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 24 May 2018

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News

Hepatitis A virus link to atopic disease

A declining prevalence of hepatitis A virus infection may contribute to an increase in atopic disease, find researchers in this week's issue of Nature.

News image

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Atopic diseases, such as asthma, allergic rhinitis and dermatitis, are caused by a combination of environmental and genetic factors.

Exposure to HAV is associated with poor hygiene, large family size and attendance at day-care centers. These are all factors which are inversely associated with atopy.

In this study, researchers from the United States determined that that infection by hepatitis A virus (HAV) may protect individuals from atopy.

Infection with HAV may have protected many individuals against atopy.
Nature

The research team identified TIM-1 as a candidate gene for atopy and asthma in a region of mouse chromosome 11. This is homologous to a segment of human chromosome 5q31–33 that has been linked to atopy.

The team investigated whether the interaction between HAV and TIM-1 on lymphocytes can modify T cells in a way that protects against atopy. They also examined whether polymorphisms in TIM-1 can alter susceptibility to atopy.

The researchers identified a 6-amino-acid insertion at residue 157 (157insMTTTVP) and 2 single-amino-acid changes. To determine the effect of 157insMTTTVP on the occurrence of atopy, the team evaluated 375 individuals who were tested for atopy and prior HAV infection.

The research team found that HAV seropositivity protects against atopy. However, this protection only occurs in individuals with the 157insMTTTVP variant of TIM-1.

Prior to 1970, the seroprevalence of antibodies against HAV approached 100% in Western countries. Therefore infection with HAV may have protected many individuals against atopy.

However, reduction in family size and improved public health has caused anti-HAV seroprevalence to fall to between 25 and 30%, while the prevalence of atopic disease has doubled.

The interaction between HAV and TIM-1 genotype may contribute to the etiology of atopic diseases, and provide a mechanism to account for the hygiene hypothesis.

Dr Jennifer McIntire's team concluded, "Our finding…indicates that exposure to a specific pathogen may influence the expression of atopy".

"A declining prevalence of HAV infection could contribute to an increase in atopy by association with TIM-1".

"It will be necessary to determine whether HAV exposure must occur during childhood to have a protective effect".

Also, "Whether HAV can mitigate the severity of existing atopic disease, and whether HAV vaccination can reproduce the effects of natural HAV infection".

Nature 2003; 425: 576
13 October 2003

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