RSV in infancy and
Asthma
Respiratory Syncytial Virus (RSV)
also known as bronchiolitis is an infection in the upper respiratory tract that
typically happens before the age of 2. Some children get a more severe form and
develop lower airway symptoms as well. Typically only 1-2% of infants are
hospitalized with RSV when infection occurs. This disease can leave kids
wheezing for several years after the infection has occurred. There is little
evidence at this time suggesting if RSV is nonallergenic or if it is an onset
of IgE associated asthma. RSV primes the memory T-cells that make Interferon-c
(INF-c) and are also associated with IL-4 producing T-cells that are activated
during RSV infections. There are many studies that show that there is a strong
relationship between RSV and asthma or allergies.
With a normal child a RSV infection
is mild and they develop a predominant Th1 antiviral response that clears the
infection. The memory T-cells are dominated by IFN-c production rather than
IL-4. In children that develop a more severe form of RSV (when hospitalization is
needed) a strong INF-c response occurs along with an IL-4 response which leads
to the accumulation of antiviral-T cells in the lungs causing an impairment of
the respiratory tract. Post infection both IL-4 and IFN-c T-cells are
maintained as memory cells that recirculate in the blood. There is some
evidence that children who are administered a polyclonal antiviral antibody
therapy have a delay in RSV infection and show improved lung function.
There are several different
mechanisms that can explain the association between asthma and RSV. Experiments
with animals suggest that RSV may contribute to post bronchiolitic symptoms and
when inhaled allergens are delivered to these animals the effects are enhanced
by a RSV infection. In these studies they link IL-4 production and a type 2
cytokine response with enhanced lung disease during the viral infection--this
is also a common feature in asthma and atopy. This mechanism has yet to be proven in humans.
Results in infant peripheral blood
mononuclear cells can be used to show that RSV increases the risk of atopy and
provides an IL-4 rich environment in which encountering airborne allergens can
create an increased memory T-cell response. Other studies suggest that there is
an increase of Th2 response which is medicated by overexpression of the IL-4
which only provides preliminary evidence for a genetic link between RSV and
asthma. The last suggestion is that there is a genetic defect that is
associated with the delay in postnatal maturation of Th1 function that gives
susceptibility to both severe viral infection in the lungs as well as allergies
and asthma in childhood.
Eosinophil cationic protein is created
in the serum of children with asthma and with children with bronchiolitis. This
suggests the degranulation of the eosinophil’s in both conditions. This
increase in antigen specific enhancement of IL-4 production may be able to
explain the link between RSV and asthma as well as chronic wheezing during
childhood.
Referances
Severe Respiratory Syncytial Virus Bronchiolitis in Infancy and Asthma
and Allergy at Age 13. http://ajrccm.atsjournals.org/content/171/2/137.full.pdf
Enhanced IL-4 responses in
children with a history of respiratory
syncytial virus
bronchiolitis in infancy P. http://erj.ersjournals.com/content/20/2/376.full.pdf
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