Decreased serum tryptophan in patients with HIV-1 infection correlates with increased neopterin and neurologic/psychiatric symptoms

Article Abstract:

Infection with human immunodeficiency virus, type 1 (HIV-1) frequently involves complications that affect nerve cells, causing symptoms of dementia and polyneuropathy (dysfunction of the peripheral nerves, with symptoms including cramps and impairment of the senses, especially touch; disturbances of nervous function in the extremities; and loss of tendon reflexes). The mechanisms behind the dysfunction and destruction of nerve cells are not understood. It is thought that there is a defect in the metabolism of the amino acid tryptophan. Patients with advanced HIV infection have reduced concentrations of tryptophan, and correspondingly increased concentrations of kynurenine (a compound which is produced when tryptophan is broken down), compared with concentrations in normal individuals. The concentrations of neopterin, tryptophan, and kynurenine were analyzed in 23 patients infected with HIV, 10 of whom had polyneuropathy, three had dementia, and one had both dementia and polyneuropathy. Patients with polyneuropathy or dementia had lower concentrations of tryptophan than the patients without these disorders. The concentrations of tryptophan in the three patients with dementia were the lowest of all. Therefore, there were significant associations between reduced concentrations of tryptophan levels and the existence of neurologic and psychiatric symptoms. Levels of neopterin and kynurenine were higher in HIV-infected patients than in normal individuals but did not vary between patients with and without neurologic symptoms. Neopterin is produced by cells in the immune system when they are stimulated to produce an immune response. Factors, such as interferon-gamma and tumor necrosis factor-alpha, produced during an immune response cause the reduction of tryptophan. Thus, the low levels of tryptophan and high levels of neopterin may be the result of chronic stimulation of the immune system in patients with HIV-1 infection. (Consumer Summary produced by Reliance Medical Information, Inc.)

Psychological aspects, Causes of, Dementia, AIDS (Disease), Peripheral nerve diseases, Peripheral nervous system diseases, Amino acid metabolism, Tryptophan metabolism

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Elevated concentrations of circulating intercellular adhesion molecule 1 (ICAM-1) in HIV-1 infection

Article Abstract:

Individuals infected with HIV-1 may have increased blood levels of a circulating form of intercellular adhesion molecule 1 (c-ICAM-1). c-ICAM-1 is a substance that can interfere with normal function of the immune system. A study compared the blood levels of c-ICAM-1 in 76 individuals infected with HIV-1 to those of 22 healthy individuals without HIV-1 infection. Blood levels of c-ICAM-1 were significantly higher in the HIV-infected individuals than in the healthy individuals. Blood levels of c-ICAM-1 in HIV-infected individuals were not related to blood levels of CD4+ T-cells or severity of disease. Increased blood levels of c-ICAM-1 in HIV-infected individuals were associated with increased blood levels of interleukin-6 and increased levels of neopterin in the urine. Levels of neopterin in the urine are related to disease progression in HIV-infected individuals.

Measurement, Cell adhesion molecules

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Role of neopterin and 7,8-dihydroneopterin in human immunodeficiency virus infection: marker for disease progression and pathogenic link

Article Abstract:

Neopterin and its derivative, 7,8-dihydroneopterin, appear to be a marker for the progression of HIV infection. These compounds are produced naturally by activated immune cells, most notably, monocytes and macrophages. Consequently, neopterin levels are elevated during viral infections and autoimmune diseases. Neopterin levels increase during the acute phase of HIV infection, decline during the long asymptomatic phase and begin to rise again as the individual develops AIDS. It appears to scavenge free radicals and may trigger a type of natural cell death called apoptosis.

Cytokines, Cellular immunity

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