by Madhumathi Palaniappan on  June 14, 2017 at 10:58 AM Research News
New Insights on the Causes That Increase Shingles Risk
Varicella zoster virus infections can cause chickenpox. However, the virus could remain dormant in the nervous system and can be reactivated to cause herpes zoster, shingles. This is characterized by a painful skin rash and blisters that predominantly affect the elderly.

Shingles can also occur at a higher rate in people who are diagnosed with coronary heart disease (CAD), that affects the immune system function in part through changes in the infection-responsive immune cells that is called as macrophages.

The specific immune mechanisms that are underlying in age- and CAD-related viral reactivation are not well understood.


This week in the JCI, a study led by Cornelia Weyand at Stanford University reports that macrophages derived from individuals diagnosed with CAD suppress the activation and proliferation of T cells.

Excessive accumulation of the metabolic intermediate pyruvate in these macrophages increased expression of a signaling molecule called PD-L1 that drives T cell suppression. The overabundance of pyruvate in macrophages suggests that metabolic dysregulation may contribute to immune dysfunction in individuals affected by CAD.

The activity of this immunosuppressive pathway in CAD patients provides insights into a mechanism for immune deficiencies that permit reactivation of long-latent viruses. These findings are a step toward developing new strategies that correct metabolic dysregulation in immune cells to prevent shingles and other infections in at-risk populations.



Source: Eurekalert

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