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ShareFeb. 24, 1997 — Johns Hopkins Medical Institutions
Office Of Communications and Public Affairs
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February 21, 1997
"This suggests we might one day be able to reduce the incidence of allergy and asthma by vaccinating children against mild childhood viral diseases that traditionally haven't received much attention."
ASTHMA AND ALLERGY--THE REVENGE OF THE VIRAL NERD? New Evidence Links Mild Infections to Development of Allergy and Asthma
Johns Hopkins scientists have found the first hard evidence that viral infections can help cause asthma and allergies, a connection long suspected but never directly confirmed in the lab.
Hopkins researchers showed that weak viral infections can cause immune system B cells to produce immunoglobin E or IgE, a protein that orchestrates the reactions that cause allergies and many cases of asthma.
"This suggests we might one day be able to reduce the incidence of allergy and asthma by vaccinating children against mild childhood viral diseases that traditionally haven't received much attention," says Farhad Imani, Ph.D., instructor of medicine, who presents his results at the annual meetings of the American Academy of Allergy, Asthma and Immunology.
"We've suspected that there might be a connection since the late 70s, when studies found that kids who had more viral infections were more likely to have asthma and allergy later in life," says Imani. More recent animal studies have shown that viral infection can increase IgE levels in the blood.
In test tube studies, Imani and his colleagues exposed human B cells, which recognize and attack a particular type of intruder, to rhino and vaccinia viruses. B cells normally attack germs with immunoglobins type M or G (IgM or IgG). Imani found that after viral infections, many of the cells switched to making IgE.
"Basically, if you have a group of B cells that is producing IgE, you're going to be allergic to whatever that group of B cells is sensitive to," Imani explains.
Ironically, stronger viruses capable of causing serious disease were less likely to trigger the switch to IgE than wimpier viruses rapidly defeated by the immune system.
"This appears to be because the weaker viruses activate anti-viral protein kinase, a protein that the B cell uses to defend itself," Imani explains. "This kinase also helps stimulate the start of IgE production in the B cell."
The more sophisticated viruses have found ways to evade the kinase, but many simpler viruses still cannot avoid it.
"These weaker viruses might not cause much suffering during the infection, but they could be causing pain farther down the road by helping the development of allergies."
Imani plans further studies both to determine which viruses will switch on IgE and to flesh out the link between the activation of anti-viral protein kinase and the start of IgE production.
The study was funded by the American Lung Association, the National Institutes of Health, and the Hopkins School of Medicine. Other authors were Kelly Rager, Branimir Catipovic, M.D., Vincenzo Casolaro, M.D., David Proud, Ph.D., J.O. Langland, Ph.D., Bertram Jacobs, Ph.D., and David Marsh, Ph.D.
--JHMI--
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