Human cytomegalovirus, HCMV, infects most of the population by adultho
od; the primary infection is often accompanied by transient neutropeni
a and thrombocytopenia, and is followed by a period asymtomatic viral
latency. In the setting of bone marrow transplantation, however, the i
mmunosuppressed state of the recipient enables HCMV to re-activate or
to infect the individual and cause serious sequelae. These range from
hepatitis and gastrointestinal disease to interstitial pneumonia and h
ematologic abnormalities, which are more common in the allograft setti
ng. Little is currently known about the mechanisms by which HCMV cause
s these hematologic abnormalities. In this review, we discuss experime
ntal models which are helping investigators understand the immunology
and pathology of CMV infection. We also summarize the in vivo and in v
itro studies of the effects of HCMV on human hematopoiesis. Several po
ssible mechanisms that could explain the deleterious effect of HCMV on
human hematopoietic function include: 1) alteration of accessory cell
function by inducing the production of inhibitory cytokines; 2) pertu
rbation of stromal cell function resulting in a decreased production o
f hematopoietic factors or by altering cell surface adhesion molecule
expression; 3) by direct infection of the hematopoietic stem or progen
itor cells. It is likely that the pathogenesis of this syndrome is mul
tifactorial therefore requiring a broad therapeutic approach. This wou
ld include the use of antiviral agents, hematopoietic growth factors a
nd donor derived HCMV specific cytolytic cells.