Human Cytomegalovirus Infection of Endothelial Cells Triggers Platelet Adhesion and Aggregation

Rahbar, Afsar; Söderberg‐Nauclér, Cecilia

doi:10.1128/jvi.79.4.2211-2220.2005

Cited by 106 publications

(96 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…43 We observed increased expression of CD34 and CD45 in HCMV infected ASCs. Although generally considered to be a marker of haematopoietic progenitor cells, it is now agreed that there is positive CD34 expression on a subset of freshly isolated ASCs.…”

Section: Discussionmentioning

confidence: 55%

Human cytomegalovirus infection of human adipose-derived stromal/stem cells restricts differentiation along the adipogenic lineage

et al. 2015

View full text Add to dashboard Cite

Human adipose-derived stromal/stem cells (ASCs) display potential to be used in regenerative stem cell therapies and as treatments for inflammatory and autoimmune disorders. Despite promising use of ASCs as therapeutics, little is known about their susceptibility to infectious agents. In this study, we demonstrate that ASCs are highly susceptible to human cytomegalovirus (HCMV) infection and permissive for replication leading to release of infectious virions. Additionally, many basic ASC functions are inhibited during HCMV infection, such as differentiation and immunomodulatory potential. To our knowledge this is the first study examining potential adverse effects of HCMV infection on ASC biology. Our results suggest, that an active HCMV infection during ASC therapy may result in a poor clinical outcome due to interference by the virus.

show abstract

Section: Discussionmentioning

confidence: 55%

Human cytomegalovirus infection of human adipose-derived stromal/stem cells restricts differentiation along the adipogenic lineage

et al. 2015

View full text Add to dashboard Cite

show abstract

“…In animal transplantation models, EC activation by CMV results in consumptive coagulopathy (142,143). Increased thrombogenicity is inhibited by foscarnet and ganciclovir, suggesting a role for active viral replication in thrombosis (144).…”

Section: Procoagulant Effectsmentioning

confidence: 99%

The Cell Biology of Cytomegalovirus: Implications for Transplantation

Kaminski

Fishman

2016

American Journal of Transplantation

View full text Add to dashboard Cite

Interpretation of clinical data regarding the impact of cytomegalovirus (CMV) infection on allograft function is complicated by the diversity of viral strains and substantial variability of cellular receptors and viral gene expression in different tissues. Variation also exists in nonspecific (monocytes and dendritic cells) and specific (NK cells, antibodies) responses that augment T cell antiviral activities. Innate immune signaling pathways and expanded pools of memory NK cells and cd T cells also serve to amplify host responses to infection. The clinical impact of specific memory T cell anti-CMV responses that cross-react with graft antigens and alloantigens is uncertain but appears to contribute to graft injury and to the abrogation of allograft tolerance. These responses are modified by diverse immunosuppressive regimens and by underlying host immune deficits. The impact of CMV infection on the transplant recipient reflects cellular changes and corresponding host responses, the convergence of which has been termed the "indirect effects" of CMV infection. Future studies will clarify interactions between CMV infection and allograft injury and will guide interventions that may enhance clinical outcomes in transplantation.

show abstract

“…It reduces sensitivity to NO, decreases endothelial NOS, and increases inducible NOS expression in human coronary artery allografts (29). Platelet adhesion, a marker of inflammation, was increased in HCMV-infected human pulmonary artery endothelial cells (48) and in postcapillary venules from mice with a persistent mCMV infection (28). Therefore, immune response mediators that increase during active or latent mCMV infections likely contribute to the vascular dysfunction and vasculopathies.…”

Section: Discussionmentioning

confidence: 99%

Vascular dysfunction in young, mid-aged and aged mice with latent cytomegalovirus infections

Gombos

Brown

Teefy

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Gombos RB, Brown JC, Teefy J, Gibeault RL, Conn KL, Schang LM, Hemmings DG. Vascular dysfunction in young ec50, mid-aged and aged mice with latent cytomegalovirus infections. Am J Physiol Heart Circ Physiol 304: H183-H194, 2013. First published November 2, 2012; doi:10.1152/ajpheart.00461.2012.-Human cytomegalovirus (HCMV) is associated with vascular diseases in both immunosuppressed and immunocompetent individuals. CMV infections cycle between active and latent phases throughout life. We and others have shown vascular dysfunction during active mouse CMV (mCMV) infections. Few studies have examined changes in physiology during latent CMV infections, particularly vascular responses or whether the negative effects of aging on vascular function and fertility will be exacerbated under these conditions. We measured vascular responses in intact mesenteric and uterine arteries dissected from young, mid-aged, and aged latently mCMV-infected (mCMV genomes are present but infectious virus is undetectable) and agematched uninfected mice using a pressure myograph. We tested responses to the ␣ 1-adrenergic agonist phenylephrine, the nitric oxide donor sodium nitroprusside, and the endothelium-dependent vasodilator methacholine. In young latently mCMV-infected mice, vasoconstriction was increased and vasodilation was decreased in mesenteric arteries, whereas both vasoconstriction and vasodilation were increased in uterine arteries compared with those in age-matched uninfected mice. In reproductively active mid-aged latently infected mice, mesenteric arteries showed little change, whereas uterine arteries showed greatly increased vasoconstriction. These vascular effects may have contributed to the decreased reproductive success observed in mid-aged latently mCMV-infected compared with age-matched uninfected mice (16.7 vs. 46.7%, respectively). In aged latently infected mice, vasodilation is increased in mesenteric and uterine arteries likely to compensate for increased vasoconstriction to mediators other than phenylephrine. The novel results of this study show that even when active mCMV infections become undetectable, vascular dysfunction continues and differs with age and artery origin. uterine arteries; mesenteric arteries; infertility; vascular function; pressure myograph HUMAN CYTOMEGALOVIRUS (HCMV) is a member of the ␤-Herpesviridae family (50). In the human population, it infects 40 to 80% of individuals (10). Although in the general population it is thought to be mostly asymptomatic, infection has been associated with tumorigenesis, transplant rejection, vascular diseases such as atherosclerosis and restenosis, and increased mortality and hypertension (9,19,23,26,33,62,64). The mechanisms whereby HCMV infections result in vasculopathy are still unclear.

show abstract

Human Cytomegalovirus Infection of Endothelial Cells Triggers Platelet Adhesion and Aggregation

Cited by 106 publications

References 39 publications

Human cytomegalovirus infection of human adipose-derived stromal/stem cells restricts differentiation along the adipogenic lineage

Human cytomegalovirus infection of human adipose-derived stromal/stem cells restricts differentiation along the adipogenic lineage

The Cell Biology of Cytomegalovirus: Implications for Transplantation

Vascular dysfunction in young, mid-aged and aged mice with latent cytomegalovirus infections

Contact Info

Product

Resources

About