Endothelial damage caused by cytomegalovirus and human herpesvirus-6

Abstract

Summary:Infection with cytomegalovirus (CMV) or human herpesvirus-6 (HHV-6) may have a role in vascular endothelial damage after bone marrow transplantation (BMT). In total, 41 patients who underwent BMT were classified into four groups (12, 10, 7, and 12 patients who were infected with both CMV and HHV-6, CMV alone, HHV-6, and neither virus, respectively). Levels of thrombomodulin, plasminogen activator inhibitor-1, and cyclic GMP were 7.571.7 FU/ml, 76.4724.1 ng/ml, and 9.5171.1 pmol/ ml, respectively, in the patients with both viruses, while the respective values were 2.970.67 FU/ml, 33.878.09 ng/ ml, and 2.9071.4 pmol/ml in patients infected with CMV alone, 4.870.96 FU/ml, 47.779.21 ng/ml, and 5.4870.55 pmol/ml in patients with HHV-6 alone, and 1.670.39, 17.577.88 ng/ml, and 0.4570.3 in those with neither virus. All three markers were significantly higher in the three groups with at least one virus than in the uninfected patients (Po0.05), and were also higher in patients with HHV-6 alone than in those with CMV alone (Po0.05). These results suggest that infection by CMV or HHV-6 causes vascular endothelial injury, with HHV-6 having a stronger effect than CMV, and combined infection having a stronger effect than either virus alone. Such viral infection may be a cause of thrombotic microangiopathy after BMT.

Intestinal thrombotic microangiopathy following reduced-intensity umbilical cord blood transplantation

“…19 Gastrointestinal damage due to preparative regimens might contribute to the development of intestinal TMA in our study. CMV infection, which is another putative etiology of TMA, 17 was Table 3 Summary of macroscopic and pathological findings documented in four patients, and all were located in the gut. CMV colitis might be associated with intestinal TMA following RI-CBT.…”

“…2,12 There is little information on the pathogenesis of intestinal TMA following RI-CBT. TMA after myeloablative HSCT has a multifactorial etiology that includes immunosuppressive agents, 14,15 total body irradiation (TBI), 16 CMV infection, 17 and acute GVHD. 18 These factors injure the vascular endothelium of many organs.…”

Human herpesvirus type 6 reactivation after haematopoietic stem cell transplantation

“…[21][22][23] This is possibly caused by the low number of patients and variation in the conditioning regimens. In vitro data showed that HHV6 can infect hematological progenitor cells and reduce colony formation, which may explain the delayed engraftment after HSCT.…”

Thrombocytopenia and hemostatic disorders in chronic graft versus host disease

“…[68][69][70][71][72] CMV or human herpes virus-6 in post-alloBMT patients may also cause vascular endothelial injury, which could lead to development of thrombotic microangiopathy. 73 Cytokine-induced thrombocytopenia It is possible that similar mechanisms are responsible for the thrombocytopenia in infection and cGVHD. Serum cytokine levels including granulocyte colony-stimulating factor (G-CSF), macrophage CSF (M-CSF), interleukin1a, interleukin-1b, and interleukin-6 may be significantly increased in both conditions, and may lead to the activation of monocytes and macrophages, leading to the increased platelet consumption.…”