About this Research Topic
In contrast to asthma, few studies have studied a connection between viral infections and food allergy. Although some studies have found associations between viral lower respiratory viral infections (LRI) and development of allergic sensitization—including food allergens—none of them has reported a causal role for the respiratory viral LRI in the development of clinical food allergy. In addition, a positive relationship between food allergen sensitivity and wheezing has been reported. Since most wheezing episodes studied were a result of a viral LRI, this can be taken as indirect evidence for a relationship between respiratory viral infections and food allergy. However, it seems that respiratory viral infections would involve the wrong mucosal immune surface in the translation of viral into atopic disease.
Therefore, a more fitting question would be whether viral infection of the gastrointestinal tract can lead to the development of clinical food allergy. While no human study has been published that directly addresses this question, it may be possible to examine the disparate prevalence of food allergy in different environments to gain some insight. While the prevalence of food allergy in developed countries may have reached a plateau, it remains well above that found in developing countries.
This is relevant because bacteria (e.g., Shigella and enterophathogenic and enterotoxigenic E. coli) are far more common causes of pediatric diarrhea in developing countries, whereas the majority of pediatric diarrhea in developed countries is of viral origin (e.g., rotavirus). Therefore, these data provide circumstantial evidence that viral gastrointestinal infections may associate with the development of food allergy.
It has been found that during an acute infection with the murine norovirus type 1 (MNV-1, a single-stranded RNA virus of the family Caliciviridae), FcεRI can be induced on gastrointestinal lamina propria cDC analogous to what happens with lung cDC during respiratory Sendai virus infection. Furthermore, a single oral exposure to ovalbumin during the intestinal infection could result in detectible ovalbumin-specific IgE in the serum, In a different mouse model that utilizes reovirus (a double-stranded RNA virus of the family Reoviridae), the administration of peanut extract with the viral inoculation increased peanut-specific IgG2a, but did not alter the peanut-specific IgE level. Unfortunately, neither of these models is robust because the viruses used caused only mild gastrointestinal disease despite being natural rodent pathogens.
As a result, it appears that further insights into the possible role of viruses in food allergy will need to await further epidemiological observations. One interesting intervention is the use of the rotavirus vaccine. If rotavirus (a double-stranded RNA virus of the family Reoviridae, like reovirus) infections could lead to increased food allergy, then (much like anti-RSV treatments) use of a rotavirus vaccine should reduce the development of food allergies. Whether or not this is true awaits further study.
Keywords: Food allergy, viruses, immunology, infections
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