The Link Between Human Cytomegalovirus (HCMV) and Hypertension
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT01113359|
Recruitment Status : Unknown
Verified April 2010 by Beijing Chao Yang Hospital.
Recruitment status was: Recruiting
First Posted : April 29, 2010
Last Update Posted : April 29, 2010
It has been reported that mouse cytomegalovirus infection alone can elevate the blood pressure in mice. Since HCMV has uniquely evolved with its human host, with little genetic similarity to the animal CMV counterparts, and it only replicates in human, an epidemiological study is required to define the relevance of HCMV infection and expression of hcmv-miRNA-UL112 to the pathogenesis of essential hypertension.
The investigators found that hcmv-miR-UL112, a human cytomegalovirus (HCMV)-encoded miRNA, was highly expressed in the hypertensive patients. Among the top miRNA target predictions, the investigators demonstrate that IRF-1 is a direct target gene of hcmv-miR-UL112, along with MICB that has been previously reported. Both IRF-1 and MICB play critical roles in immuno/inflammatory and anti-infection response. Thus, the investigators speculated that IRF-1 and MICB repression by hcmv-miR-UL112 could be considered a unifying mechanism that evades the host response at several levels: antiviral, inflammatory, and immune. In addition, there is an increasing evidence that IRF-1 may be important in apoptosis, angiogenesis, neointima formation and the pathogenesis of vascular diseases. IRF-1 can up-regulate angiotensin II type 2 receptor (AGTR2) that exerts antiproliferative and proapoptotic actions and affects regulation of blood pressure. It has been reported that the targeted disruption of the mouse AGTR2 gene resulted in a significant increase in blood pressure and increased sensitivity to angiotensin II. The nitric oxide synthase expression and NO synthesis in macrophages and distinct cardiomyocytes are induced and controlled by IRF-1 in response to inflammation, important steps in vascular biology that may improve endothelial function and inhibit smooth muscle cell migration, and a key pathophysiological event in hypertension. Collectively, these reports support a strong relationship between IRF-1 regulation and hypertension, indicating a potential role of hcmv-miR-UL112 and HCMV infection in the pathogenesis of hypertension.Thus, the investigators want to investigate the potential link between HCMV infection and essential hypertension.
|Condition or disease|
|HCMV Infection Hypertension|
|Study Type :||Observational|
|Estimated Enrollment :||300 participants|
|Observational Model:||Case Control|
|Official Title:||The Potential Link Between HCMV Infection and Essential Hypertension|
|Study Start Date :||April 2010|
|Estimated Primary Completion Date :||May 2010|
|Estimated Study Completion Date :||May 2010|
- The positive rate of HCMV infection in hypertensive patients and healthy control [ Time Frame: 1 month ]
- HCMV copies number per ml plasma of hypertensive patients and healthy controls [ Time Frame: 1 month ]
Biospecimen Retention: Samples Without DNA
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01113359
|Beijing, Chaoyang, China, 100020|
|Contact: Jun Cai, MD +86 10 85231217 firstname.lastname@example.org|
|Sub-Investigator: Jun Cai, MD|
|Principal Investigator:||Xin-Chun Yang, MD||Beijing Chao Yang Hospital|