View clinical trials related to Cytomegalovirus Infections.
Filter by:Cytomegalovirus (CMV) is the most common cause of congenital infection, with approximately 0.5% of pregnant women being infected during pregnancy. CMV transmission to the fetus occurs in about one third of women who are infected in first trimester. Babies infected before birth are at risk for serious neurological complications such as intellectual disability, seizures, deafness, and even death. Most couples facing a diagnosis of congenital cytomegalovirus infection in their unborn baby focus heavily on the predicted neurological outcome for their child. To date, methods to assess brain development in fetuses have been mainly limited to detecting structural brain abnormalities by ultrasound. However, these ultrasound signs may not become apparent until very late in pregnancy, and some neurological disability is not accompanied by any structural brain changes. More research on methods of predicting neurodevelopmental outcome independent of structural brain malformations before third trimester is urgently needed. The purpose of this study is to investigate a new method of studying the health of unborn babies using amniotic fluid. Amniocentesis is often performed after maternal CMV infection to diagnose fetal infection. Prior research by Dr Hui has demonstrated that cell free RNA in amniotic fluid can provide meaningful information from multiple organs including the fetal brain. The investigators propose to collect and analyse a small sample of amniotic fluid to detect which genes are turned "on" or "off" (gene expression) in a fetus that has a congenital CMV infection, compared to those without any infection. The genes that are differentially expressed in CMV infected fetuses will then be analysed to provide information on the broad physiological processes that are altered due to the infection ("functional analysis") and identify neurodevelopmental gene transcripts of interest for future studies ("biomarker discovery").
Coronary artery disease is a contraction of the coronary arteries that prevent adequate blood supply to the heart muscle is called CAD. Usually caused by atherosclerosis, it may be advanced to the point where the heart muscle is injured due to lack of blood supply. Such damage may result in infarction, arrhythmias, and heart failure(1,2). Telomeres are short in circulating leucocytes in patients with coronary artery disease but the precise mechanism is not well-known (3). Telomere and telomerase are affected by cytomegalovirus (CMV) infection due to its effect on increasing the number of highly differentiated T cells that are characterized by shorter telomere length (TL) and lowered telomerase activity (TA). Both genetic and environmental factors have been connected with individual distinction in TL.Cardiovascular risk factors such as smoking, diabetes mellitus, hypertension, obesity, and stress have been considered to upsurge inflammation, oxidative stress, therefore accelerating TL shortening (1,2) It has also been observed that telomere loss in type 2 diabetic patients contributes to oxidative stress and endoplasmic reticulum stress while telomere shortening has also been proposed that it can serve as an independent risk factor of T2DM and it can measure disease progression(4). Moreover, telomeric length in peripheral blood mononuclear cells (PBMCs) is associated with the duration of disease and good glycemic control seems to be protective for telomeric loss (5). Growth differentiation factor-15 (GDF-15) is a member of the transforming growth factor (TGF)-β superfamily. GDF-15, recently identified as one of the new cardioprotective cytokines. It is highly expressed in cardiomyocytes, adipocytes, macrophages, endothelial cells, and vascular smooth muscle cells in normal and pathological condition. GDF-15 increases during tissue injury and inflammatory states and is associated with cardiometabolic risk(6). Dipeptidyl peptidase inhibitors (DPP4 -I) are called gliptins which increase the incretin levels and therefore prolong the post-prandial insulin action(7). Diana et al reported that In type 2 diabetic patients, leukocyte telomere was significantly shorter than control groups and was significantly elongated after intervention by sitagliptin(8). The common feature of all risk factors of CAD and T2DM imbalance between pro- and anti-oxidative factors in the organism with an increased production of reactive oxygen species (ROS).Nuclear factor erythroid-derived factor 2-related factor 2(Nrf2) is a family of transcription factors which plays an important role in protection against CVD and DM by regulating antioxidant enzymes in cells after ROS exposure (9). In our study, we will propose a model, which would provide the basis to establish a marker for chronic reactivation of CMV and shed more light into the pathophysiology of CMV infection in patients with CAD in relation to GDF-15 and NrF2 and their implications on disease progression. Ultimately, this would then enable us to identify patients at risk and develop novel strategies for future treatment and prevention of heart diseases in our country. In light of our project research, the question arises whether telomere length could represent a marker of chronic CMV reactivation and uncertainty their length will be modified by the effect of DPP-4 or not?
CMV infection is common in transplant patients and can cause graft loss. CMV is a major factor in increasing morbidity, and post-transplant costs. The CMV infection is associated with many deleterious indirect effects including rejection, interstitial fibrosis and tubular atrophy, mortality. In addition to the potential for undesirable clinical outcomes associated with CMV, there is also a negative economic aspect. Patients who developed CMV events have been found to use significantly more inpatient and outpatient resources than patients without CMV disease. Universal prophylaxis is associated with high treatment cost and the potential for drug-related toxicity. It can be speculated that use of EVR may offer additional economic benefits in terms of decreased utilization associated with prevention of CMV disease, and reduce use of costly prophylaxis. Any efforts to reduce costs in renal transplants are very important and may have a great impact in total cost of a renal program. And the other hand, the clinical data suggest that EVR is associated with a decrease in CMV incidence compared to mycophenolic acid (MPA). CMV replication is dependent upon 1 ou 2 mTor pathways and in vitro studies support an association between mTor inhibitors and decreased CMV infection and disease. In cardiac transplantation, the use of EVR was associated with a lower incidence of CMV events. Some clinical trials data have also shown that use of EVR was associated with a lower incidence of CMV infection compared to MPA following renal transplantation. Brennan et al compared the incidence of CMV in three clinical trials using EVR versus MPA in De Novo renal transplants. They pooled for analysis the studies B201, B251 and A2309, all double-blind, randomized, parallel-groups that compared the incidence of freedom form and incidence of CMV between EVR groups and MPA groups. The results of this pooled analysis of over 2000 patients de novo renal transplant demonstrated that EVR was associated with a decrease in and delay in the time of onset of CMV events compared to MPA. Our hypothesis is that basiliximab in combination with low dose tacrolimus, everolimus and prednisone may result in comparable efficacy (BCAR) observed in patients receiving tacrolimus/mycophenolate/prednisone but with a better safety profile (CMV infection) and cost-effectiveness.