title: Rabbits transfused with human immunodeficiency virus type 1-infected blood develop immune deficiency with CD4+ lymphocytopenia in the absence of clear evidence for HIV type 1 infection.
abstract: Rabbits can be infected with human immunodeficiency virus (HIV-1), but no disease signs similar to acquired immunodeficiency syndrome (AIDS) have been reported to date. In our attempt to develop types of HIV-1 more virulent for rabbits, an immunodeficiency characterized by CD4+ lymphocytopenia and opportunistic infection was induced by transfusion from HIV-1-infected rabbits. The original donor was infected for 27 months; initial passage resulted in infection of two rabbits. Transfusions from these two infected rabbits. Transfusions from these two infected rabbits caused immunodeficiency in 12 recipients. One rabbit died at 3 months and a second at 8 months postransfusion with lymphocyte depletion in lymphoid organs; one of these and another of the CD4+ lymphocytopenic rabbits had opportunistic infections. Lentivirus-like particles were detected in thymus and spleen from an affected rabbit. Despite appearance of AIDS-like disease signs, antibodies to HIV-1 probes were detected in rabbits receiving passaged blood. However, RNA transcripts hybridizing with HIV-1 probes were detected in organs of some rabbits, implicating the initial HIV infection in the disease. Transfusion from uninfected donors produced no signs of immunodeficiency, which suggests the involvement of an HIV-related agent. The present data do not allow definitive characterization of the agent(s) involved in the immunodeficiency. Possibilities include activation of a rabbit retrovirus or, alternatively, development of a mutated HIV-1 strain.
authors.affiliation: Laboratory of Immunogenetics, National Institute of Allergy and Infectious Disease, NIH-Twinbrook II Facility, Rockville, Maryland 20852, USA.
authors.forename: R M
authors.initials: RM
authors.lastname: Simpson
authors.forename: B S
authors.initials: BS
authors.lastname: Hubbard
authors.forename: D W
authors.initials: DW
authors.lastname: Alling
authors.forename: R
authors.initials: R
authors.lastname: Teller
authors.forename: M A
authors.initials: MA
authors.lastname: Fain
authors.forename: F S
authors.initials: FS
authors.lastname: Bowers
authors.forename: T J
authors.initials: TJ
authors.lastname: Kindt
mesh_terms: D000818:Animals; D001769:Blood / Q000821:virology*; D001803:Blood Transfusion; D015496:CD4-Positive T-Lymphocytes / Q000473:pathology*; D015658:HIV Infections / Q000276:immunology / Q000503:physiopathology / Q000635:transmission*; D015497:HIV-1 / Q000276:immunology / Q000472:pathogenicity*; D006801:Humans; D007153:Immunologic Deficiency Syndromes / Q000276:immunology / Q000503:physiopathology / Q000821:virology*; D008198:Lymph Nodes / Q000821:virology; D008854:Microscopy, Electron; D012367:RNA, Viral / Q000032:analysis; D011817:Rabbits; D013154:Spleen / Q000648:ultrastructure / Q000821:virology; D013950:Thymus Gland / Q000648:ultrastructure / Q000821:virology
chemical_list: D012367:RNA, Viral