Document 0704
 DOCN  M9550704
 TI    Marrow accessory cell infection and alterations in hematopoiesis
       accompany severe neutropenia during experimental acute infection with
       feline immunodeficiency virus.
 DT    9505
 AU    Linenberger ML; Beebe AM; Pedersen NC; Abkowitz JL; Dandekar S;
       Department of Medicine, University of Washington Seattle 98195.
 SO    Blood. 1995 Feb 15;85(4):941-51. Unique Identifier : AIDSLINE
       MED/95152072
 AB    Severe neutropenia and bone marrow (BM) morphologic abnormalities occur
       during experimentally induced primary infection with feline
       immunodeficiency virus (FIV), a lentivirus biologically similar to human
       immunodeficiency virus (HIV). To further characterize the mechanisms
       involved in this acute infection model of lentivirus-induced BM
       suppression, peripheral blood counts, histologic BM studies, and BM
       culture assays were performed on 12 cats that underwent necropsy at
       regular intervals postinoculation (PI) with FIV Petaluma. Plasma viremia
       developed at week 3 PI and neutropenia was initially detected at week 6
       PI. Low neutrophil counts, but normal hematocrits and platelet counts,
       persisted through week 12 PI. Infected BM mononuclear cells and
       megakaryocytes were identified by in situ hybridization assays for FIV
       nucleic acids in BM sections of cats that underwent necropsy at weeks 4
       to 12 PI, correlating with detection of soluble FIV p24 antigen and
       identification of infected mononuclear and macrophage cells in BM
       buffy-coat cell cultures from these cats. At weeks 1.5 to 4 PI, the mean
       frequencies (number per 10(5) BM mononuclear cells) of erythroid
       progenitors (erythroid colony-forming units [CFU-E] and erythroid
       burst-forming units [BFU-E] and granulocyte/macrophage progenitors
       (CFU-granulocyte/macrophage [CFU-GM]) were increased to 508 +/- 74, 143
       +/- 24, and 110 +/- 17, respectively (n = 5 cats) as compared with
       controls (172 +/- 24, 86 +/- 26, and 44 +/- 10; n = 3 cats; P < .02),
       and the percentages of progenitors in the DNA-synthetic phase of the
       cell cycle were equivalent to controls. In contrast, the progenitor
       frequencies at weeks 6 to 12 PI were significantly decreased (72 +/- 16,
       43 +/- 6, and 19 +/- 4, respectively; n = 7 cats; P < .01), and these
       progenitors were more frequently in S-phase. Autologous serum
       significantly inhibited (P < .05) the growth of CFU-GM in 6 of 9 cats
       and failed to support the maximal growth of BFU-E in 4 of 9 cats studied
       at weeks 4 to 12 PI, whereas no such abnormalities were observed in
       colony assays containing autologous sera from control cats (n = 3) or
       cats studied at weeks 1.5 or 3 PI (n = 3). In comparison, sera from
       FIV-infected cats did not inhibit the growth of normal, allogeneic
       progenitors. However, FIV serum frequently failed to support maximal in
       vitro growth of normal CFU-GM as compared with uninfected allogeneic
       sera, further suggesting a lack of progenitor growth-promoting
       substances in infected cat sera.(ABSTRACT TRUNCATED AT 400 WORDS)
 DE    Animal  Bone Marrow/PATHOLOGY/PHYSIOPATHOLOGY/*VIROLOGY  Cats  Cell
       Cycle  Cells, Cultured  DNA, Viral/ANALYSIS  Feline Acquired
       Immunodeficiency Syndrome/BLOOD/*PATHOLOGY/  *PHYSIOPATHOLOGY
       *Hematopoiesis  Hematopoietic Stem Cells/*PATHOLOGY  Immunodeficiency
       Virus, Feline/ISOLATION & PURIF/*PHYSIOLOGY  In Situ Hybridization
       Kinetics  Neutropenia/*ETIOLOGY  RNA, Viral/ANALYSIS  Support, U.S.
       Gov't, P.H.S.  Time Factors  Viremia/BLOOD/PATHOLOGY/PHYSIOPATHOLOGY
       JOURNAL ARTICLE

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