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Human cytomegalovirus suppression of and latency in early hematopoietic
progenitor cells
H Sindre, GE Tjoonnfjord, H Rollag, T Ranneberg-Nilsen, OP Veiby, S Beck, M Degre and K Hestdal
Kaptein W Wilhelmsens og Frues Institute of Microbiology, The National
Hospital, Oslo, Norway.
Bone marrow cells (BMC) are involved in the pathogenesis of human
cytomegalovirus++ (HCMV) infections, and the hematopoietic cells are
probable sites of HCMV latency in healthy donors. In vitro studies have
indicated both a direct inhibitory effect of HCMV on proliferation and
differentiation of myeloid bone marrow progenitors and an impairment of
bone marrow stroma cell function by HCMV. The purpose of the present study
was to establish whether the suppressing effect could be limited to subsets
of immature CD34+ BMC and to investigate the role of immature cell
populations as possible sites of HCMV latency. CD34+ cells from healthy
HCMV-seropositive and -seronegative donors were sorted according to the
expression of HLA-DR (CD34+ HLA-DR+ and CD34+ HLA-DR- cells). The
progenitor growth of hematopoietic progenitor cells from seronegative
donors was examined by colony and single-cell assays after in vitro
infection with HCMV. To determine the susceptibility of the CD34+ cells to
HCMV infection in vitro and in vivo, cells of both subsets from
seronegative and seropositive donors were analyzed for the presence of HCMV
DNA by polymerase chain reaction. HCMV infection in vitro inhibited the
interleukin-1alpha (IL-1alpha)-, IL-3-, granulocyte colony-stimulating
factor-, granulocyte-macrophage colony-stimulating factor-, and stem cell
factor-induced proliferation in single-cell assays of CD34+ HLA-DR- cells
by 34%. In contrast, the colony growth of the CD34+ HLA-DR+ subset was
suppressed in cells from only 3 of the 8 donors. However, in vitro HCMV
infection of the CD34+ HLA-DR+ progenitor cells inhibited the proliferation
of all donors tested when hematopoietic growth factors were used
individually to promote progenitor growth. In addition, the formation of
burst-forming units- erythroid and colony-forming units-granulocyte,
erythrocyte, monocyte, megakaryocyte was reduced 40% to 60% by HCMV in
vitro. In contrast, the growth of high proliferative potential
colony-forming cells was not inhibited after in vitro HCMV infection.
Furthermore, HCMV DNA was detected in both CD34+ HLA-DR- and CD34+ HLA-DR+
progenitors from in vitro-infected HCMV-seronegative donors and cells from
HCMV- seropositive donors. Taken together, the early progenitors defined as
CD34+ HLA-DR- and CD34+ HLA-DR+ are directly suppressed in their
proliferation by HCMV in vitro, and hematopoietic stem cells are also sites
of HCMV latency in healthy HCMV-seropositive donors.
Volume 88,
Issue 12,
pp. 4526-4533,
12/15/1996
Copyright © 1996 by The American Society of Hematology
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