A new study provided further support for the hygiene hypothesis after showing that murid herpesvirus 4 (MuHV-4) inhibited the development of house dust mite (HDM)-induced experimental asthma by modulating lung innate immune cells.
Asthma affects over 300 million people worldwide and there has been a substantial increase in prevalence observed in the Western countries. The hygiene hypothesis postulates that the recent increase in allergic diseases such as asthma and hay fever observed in Western countries is linked to reduced exposure to childhood infections, when there is a window of opportunity for becoming sensitized to allergens. Studies have shown that early-life infection of children with Epstein-Barr virus (EBV) can help to protect the children against persistent sensitization to immunoglobulin E (IgE). The increased incidence of allergic asthma could therefore be associated in part with the increased age of seroconversion to EBV or to other herpesviruses that is observed in developed countries.
A study led by Dr. Fabrice Bureau and Laurent Gillet, which was published in Nature Immunology investigated in BALB/c and C57BL/6 mice how infection of gammaherpesvirus affected the development of allergic asthma. Researchers found that respiratory infection with MuHV-4 conferred strong and lasting protection against airway allergy through the replacement of resident alveolar macrophages (AMs) with recruited regulatory monocytes of bone marrow (BM) origin.
The results from this study indicate that replacement of embryonic AMs by regulatory monocytes is a major mechanism underlying the long-term training of lung immunity after infection.