June 13 (UPI) -- Stanford researchers have found coronary artery disease is linked to a higher risk of shingles due to defective immune cells muting the body's immune response.
Individuals with coronary artery disease are at an elevated risk for shingles because aberrant immune cells reduce the body's immune response to viral pathogens like the virus that causes shingles, the researchers report in a study published June 12 in The Journal of Clinical Investigation.
Shingles' incidence increases significantly after age 50, with about half of all people over age 80 having experienced an attack.
Shingles is a leftover from childhood infection by varicella zoster, the virus that causes chickenpox. Even after the body's immune system defeats the active infection, the virus lives on inside nerve ganglions.
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In older or immune-compromised people, the long-dormant virus can reactivate, crawl along the nerve fiber and emerge at nerve endings as a painful skin rash that's exceedingly difficult to treat.
Previous studies have shown that macrophages -- cells of the immune system that are formed in response to infection that recognize, engulf and destroy target cells -- in patients with coronary artery disease have excessive amounts of molecules involved in the uptake of glucose.
"Coronary artery disease patients' glucose-guzzling macrophages, it turns out, exert the same paralyzing effect on T cells that cancers cells do, in much the same way," Dr. Cornelia Weyand, professor and chief of immunology and rheumatology at Stanford, said in a press release.
Macrophages are attracted to wound sites such as coronary artery vessels, which can develop tiny scars or tears. Previous studies demonstrated that while macrophages may have good intentions, those that are predisposed to glucose gluttony may go off-task, become inflammatory and make the problem worse.
The inflammatory macrophages accelerate plaque buildup in coronary arteries and make it brittle, which can then break off, block blood flow and cause a heart attack. Coronary artery disease accounts for half of all deaths in the United States. The current study showed glucose-addicted macrophages in atherosclerotic lesions are unable to spur T-cells' antiviral activity and actively prevent it.
"Finding out why this happens is the next frontier," Weyand said of the next steps for researchers.
