Influence of cytomegalovirus infection in the development of cardiac allograft vasculopathy after heart transplantation

Delgado, Juan; Reyne, Ana García; Dios, Santiago de; López‐Medrano, Francisco; Jurado, Alfonso; Juan, Rafael San; Ruiz-Cano, María J.; Folgueira, María Dolores; Gómez-Sánchez, Miguel Ángel; Aguado, José María; Lumbreras, Carlos

doi:10.1016/j.healun.2015.03.015

Cited by 82 publications

(80 citation statements)

References 41 publications

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“…Th T e strength h of the study is to provide d evide d nce that the identification of the CD CD16 profi f le Previous studies have identified CMV infection as a risk factor associated with the development of allograft vascular lesions 33,34 . In the present cohort, the FCGR3A-VV genotype was identified as a risk factor associated with viral infections.…”

Section: Discussionmentioning

confidence: 99%

Genetic and Functional Profiling of CD16-Dependent Natural Killer Activation Identifies Patients at Higher Risk of Cardiac Allograft Vasculopathy

et al. 2018

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Section: Discussionmentioning

confidence: 99%

Genetic and Functional Profiling of CD16-Dependent Natural Killer Activation Identifies Patients at Higher Risk of Cardiac Allograft Vasculopathy

et al. 2018

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“…Both direct and indirect effects are often present simultaneously, and the relative clinical contributions of any of these mechanisms are uncertain. In general, CMV seropositivity and receipt of seropositive organs and viremia are linked in many, but not all, studies to diminished long-term graft function (16)(17)(18)(19)(20)(21)(22)(23)(24)(25). Furthermore, most studies have indicated that successful antiviral prophylaxis has a beneficial effect on long-term graft function (8).…”

Section: Introductionmentioning

confidence: 99%

The Cell Biology of Cytomegalovirus: Implications for Transplantation

Kaminski

Fishman

2016

American Journal of Transplantation

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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.

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“…In the immunocompromised and neonatal populations, CMV is a major source of morbidity and mortality [2]. CMV is the leading cause of permanent congenital disability in the United States [3] and also a source of organ transplant failure [4,5,6]. …”

Section: Introductionmentioning

confidence: 99%

The Microtubule Inhibitor Podofilox Inhibits an Early Entry Step of Human Cytomegalovirus

Cohen

Schwarz

Vigant

et al. 2016

Viruses

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Human cytomegalovirus is a ubiquitous β-herpesvirus that infects many different cell types through an initial binding to cell surface receptors followed by a fusion event at the cell membrane or endocytic vesicle. A recent high-throughput screen to identify compounds that block a step prior to viral gene expression identified podofilox as a potent and nontoxic inhibitor. Time-of-addition studies in combination with quantitative-PCR analysis demonstrated that podofilox limits an early step of virus entry at the cell surface. Podofilox was also able to drastically reduce infection by herpes simplex 1, an α-herpesvirus with a very similar entry process to CMV. Podofilox caused a reduced maximal plateau inhibition of infection by viruses with single step binding processes prior to fusion-like Newcastle disease virus, Sendai virus, and influenza A virus or viruses that enter via endocytosis like vesicular stomatitis virus and a clinical-like strain of CMV. These results indicate that microtubules appear to be participating in the post-binding step of virus entry including the pre- and post-penetration events. Modulation of the plasma membrane is required to promote virus entry for herpesviruses, and that podofilox, unlike colchicine or nocodazole, is able to preferentially target microtubule networks at the plasma membrane.

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Influence of cytomegalovirus infection in the development of cardiac allograft vasculopathy after heart transplantation

Cited by 82 publications

References 41 publications

Genetic and Functional Profiling of CD16-Dependent Natural Killer Activation Identifies Patients at Higher Risk of Cardiac Allograft Vasculopathy

Genetic and Functional Profiling of CD16-Dependent Natural Killer Activation Identifies Patients at Higher Risk of Cardiac Allograft Vasculopathy

The Cell Biology of Cytomegalovirus: Implications for Transplantation

The Microtubule Inhibitor Podofilox Inhibits an Early Entry Step of Human Cytomegalovirus

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