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Inherited Herpes Virus Increases the Risk of Angina Reports HHV-6 Foundation
Date:7/6/2015

SANTA BARBARA, Calif., July 6, 2015 /PRNewswire/ -- Approximately 1% of the population inherits a common herpes virus that is integrated into their chromosomes. These individuals are three times more likely to develop angina, according to a new study published in one of the nation's leading medical journals by researchers from the Universite Laval Faculty of Medicine in Canada. 

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The virus, known as human herpesvirus 6 (HHV-6) causes roseola (also known as "sixth disease") and occasional seizures in infants as well as cognitive dysfunction and encephalitis in those with compromised immune systems. Like all herpes viruses, HHV-6 establishes latency in the cells, and can reactivate under certain conditions.  What makes this virus different, however, is that it integrates into the chromosome of the cell. This means that when the virus infects the sperm or human eggs, children can inherit the latent virus in every cell.

"Inheriting a latent herpes virus in each of your cells can create a significant hazard if they activate," commented the study's lead investigator Louis Flamand. "Furthermore, individuals with immune deficiencies or specific drug or chemical exposures may be at an even higher risk," he said.  Flamand has called for screening for this inherited condition at birth and before transplant procedures.

To determine the impact of inheriting a herpesvirus, the group analyzed biological samples of nearly 20,000 people to find 113 individuals with the condition, and then analyzed stored medical data. The reason behind the increased rate of angina is still under investigation. One theory proposed is that the integrated HHV-6 virus may exit the chromosome and infect the cells lining the arteries. Another theory is that the angina could be due to the fact that individuals with integrated herpes virus end up with shorter chromosome tips or telomeres, and short telomeres are associated with a number of conditions including cancer and angina. Flamand's group measured the telomere length in the individuals with integrated virus and angina, and found that they were 24% shorter. 

 "Short telomeres are associated with premature cellular death. If this occurs in cells lining the blood vessels, it could trigger inflammatory reactions and the start of atherosclerotic plaque development that precede angina," said Flamand.

Flamand and colleagues are currently working on a study to determine if angina patients with inherited herpes virus have active HHV-6 infections. One clue is that a German cardiology group reported last year that two thirds of their 19 heart failure patients with integrated virus had signs of active infection. These patients improved after six months of antiviral treatment.

"We are concerned that certain drugs such as steroids and certain types of drugs or supplements could accidentally activate the integrated herpesvirus in otherwise healthy individuals," said Dharam Ablashi, scientific director of the HHV-6 Foundation. "We need much larger studies to explore potential disease associations and the impact of chemical and drug exposures in these patients."

The report was published in the latest issue of the Proceedings of the National Academy of Sciences.

Contact:

Kristin Loomis

Executive Director,

HHV-6 Foundation

Santa Barbara, California

805-705-7766

Kristin_Loomis@HHV-6Foundation.org

 

Additional links:

Chromosomally integrated human herpesvirus 6 in heart failure: prevalence and treatment

Expert Opinion: Dr. Louis Flamand calls for screening of transplant organs and cells for ciHHV-6 status

This content was issued through the press release service at Newswire.com. For more info visit: www.newswire.com


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SOURCE HHV-6 Foundation
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