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Published on: August 1, 2018
Association of pathogen burden and hypertension: the Persian Gulf Healthy Heart Study
Katayoun Vahdat1, Mohammad Reza Pourbehi, Afshin Ostovar
1Department of Infectious Diseases, Persian Gulf Tropical Medicine Research Centre, Bushehr University of Medical Sciences, Bushehr, Iran.
Insights
Chronic infections from cytomegalovirus (CMV), Chlamydia pneumoniae, herpes simplex virus 1 (HSV-1), and Helicobacter pylori were studied for links to hypertension. While pathogen burden was not associated with hypertension, coinfection with H. pylori and C. pneumoniae showed a significant link.
Area of Science:
- Infectious disease epidemiology
- Cardiovascular health
- Microbial-host interactions
Background:
- Chronic infections with cytomegalovirus (CMV), Chlamydia pneumoniae, herpes simplex virus 1 (HSV-1), and Helicobacter pylori are potential contributors to essential hypertension.
- The association between the aggregate number of these pathogens (pathogen burden) and hypertension remains unclear.
Purpose of the Study:
- To investigate the relationship between individual chronic infections (CMV, C. pneumoniae, HSV-1, H. pylori) and hypertension.
- To determine if an increased pathogen burden is associated with essential hypertension.
- To examine the impact of coinfections on hypertension risk.
Main Methods:
- Sera from 1,754 adults (≥25 years) were analyzed for immunoglobulin G antibodies to C. pneumoniae, HSV-1, H. pylori, and CMV using ELISA.
- Pathogen burden was defined as the aggregate number of seropositive infections.
- Hypertension was classified using World Health Organization criteria.
Main Results:
- Helicobacter pylori seropositivity was independently associated with hypertension (OR = 1.37; P = 0.02).
- No significant independent association was found between overall pathogen burden and hypertension.
- Coinfection with H. pylori and C. pneumoniae showed a significant association with hypertension (OR = 1.68; P = 0.008) after adjusting for confounders.
Conclusions:
- Pathogen burden was not found to be associated with essential hypertension.
- Coinfection with Chlamydia pneumoniae and Helicobacter pylori demonstrated a significant independent association with essential hypertension, irrespective of cardiovascular risk factors and chronic low-grade inflammation.
Background:
Chronic infection with cytomegalovirus (CMV), Chlamydia pneumoniae, herpes simplex virus 1 (HSV-1), and Helicobacter pylori may contribute to essential hypertension. However, the evidence now available does not clarify whether the aggregate number of pathogens (pathogen burden) may be associated with hypertension.
Methods:
Sera from 1,754 men and women aged ≥25 years were analyzed for immunoglobulin G antibodies to C. pneumoniae, HSV-1, H. pylori, and CMV using enzyme-linked immunosorbent assay. The aggregate number of seropositives to the studied viral and bacterial agents was defined as pathogen burden. Hypertension was defined according to World Health Organization criteria.
Results:
A total of 459 (26.3%) of the subjects had hypertension. In the hypertensive group, 4.2% had 0 or 1 pathogens present, 20.6% had 2, 43.2% had 3, and 32.1% had 4; in the normotensive group, 7.9% had 0 or 1, 28.4% had 2, 42.7% had 3, and 21.0% had 4. Of the 4 studied pathogens, H. pylori seropositivity showed a significant independent association with hypertension (odds ratio (OR) =1.37; 95% confidence interval (CI) =1.05-1.79; P = 0.02). In multiple logistic regression analyses, the pathogen burden did not show a significant independent association with hypertension. Coinfection with H. pylori and C. pneumoniae was significantly associated with hypertension compared with double seronegativity after adjustment for age, sex, chronic low-grade inflammation, and cardiovascular risk factors (OR = 1.68; 95% CI = 1.14-2.47; P = 0.008].
Conclusions:
The pathogen burden was not associated with hypertension. However, coinfection with C. pneumoniae and H. pylori showed a significant association with essential hypertension, independent of cardiovascular risk factors and chronic low-grade inflammation.
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