The Link Between Human Cytomegalovirus (HCMV) and Hypertension

NCT ID: NCT01113359

Last Updated: 2010-04-29

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

UNKNOWN

Total Enrollment

300 participants

Study Classification

OBSERVATIONAL

Study Start Date

2010-04-30

Study Completion Date

2010-05-31

Brief Summary

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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.

Detailed Description

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Conditions

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HCMV Infection Hypertension

Keywords

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HCMV infection Hypertension The Potential Link Between HCMV Infection and Essential Hypertension

Study Design

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Observational Model Type

CASE_CONTROL

Study Time Perspective

CROSS_SECTIONAL

Study Groups

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study group

hypertensive patients

No interventions assigned to this group

control group

healthy volunteer

No interventions assigned to this group

Eligibility Criteria

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Inclusion Criteria

* Patients with essential hypertension are assessed for potential secondary causes, for the severity of hypertension, other risk factors and for end-organ damage
* Aged between 30 to 60 years
* Untreated (whole day average \> 140/90 mmHg) or treated hypertension whole-day average \< 140/85), as determined by 24-hour blood pressure monitoring.

Exclusion Criteria

* Cancer
* Diabetes
* Smoking
* Renal failure
* Stroke
* Peripheral artery disease
Minimum Eligible Age

30 Years

Maximum Eligible Age

60 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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Beijing Chao Yang Hospital

OTHER

Sponsor Role lead

Responsible Party

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Beijing Chao Yang Hospital

Principal Investigators

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Xin-Chun Yang, MD

Role: PRINCIPAL_INVESTIGATOR

Beijing Chao Yang Hospital

Locations

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Jun Cai

Beijing, Chaoyang, China

Site Status RECRUITING

Countries

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China

Facility Contacts

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Jun Cai, MD

Role: primary

Other Identifiers

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YXinchun

Identifier Type: REGISTRY

Identifier Source: secondary_id

BJCY-CV-2010001

Identifier Type: -

Identifier Source: org_study_id