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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #152719

Title: THE PROTEIN METABOLIC RESPONSE TO HIV INFECTION IN YOUNG CHILDREN

Author
item Jahoor, Farook
item ABRAMSON, STUART - BCM, PEDIATRICS
item Heird, William

Submitted to: The American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/24/2003
Publication Date: 7/20/2003
Citation: JAHOOR, F., ABRAMSON, S., HEIRD, W.C. 2003. THE PROTEIN METABOLIC RESPONSE TO HIV INFECTION IN YOUNG CHILDREN. AMERICAN JOURNAL OF CLINICAL NUTRITION. 78(1):182-189.

Interpretive Summary: Infants born to women infected with the virus (HIV) that causes AIDS can also become infected by the virus. These babies grow at a much slower rate compared to healthy babies. Although it is known that repeated infections with bacteria will slow a child's growth, these babies grow at a much slower rate even before they get such infections. In this study we wanted to find out why young children with HIV infection grew slower than healthy children without HIV. We found that these children's dietary intake of energy and protein were much lower than normal healthy children, but they broke down and excreted a greater amount of the protein that they were eating. Hence they had less protein and energy available to support a normal growth rate. The findings of this study suggest that feeding babies with HIV a formula with a higher energy and protein content may enable them to maintain a normal growth rate.

Technical Abstract: BACKGROUND: Growth failure often precedes secondary infections in HIV-infected infants and children, suggesting that inadequate protein deposition may be an early manifestation of infection by the virus. However, the protein metabolic response elicited by the virus in young children is unknown. OBJECTIVE: We compared children with HIV infection and age-matched children without HIV infection with regard to whole-body and splanchnic protein kinetics and synthesis of acute phase proteins (APPs). DESIGN: Whole-body and splanchnic leucine kinetics and fractional and absolute synthesis rates of 2 positive and 4 negative APPs were measured in 6 asymptomatic, HIV-infected children (4 males and 2 females) aged 6-17 mo and 4 uninfected children (3 females and 1 male) aged 7-9 mo who were in the fed state. RESULTS: Compared with the control children, the HIV-infected children had significantly lower dietary energy and protein intakes and leucine balance and significantly faster leucine flux and fractional splanchnic leucine extraction; there was no significant difference between the groups in leucine oxidation rates. The HIV-infected children also had significantly higher plasma concentrations and absolute synthesis rates of the positive APPs and a significantly higher fractional synthesis rate of fibrinogen. The concentrations of 2 of the 4 negative APPs, albumin and HDL apolipoprotein A-I, were significantly lower in the HIV-infected children but were not associated with slower synthesis rates. CONCLUSIONS: Children with HIV infection but without secondary infection have reduced protein balance because of an inability to down-regulate protein catabolism. Furthermore, the acute phase protein response elicited by HIV infection is characterized by higher concentrations and synthesis rates of positive APPs without lower concentrations of some negative APPs.