HUMAN RETROVIRUSES: AFTER A DECADE OF DISCOVERY (MEETING ABSTRACT)

Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.

HUMAN RETROVIRUSES: AFTER A DECADE OF DISCOVERY (MEETING ABSTRACT)

Fifteenth Symposium of the International Association for Comparative Research on Leukemia and Related Diseases. October 6-11, 1991, Padova/Venice, Italy, p. 29, 1991.. Unique Identifier : AIDSLINE ICDB/92682385
Gallo RC; Lab. of Tumor Cell Biology, NCI, Bethesda, MD

Abstract: In the last decade, four human retroviruses have been discovered belonging to two different types: leukemia viruses (HTLVs) and immunodeficiency viruses (HIVs). Similar viruses have been found in primates and ungulate animals with analogous disease outcomes. HTLV-1 primarily causes adult T-cell leukemia (ATL), tropical spastic paraparesis or HTLV-1-associated myelopathy, and is associated with some cases of B-cell leukemia. HTLV-II is linked to relatively chronic forms of leukemia and more recently detected on iv drug abusers. HIV-1 and HIV-2 primarily induce immunodeficiency, severe neurological disorders and indirectly induce tumors. Recent epidemiological studies indicate that HIV is currently spreading more in iv drug abusers than in other risk groups, especially in female prostitutes or those with partners who are drug abusers, and in their babies. HTLVs and HIVs show remarkable parallels in properties like CD4+ T-cell tropism, modes of transmission, latency, immunosuppressive effects, as well as in overall molecular characteristics (eg, nature of structural proteins) and transcription of regulatory proteins from doubly spliced mRNA. The main differences in these viruses are HTLVs induce cell proliferation, where HIVs induce cytopathic destruction; HTLV genome is less complex than that of HIV; HTLVs infect almost all T-cell subsets, some B cells, but not cells of monocytoid lineage, whereas HIVs infect CD4+ cells including T cells and a wide variety of monocyte/macrophage-derived cells; HTLVs are less transmissible than HIVs; HTLV genomes show very little difference, whereas the HIV genome shows significant variation, posing great difficulties for vaccine or chemotherapy studies. The induction of ATL by HTLV-1 is mediated by the tax gene product which can activate several cellular genes (eg, IL-2, IL-2 receptor, and TNF) and when released extracellularly by infected cells, it can induce proliferation of uninfected cells. The induction of immunodeficiency by HIV is mediated through both its direct or indirect effects on cells of the immune system. The appearance of Kaposi's sarcoma (KS) is increased several thousandfold in HIV-1-infected individuals, although the virus genome or its expression is not found in KS lesions. The HIV tat gene product appears in vitro to act as a growth factor for KS cells derived from AIDS patients. A more potent growth factor (30 kD) for these cells is produced by activated T cells. Immunocytochemical studies of KS cells suggests that these cells may originate from smooth muscle cell precursors. The in vitro culture of these cells releases a variety of growth factors which can function both in an autocrine and a paracrine manner. HIV thus may play an indirect role in the formation of Kaposi's tumor.

Keywords: Cell Division CD4-Positive T-Lymphocytes Female Human HIV Infections/*COMPLICATIONS/PATHOLOGY/TRANSMISSION HTLV-I Infections/*COMPLICATIONS/GENETICS/IMMUNOLOGY HTLV-II Infections/*COMPLICATIONS/GENETICS/IMMUNOLOGY Leukemia, B-Cell/ETIOLOGY Leukocyte Count Male Prostitution Substance Abuse, Intravenous Transcription, Genetic Viral Regulatory Proteins ABSTRACT
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M9290919

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