Elevated serum levels of soluble tumour necrosis factor receptors (sTNF‐R) in patients with HIV infection

• Published in: Clinical and experimental immunology Vol. 89; no. 3; pp. 351 - 355
• Main Authors: KALINKOVICH, A., ENGELMANN, H., HARPAZ, N., BURSTEIN, R., BARAK, V., KALICKMAN, I., WALLACH, D., BENTWICH, Z.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.09.1992; Blackwell
• Subjects: AIDS/HIV; Biological and medical sciences; Enzyme-Linked Immunosorbent Assay; HIV infection; HIV Infections - blood; HIV Seropositivity - blood; HIV Seropositivity - pathology; Homosexuality; human immunodeficiency virus; Humans; Immunodeficiencies; Immunodeficiencies. Immunoglobulinopathies; Immunopathology; Male; male homosexuals; Medical sciences; Receptors, Cell Surface - analysis; Receptors, Cell Surface - chemistry; Receptors, Tumor Necrosis Factor; Solubility; soluble tumour necrosis factor receptors; tumour necrosis factor; Human; Immunopathology; Seropositivity; Pathogenesis; Retroviridae; AIDS; Hemopathy; Soluble form; Infection; Virus; Tumor necrosis factor; Viral disease; Lentivirinae; Serum; Human immunodeficiency virus; Biological receptor
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.1992.tb06961.x

SUMMARY Serum levels of the soluble form of tumour necrosis factor receptor type II (p75) (sTNF‐R) were determined in HIV‐infected individuals and risk groups and were then correlated with the course of infection and prognosis. sTNF‐R levels were determined by an ELISA with MoAbs and polyclonal antibodies to urine‐derived sTNF‐R proteins. The mean ±s.e. levels of sTNF‐R in the sera of 49 HIV+ male homosexuals, 34 HIV− male homosexuals and 44 matched controls were 6.1 ± 0.3 ng/ml, 4.4 ± 0.3 ng/ml and 3.4 ± 0.2 ng/ml, respectively. All these values were significantly different between each of the groups (P < 0.001‐0.05). Sequential studies of sTNF‐R revealed higher levels following seroconversion in 5/8 individuals, remained persistently high during the asymptomatic phase of the infection and became even more elevated in some ARC and AIDS patients. At the same time TNF‐α was undetectable in sera obtained from HIV+ male homosexuals and from healthy controls. This was independent of stage of HIV infection, serum sTNF‐R level and type of ELISA kit used. These findings suggest that TNF‐α/TNF‐R system is turned on before and during HIV infection and raise the possibility that sTNF‐R, the natural inhibitor of TNF, may be of importance in determining the course and probably prognosis of the disease.