Cytomegalovirus (CMV) has been reported to cause delayed marrow engraftmenl and even graft failure afler BMT. tt has been also reported that platelet recovery is delayed in CMV-seroposiiive patients following BMT. We have thus examined the hematopoiesis of MCMV infected mice which could be used as a model of latent CMV infection. As we have reported, bone marrow (BM) cellularity and number of hernatopoietic progenitor cells (HPCs) decreased in the acute phase of MCMV infection. However, 4 weeks postinfection (pi) of B ALB/c mice with 0.2LD50 of MCMV, where viral replication is not detected in any organs except salivary glands, BM cellularity recovered to the control level. Furthermore, numbers of CFU-GM, BFU-E, and lineage marker negative, c-kil and Sca-1 positive (Lin"c-kit+Sca-1+) cells have also recovered to the control level. However, autologous BM reconstitution in MCMV latently infected mice after intravenous 5-FU(150mg/kg) injection significantly delayed compared with control (P<.05). We then examined the function of hernatopoietic microenvironment to explain this delayed marrow reconstitution. Firstly, mice 4 weeks pi and control mice were irradiated (8.5Gy) and IxIO5 normal BM cells were transferred. Surface colonies of spleens (CFU-S) on day8 and day 12 after the transfer were significantly reduced in MCMV infected mice. Secondly, long-term bone marrow culture was established and the production of non-adherent cells decreased rapidly after recharging normal bone marrow cells in MCMV infected mice. In addition, MCMV IE gene was detected in adherent, but not in non-adherent cells by PCR and in situ hybridization. These results suggests that MCMV exclusively infects microenvironment in MCMV latently infected mice and impairs its supporting capability.
|出版ステータス||Published - 1997 12月 1|
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