EFFECTS OF HIV ON MALNUTRIONED PATIENTS
Protein-energy malnutrition, now known as protein-energy undernutrition, is an energy deficit due to chronic deficiency of all macronutrients. In children, it causes widespread atrophy of lymphoid tissues, particularly T-lymphocyte areas, arrest of lymphocyte development, reduced numbers of circulating mature CD4 helper cells, and impairment of antibody production to T-dependent antigens..
Deficiencies of essential amino acids can depress the synthesis of proteins responsible for production of cytokines released by lymphocytes, macrophages, and other body cells, complement proteins, kinins, clotting factors, and tissue enzymes activated during acute phase responses. allowing damaging effects of free oxygen radicals, depress T suppressor cells, and stimulate T helper cells.
Iron deficiency results in impaired phagocytic killing, less response to lymphocyte stimulation, fewer natural killer cells, and reduced interferon production. Selenium serves as an antioxidant and contributes to antibody responses and cytotoxicity of natural killer cells.
In children with HIV infection, selenium concentration in plasma appear to correlate with their immune functions. Similar changes are also seen in patients with copper deficiency. Copper concentrations often increase during infection as a result of stimulation of the hepatic production of ceruloplasmin.
Whereas micronutrient deficiencies may affect replication of the invading virus, they also induce several metabolic alterations in the body. This includes changes in whole-body protein turnover, increased urinary nitrogen loss
During infections, reactive oxygen molecules and pro-oxidant cytokines are released from activated phagocytes leading to increased consumption of vitamins like vitamin E and C and carotene which serve as antioxidants and minerals like zinc, copper, manganese, and selenium, which serve as components of antioxidant enzymes. 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.
Maternal micronutrient deficiencies may also increase viral load in blood, cervicovaginal secretions, and breast milk, and hence aid in utero, intrapartum, and postnatal mother-to-child HIV transmission, respectively, and affect immune functions and susceptibility of the unborn or young breast-fed child. HIV infection in nutritionally deprived individuals intensifies the nutritional deficits and further enhances cellular oxidative stress. This affects the functions of transcription factors and contributes to HIV replication and progression.
Although HIV attacks only a limited variety of T-lymphocyte subspecies, AIDS-induced malnutrition can lead to the secondary development of NAIDS through the action of proinflammatory cytokines. Also, malnutrition could hasten the development of AIDS in an HIV-infected person.
Conclusion
Since the realization of HIV as a potential disaster for the immune system, several advancements in its treatment, diagnosis, and supportive regimens have been made, still many deaths in AIDS are being attributed to malnutrition and its poor management.
Jane Ndinda
Deficiencies of essential amino acids can depress the synthesis of proteins responsible for production of cytokines released by lymphocytes, macrophages, and other body cells, complement proteins, kinins, clotting factors, and tissue enzymes activated during acute phase responses. allowing damaging effects of free oxygen radicals, depress T suppressor cells, and stimulate T helper cells.
Iron deficiency results in impaired phagocytic killing, less response to lymphocyte stimulation, fewer natural killer cells, and reduced interferon production. Selenium serves as an antioxidant and contributes to antibody responses and cytotoxicity of natural killer cells.
In children with HIV infection, selenium concentration in plasma appear to correlate with their immune functions. Similar changes are also seen in patients with copper deficiency. Copper concentrations often increase during infection as a result of stimulation of the hepatic production of ceruloplasmin.
Whereas micronutrient deficiencies may affect replication of the invading virus, they also induce several metabolic alterations in the body. This includes changes in whole-body protein turnover, increased urinary nitrogen loss
During infections, reactive oxygen molecules and pro-oxidant cytokines are released from activated phagocytes leading to increased consumption of vitamins like vitamin E and C and carotene which serve as antioxidants and minerals like zinc, copper, manganese, and selenium, which serve as components of antioxidant enzymes. 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.
Maternal micronutrient deficiencies may also increase viral load in blood, cervicovaginal secretions, and breast milk, and hence aid in utero, intrapartum, and postnatal mother-to-child HIV transmission, respectively, and affect immune functions and susceptibility of the unborn or young breast-fed child. HIV infection in nutritionally deprived individuals intensifies the nutritional deficits and further enhances cellular oxidative stress. This affects the functions of transcription factors and contributes to HIV replication and progression.
Although HIV attacks only a limited variety of T-lymphocyte subspecies, AIDS-induced malnutrition can lead to the secondary development of NAIDS through the action of proinflammatory cytokines. Also, malnutrition could hasten the development of AIDS in an HIV-infected person.
Conclusion
Since the realization of HIV as a potential disaster for the immune system, several advancements in its treatment, diagnosis, and supportive regimens have been made, still many deaths in AIDS are being attributed to malnutrition and its poor management.
Jane Ndinda
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