A transmission electron micrograph (four views) of a herpes simplex virus. Courtesy David Gregory and Debbie Marshall, Wellcome Images. 
Herpes Virus Exploits Immune Response to Bolster Infection
Researchers at the University of California, San Diego School of Medicine and colleagues report that the herpes simplex virus type-1 (HSV-1), which affects an estimated 50 to 80 percent of all American adults, exploits an immune system receptor to boost its infectivity and ability to cause disease.
The findings are published in the June 6, 2013 issue of Nature Communications.
HSV-1 is a persistent and problematic pathogen. Typically, it infects victims through oral secretions (kissing, sharing a contaminated toothbrush) or through openings in the skin. In healthy people, the result may be cold sores or fever blisters. In people with compromised immune systems, HSV-1 can pose more serious and chronic health problems. It can spread, for example, to organs like the brain, lungs and liver, where the infection may become life-threatening. Some patients, such as those with atopic dermatitis – a common form of eczema that accounts for roughly 20 percent of all dermatologic referrals, are especially vulnerable to serious complications stemming from an HSV-1 infection.
Led by principal investigator Richard L. Gallo, MD, PhD, professor of medicine and chief of UC San Diego’s Division of Dermatology, the scientists found that HSV-1 launches an infection by binding to receptors on the surface of skin cells. Ordinarily, if a cell recognizes the virus as an invader, an immune response is immediately triggered, which includes a group of proteins called scavenger receptors that help identify and remove harmful viruses.
But sometimes the process goes awry. While studying HSV-1 and scavenger receptors in cultured human skin cells, Gallo and colleagues in the Atopic Dermatitis Research Network, funded by the National Institute of Allergy and Infectious Diseases, discovered that the virus strongly interacts with a particular receptor called a macrophage receptor with collagenous structure or MARCO, which it uses to gain entry into cells.
More here

A transmission electron micrograph (four views) of a herpes simplex virus. Courtesy David Gregory and Debbie Marshall, Wellcome Images.

Herpes Virus Exploits Immune Response to Bolster Infection

Researchers at the University of California, San Diego School of Medicine and colleagues report that the herpes simplex virus type-1 (HSV-1), which affects an estimated 50 to 80 percent of all American adults, exploits an immune system receptor to boost its infectivity and ability to cause disease.

The findings are published in the June 6, 2013 issue of Nature Communications.

HSV-1 is a persistent and problematic pathogen. Typically, it infects victims through oral secretions (kissing, sharing a contaminated toothbrush) or through openings in the skin. In healthy people, the result may be cold sores or fever blisters. In people with compromised immune systems, HSV-1 can pose more serious and chronic health problems. It can spread, for example, to organs like the brain, lungs and liver, where the infection may become life-threatening. Some patients, such as those with atopic dermatitis – a common form of eczema that accounts for roughly 20 percent of all dermatologic referrals, are especially vulnerable to serious complications stemming from an HSV-1 infection.

Led by principal investigator Richard L. Gallo, MD, PhD, professor of medicine and chief of UC San Diego’s Division of Dermatology, the scientists found that HSV-1 launches an infection by binding to receptors on the surface of skin cells. Ordinarily, if a cell recognizes the virus as an invader, an immune response is immediately triggered, which includes a group of proteins called scavenger receptors that help identify and remove harmful viruses.

But sometimes the process goes awry. While studying HSV-1 and scavenger receptors in cultured human skin cells, Gallo and colleagues in the Atopic Dermatitis Research Network, funded by the National Institute of Allergy and Infectious Diseases, discovered that the virus strongly interacts with a particular receptor called a macrophage receptor with collagenous structure or MARCO, which it uses to gain entry into cells.

More here

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