How does the pathophysiology of HIV infection affect nutritional status?

Updated: Apr 09, 2019
  • Author: Fazia Mir, MD; Chief Editor: Michael Stuart Bronze, MD  more...
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Weight loss incurred in adults with HIV is multifactorial. Protein energy malnutrition is the most common form of malnutrition seen in patients with HIV disease worldwide. It is marasmus predominant and results in T-lymphocyte function and number depression numbers, [6] along with impaired complement activation resulting in further health embarrassment.

Tumor necrosis factor alpha (TNF), IL-6, and IL-1 beta elevated levels have been implicated in HIV-mediated cachexia. [7] Both in combination cause appetite suppression by affecting the hypothalamus via serotonergic pathways and accelerated proteolysis, causing skeletal muscle break down by activating the ubiquitin proteosome pathway. [8] Since anaerobic glycolysis is preferred in infection, lactic acid accumulation occurs, which can lead to appetite suppression. TNF also works by inhibiting lipoprotein lipase, which results in depletion of fat stores and further wasting.

Micronutrient deficiencies affect replication of the HIV virus, elevate hepatic protein synthesis, increased urinary nitrogen loss, insulin resistance with resultant hyperglycemia, and increased gluconeogenesis. This persistent hyperglycemia contributes to anorexia and weight loss. [9]

Malnourished patients also exhibit delayed cutaneous sensitivity, reduced bactericidal properties, [10] and impaired serological response after immunizations. During infections, reactive oxygen molecules and prooxidant cytokines are released from activated phagocytes, [11] leading to increased consumption of vitamins like vitamin E and C, and β -carotene, which serve as antioxidants and minerals like zinc, copper, manganese, and selenium, which serve as components of antioxidant enzymes. [12] Deficiencies of antioxidants cause increased oxidative stress, which leads to apoptosis of T cells and indirectly compromise cell-mediated immunity and may stimulate HIV replication.

Deficiencies of water-soluble vitamins appear to occur less frequently than those of fat-soluble vitamins, and only cobalamin (B12) deficiency is associated with HIV disease progression. [13] Zinc levels decline as HIV disease progresses, and zinc supplementation in HIV infection has been shown to improve immune responses, although clinical benefits have not been documented. Selenium supplementation trials in HIV-infected individuals failed to demonstrate improvements in CD4+ T-cell counts, rates of opportunistic infections, or mortality despite improvements in markers of oxidative stress. [14] Glutathione, an intracellular antioxidant, was noted to be reduced in children with HIV infection, especially those showing growth failure. [15]

In a recent study published by Koethe et al, an optimal BMI in the range of 25-30 was associated with the greatest increase in CD4+ T-lymphocyte count reiterating the need for appropriate nutrition in HIV patients prior to initiating ART. [16] Over nourishment, a disease of developed countries, resulting in obesity (BMI>30) has the same effects on the immune system as malnourishment. Immune dysregulation in obesity has been attributed to elevated leptin levels and leptin resistance, increased interferon gamma levels leading to depressed T-cell function. [17]

Vitamin A deficiency has been associated with the progression of HIV disease, development of secondary infections, increased HIV-associated mortality, and increased maternal-fetal transmission. [18] Fawzi and colleagues in a subsequent trial on pregnant women in Tanzania could not demonstrate reduced transmission of HIV virus to children born to mothers with HIV receiving Vitamin A supplementation in conjunction with multivitamins. [19] However, they did conclude that patients, in the multivitamin treatment arm, did have delay in progression of HIV. [20]

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