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Reuters Health Information (2003-10-08): Hepatitis A exposure plus receptor genotype may protect against atopy


Hepatitis A exposure plus receptor genotype may protect against atopy

Last Updated: 2003-10-08 13:00:26 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Among individuals who carry a particular genetic variant of the TIM-1 gene, exposure to hepatitis A virus (HAV) appears to protect from atopic diseases, according to a report in the October 9th issue of Nature.

This finding may explain the increased prevalence of atopic disease during the last two decades that coincided with improved hygiene, senior author Dr. Dale T. Umetsu told Reuters Health.

"People suspect that the reduction in infections was somehow related to the increase in asthma and allergy," he said. "Our study suggests that it's not all infections that are causing this, that it may be specific to hepatitis A virus."

Dr. Umetsu and his team at Stanford University in California recently found that two strains of mice differed in their immune response to allergens. "One strain developed asthma and allergy, and the other did not," he said. Genetic studies revealed that the strains had different forms of the TIM-1 gene.

They also found that TIM-1 is expressed on human T cells, Dr. Umetsu said. "We know that TIM-1 controls whether a T cell becomes one that causes allergy or one that protects against allergy," he said. They also observed that TIM-1 is the cell surface receptor used by hepatitis A to infect cells.

A common genetic variant of TIM-1--a six amino-acid insertion at residue 157--does not affect HAV infection rates, their report indicates. But when they genotyped 375 individuals, they found that only among those with the 157-insertion did viral seropositivity protect against atopy (p = 0.0005).

"We believe that HAV binds to TIM-1 and changes how the T cells differentiate," Dr. Umetsu said. His team is now conducting studies to further elucidate the function of the TIM family of genes, and to see if HAV exposure must occur during childhood to exert its protective effects.

Nature 2003;425:576.

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