Important note: Information in this article was accurate in 1987. The state of the art may have changed since the publication date.
Transmission of simian acquired immunodeficiency syndrome with a type D retrovirus: immunological aspects.
Clin Immunol Immunopathol. 1986 Dec;41(3):453-60. Unique Identifier : AIDSLINE MED/87052361 Wilson BJ; Shiigi SM; Zeigler JL; Olson LC; Malley A; Howard CF Jr
Abstract:
Simian acquired immunodeficiency syndrome (SAIDS) was transmitted to four of four rhesus macaques with blood from rhesus macaques naturally infected with a type D retrovirus, simian retrovirus-2 (SRV-2). Three of the four blood recipients died with SAIDS at 13, 15, and 26 weeks postinoculation. The fourth animal is alive with SAIDS. All four test monkeys became viremic and produced antiviral antibody. None of the inoculated monkeys produced measureable neutralizing antibody to SRV-2. The survivor produced higher levels of antiviral antibody than the monkeys that died. Phytohemagglutinin and concanavalin A reactivity of peripheral blood lymphocytes was depressed from weeks 6 to 12 after inoculation. Clinical findings included development of splenomegaly in all four monkeys, and diarrhea in two monkeys. Blood counts remained within the normal range except for a depression in the number of polymorphonuclear lymphocytes in two monkeys. Hematocrits were decreased in two monkeys just prior to their death. All four test monkeys developed lymph node atrophy and bone marrow hypoplasia. Total proteins and immunoglobulin production were normal. This report provides evidence that SRV-2, as well as other type D retroviruses, causes SAIDS in macaque species.
Keywords: Acquired Immunodeficiency Syndrome/MICROBIOLOGY/TRANSMISSION/ *VETERINARY Animal Antibodies, Viral/ANALYSIS Concanavalin A Lymphocyte Transformation Lymphocytes/IMMUNOLOGY Lymphoproliferative Disorders/MICROBIOLOGY/VETERINARY Macaca/*MICROBIOLOGY Macaca mulatta/*MICROBIOLOGY Monkey Diseases/MICROBIOLOGY/*TRANSMISSION Phytohemagglutinins Retroviridae/IMMUNOLOGY/*PATHOGENICITY Support, U.S. Gov't, P.H.S. JOURNAL ARTICLE
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