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Hematopoietic response to lineage‐non‐specific (rrIL‐3) and lineage‐specific (rhG‐CSF, rhEpo, rhTpo) cytokine administration in SIV‐infected rhesus macaques is related to stage of infection
Author(s) -
Bucur Silvana Z.,
Gillespie Theresa W.,
Lee Mark E.,
Adams Jonathan W.,
Bray Robert A.,
Villinger Francois,
Ansari Aftab A.,
Hillyer Christopher D.
Publication year - 2000
Publication title -
journal of medical primatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.31
H-Index - 42
eISSN - 1600-0684
pISSN - 0047-2565
DOI - 10.1034/j.1600-0684.2000.290201.x
Subject(s) - thrombopoietin , granulocyte colony stimulating factor , haematopoiesis , simian immunodeficiency virus , erythropoietin , bone marrow , immunology , biology , cytokine , medicine , immune system , stem cell , endocrinology , chemotherapy , genetics
The present study reports the hematopoietic response to the exogenous administration of recombinant rhesus interleukin‐3 (rrIL‐3) or a combination of recombinant human granulocyte colony‐stimulating factor (rhG‐CSF)/erythropoietin (Epo)/thrombopoietin (Tpo) at two different stages of SIV infection: Early‐stage (n=6, CD4+>1000/ μl and mild splenomegaly) and late‐stage (n=6, CD4+<500/μl, progressive hepatosplenomegaly and/or weight loss). SIV‐infected animals exhibited significantly impaired bone marrow (BM) and peripheral blood (PB) responses to both rrIL‐3 and rhG‐CSF/Epo/Tpo administration, as compared to historic controls. In addition, compared to early‐stage SIV‐infected animals, late‐stage SIV‐infected macaques demonstrated a more marked dysfunction, as assessed by PB and BM CD34+ content and clonogenic progenitors (colony‐forming unit). Neither rrIL‐3 nor rhG‐CSF/Epo/Tpo administration during either early‐stage or late‐stage SIV infection increased the viral load, as assessed by bDNA assay. These data suggest that hematopoietic reserve and the response to various cytokines is decreased even in early‐stage SIV infection, with the hematopoietic dysfunction progressing in parallel to SIV infection.