Human cytomegalovirus induces apoptosis in the hematopoietic cell line MO7e

Sindre, Hilde; Rollag, Halvor; Olafsen, Mette Kløvstad; Degré, Miklos; Hestdal, Kjetil

doi:10.1034/j.1600-0463.2000.d01-48.x

Cited by 11 publications

(9 citation statements)

References 34 publications

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“…Moreover, MCMV induces apoptosis in uninfected neuronal cells in vivo (30), but not in in vitro culture (30). In addition, HCMV has been reported to induce apoptosis in hematopoietic progenitor MO7 cells (51). Clearly the capacity of HCMV to block or even induce apoptosis in infected cells may be dependent on the stage of differentiation, cells of different origins and/or different culture conditions, and the virus strains involved.…”

Section: Discussionmentioning

confidence: 99%

Human Cytomegalovirus Inhibits Neuronal Differentiation and Induces Apoptosis in Human Neural Precursor Cells

Odeberg

Wolmer

Falci

et al. 2006

J Virol

145

165

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Human cytomegalovirus (HCMV) is the most common cause of congenital infections in developed countries, with an incidence varying between 0.5 and 2.2% and consequences varying from asymptomatic infection to lethal conditions for the fetus. Infants that are asymptomatic at birth may still develop neurological sequelae, such as hearing loss and mental retardation, at a later age. Infection of neural stem and precursor cells by HCMV and consequent disruption of the proliferation, differentiation, and/or migration of these cells may be the primary mechanism underlying the development of brain abnormalities. In the present investigation, we demonstrate that human neural precursor cells (NPCs) are permissive for HCMV infection, by both the laboratory strain Towne and the clinical isolate TB40, resulting in 55% and 72% inhibition of induced differentiation of human NPCs into neurons, respectively, when infection occurred at the onset of differentiation. This repression of neuronal differentiation required active viral replication and involved the expression of late HCMV gene products. This capacity of HCMV to prevent neuronal differentiation declined within 24 h after initiation of differentiation. Furthermore, the rate of cell proliferation in infected cultures was attenuated. Surprisingly, HCMV-infected cells exhibited an elevated frequency of apoptosis at 7 days following the onset of differentiation, at which time approximately 50% of the cells were apoptotic at a multiplicity of infection of 10. These findings indicate that HCMV has the capacity to reduce the ability of human NPCs to differentiate into neurons, which may offer one explanation for the abnormalities in brain development associated with congenital HCMV infection.

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Section: Discussionmentioning

confidence: 99%

Human Cytomegalovirus Inhibits Neuronal Differentiation and Induces Apoptosis in Human Neural Precursor Cells

Odeberg

Wolmer

Falci

et al. 2006

J Virol

145

165

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“…HCMV can induce growth suppression of hematoietic progenitors possibly via apoptosis [4,14]. Our group has reported that HCMV can directly infect both primary cultured CD34 ?…”

Section: Introductionmentioning

confidence: 98%

“…Conversely, apoptosis plays an important role in the dissemination and pathogenesis of several viral infections. HCMV can induce apoptosis in several cell types through different mechanisms that may favor either viral clearance or disease development [4,[8][9][10]. Recent studies have suggested that viral infections may be modulated by mitogenactivated protein kinase pathways [11,12].…”

Section: Introductionmentioning

confidence: 98%

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Human cytomegalovirus induces caspase-dependent apoptosis of megakaryocytic CHRF-288-11 cells by activating the JNK pathway

Dou

Cai

et al. 2010

Int J Hematol

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Human cytomegalovirus (HCMV) infection is usually implicated in thrombocytopenia occurring in newborns and immunocompromised patients. However, the underlying mechanisms remain elusive. This study was conducted to investigate the effects of HCMV infection on the viability of megakaryocytic CHRF-288-11 cells and the underlying mechanisms involved. RT-PCR for determining mRNA expression of HCMV immediate early gene 1 and Western blot for measuring protein expression of late HCMV gene pp65 showed that CHRF-288-11 cells were susceptible to HCMV infection. HCMV infection reduced the viability of CHRF-288-11 cells via apoptosis in a dose- and time-dependent manner. Both caspase 3 and c-Jun terminal kinase (JNK) signaling pathway were activated in the HCMV-treated CHRF-288-11 cells. z-DEVD-fmk (a caspase inhibitor) and SP600125 (a JNK inhibitor) significantly prevented the death of CHRF-288-11 cells induced by HCMV, respectively. Furthermore, inhibition of JNK activity could reduce the formation of active caspase 3 induced by HCMV. Interestingly, the co-application of antivirus drug ganciclovir and SP600125 synergistically prevented the death of CHRF-288-11 cells induced by HCMV. Collectively, these findings suggest that HCMV infection may induce the caspase-dependent apoptosis of megakaryocytic CHRF-288-11 cells by the activation of JNK signaling pathway.

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“…21 Under certain circumstances, CMV infection may even directly induce apoptosis and growth suppression, as shown for hematopoetic progenitors. 22 …”

Section: Mechanistic Considerationsmentioning

confidence: 99%

Previous Cytomegalovirus Infection and Restenosis After Coronary Stent Placement

et al. 2001

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Background-Reactivated cytomegalovirus may promote neointima formation after percutaneous coronary interventions by facilitating cell cycle progression through inhibition of the eukariotic tumor suppressor protein p53. This prospective study sought to investigate the effect of previous cytomegalovirus infection on restenosis after coronary stenting. Methods and Results-In 551 consecutive patients with successful stent placement, we determined cytomegalovirus IgG titers. Primary and secondary end points were the rate of angiographic restenosis at 6 months and the rate of target vessel reintervention at 1 year, respectively. Three hundred forty patients (62%) had a positive cytomegalovirus IgG titer. We obtained angiographic follow-up in 82% of all patients. Angiographic restenosis rate was 28.7% in patients with positive cytomegalovirus titers and 34.6% in patients with negative titers (Pϭ0.18). Between the groups with and without positive cytomegalovirus titers, there were no significant differences in late lumen loss (

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Human cytomegalovirus induces apoptosis in the hematopoietic cell line MO7e

Cited by 11 publications

References 34 publications

Human Cytomegalovirus Inhibits Neuronal Differentiation and Induces Apoptosis in Human Neural Precursor Cells

Human Cytomegalovirus Inhibits Neuronal Differentiation and Induces Apoptosis in Human Neural Precursor Cells

Human cytomegalovirus induces caspase-dependent apoptosis of megakaryocytic CHRF-288-11 cells by activating the JNK pathway

Previous Cytomegalovirus Infection and Restenosis After Coronary Stent Placement

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