Asthma attacks lead to impaired quality of life and
mortality, but the rates of admission for
acute asthma have changed little over the last 20 y
ears(
1
). We know that a combination of
allergen sensitization, allergen exposure and viral
infections trigger attacks(
2
). Although
usually these factors work together, a large allerg
en load alone can also be sufficient to
trigger an attack [thunderstorm], and although viru
ses contribute to increased symptoms,
in the context of atopic asthma, they are not the o
nly culprit. Although Influenza viruses
can be targeted by specific agents including vaccin
es, we lack strategies to treat most of
the common respiratory viruses that result in asthm
a attacks, especially rhinovirus (RV).
Interferon responses to rhinovirus are altered in a
sthmatics(
3
), but a recent study using
nebulised interferon(
4
) failed to meet its primary end point suggesting i
nteractions
between allergic and antiviral immunity are key. He
nce attention has turned to modulating
the allergic components of asthma attacks. Reducing
house dust mite allergen exposure
with impermeable covers shows promise in sensitized
children(
5
) and modulating the
response to allergens with omalizumab(
6
) are examples of this approach.