HIV-1 peptides induce a proliferative response in lymphocytes from infected persons
Article Abstract:
Cell-mediated immune responses are impaired in individuals who are infected with HIV. Lymphocytes (a type of white blood cell) from 99 subjects in various stages of HIV-1 infection were tested. The blood cells were tested with peptides (segments of protein) from various regions of the structural proteins of HTLV-III(B), a related virus, to see which peptides could induce cell proliferation, indicative of a cell-mediated immune response. The structural proteins included the gag antigens, which comprise the inner core of the virus, and the envelope protein, which comprises the outer coat of the virus. Regions of the structural proteins were identified that evoked a response in many of the patients (a common response), as were regions that evoked a response in specific patients. The gag proteins caused the most frequent response among patients, and the responses occurred in late as well as early stages of disease. Twelve common sites in the gag proteins were identified. Eighteen sites that elicited common responses were identified in the envelope protein. The sites were grouped into four regions of the protein that had not been previously known to evoke responses and two other regions that were previously known to evoke responses. The responses to the envelope protein were detectable in patients in the early stages of disease and decreased in AIDS-related complex and AIDS. The understanding of what regions of the structural proteins evoke cell-mediated immunity is important because it could lead to a vaccine against AIDS. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Journal of Acquired Immune Deficiency Syndromes
Subject: Health
ISSN: 0894-9255
Year: 1989
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Effect of cytokines on HIV release and IL-2 receptor alpha expression in monocytic cell lines
Article Abstract:
The cell line THP-1, which resembles monocytes, a type of white blood cell, was experimentally infected with the human immunodeficiency virus (HIV). The effects of various cytokines, or growth factors, such as interferon-T (IF-T), lipopolysaccharide (LPS), interleukin-2 (IL-2) and IL-6 on the HIV-infected cell line were then assessed. The cytokine IF-T can suppress viral replication or multiplication, whereas LPS can activate and induce maturation or development of monocytes. IL-2 increases certain functions of monocytes, such as killing activity against microorganisms and secretion of IL-1beta. HIV production by the HIV-infected monocytic cell line was reduced by IF-T and increased by IL-2 and IL-6. The decrease in HIV production due to IF-T was not overcome by IL-2 or LPS. The relationship between cytokine activation of IL-2 receptor alpha (a specialized protein) on the monocytic cell surface and HIV infection was examined. The expression of IL-2 receptor alpha was moderately increased by HIV infection and markedly enhanced by IL-6 and IF-T in both infected and uninfected monocytic cells. These results do not support a relationship between expression of IL-2 receptor alpha and HIV production, but suggest that the increased levels of IL-2 receptor alpha in patients with acquired immunodeficiency syndrome (AIDS) may result in part from the activation of infected monocytes by cytokines, such as IL-6, produced mainly by the monocytes. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Journal of Acquired Immune Deficiency Syndromes
Subject: Health
ISSN: 0894-9255
Year: 1990
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T-cell response to HIV in natural infection: optimized culture conditions for detecting responses to gag peptides
Article Abstract:
Four HIV peptides that illicit an immunological response from T-cells have been identified with an enhanced cell culture technique. Interleukin-2 was added to cultures, which were extended to 8-10 days duration, yielding gag 180-194 peptides not previously thought immunogenic.
Publication Name: Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology
Subject: Health
ISSN: 1077-9450
Year: 1997
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