESIGN: The participants were 106 HIV-infected outpatients and 29 uninfected control subjects (n = 89 men and 46 women; age range: 35-57 y). The HIV-infected subjects represented a broad range of disease progression. RESULTS: We found lower concentrations of plasma and erythrocyte magnesium and of erythrocyte reduced glutathione beginning early in the course of HIV-1 infection. Significantly decreased hematocrit and increased serum copper concentration developed only late in the course of the disease. Statistically significant univariate associations were found between the CD4(+) T lymphocyte count and hematocrit, plasma magnesium concentration, and plasma zinc concentration. The lowest erythrocyte magnesium concentrations occurred in HIV-infected subjects who consumed alcoholic beverages. Independent variables that were significant joint predictors of CD4(+) cell count in multiple regression analyses were hematocrit and plasma free choline and zinc concentrations. These 3 factors together explained 43% of the variability in CD4(+) cell counts. CONCLUSION: The results provide evidence that compromised nutritional and antioxidant status begin early in the course of HIV-1 infection and may contribute to disease progression.

Full Text

Duke Authors

Cited Authors

  • Bogden, JD; Kemp, FW; Han, S; Li, W; Bruening, K; Denny, T; Oleske, JM; Lloyd, J; Baker, H; Perez, G; Kloser, P; Skurnick, J; Louria, DB

Published Date

  • September 2000

Published In

Volume / Issue

  • 72 / 3

Start / End Page

  • 809 - 815

PubMed ID

  • 10966904

Pubmed Central ID

  • 10966904

International Standard Serial Number (ISSN)

  • 0002-9165

Digital Object Identifier (DOI)

  • 10.1093/ajcn/72.3.809

Language

  • eng

Conference Location

  • United States