such as "Introduction", "Conclusion"..etc
Research recently published in PLoS Medicine challenges the dogma of the antibody-dependent enhancement model (ADE) for the development of dengue hemorrhagic fever (DHF).
Dengue virus infection usually causes a severe 'flu like illness,
although symptoms may be mild in young children. DHF, however, is a
severe and sometimes fatal complication of dengue virus infection that
affects about half a million people every year. DHF patients usually
fall into two groups; children and adults who become infected with a
second dengue virus serotype after an initial ''primary'' dengue virus
infection with a different serotype, and infants with primary dengue
virus infections born to mothers who have some dengue virus immunity.
The current model for development of DHF in infants around 6 months old
is that anti-dengue virus antibodies transferred from a dengue-immune
mother to her child somehow enhance dengue virus infection, resulting
in more severe symptoms (the 'antibody-dependent enhancement' model).
A prospective nested case-control study of infant dengue carried out
by Daniel Libraty (of the University of Massachusetts Medical School,
Worcester, MA) and colleagues reveals that maternal antibodies against
dengue protect infants from the full spectrum of dengue disease. They
also found that all infants with symptomatic dengue virus infection had
antibodies with measurable ADE activity, but that there was no link
between the amount of ADE activity and the development of DHF. They
failed to find evidence supporting a role for the ADE model of
development of DHF but did find that a higher weight-for-age was a risk
factor for DHF.
The authors conclude that 'the results should encourage a rethinking
or refinement of the currently promulgated ADE model for infant DHF,
promote prospective studies of infant dengue and stimulate new
directions of research into novel potential mechanisms for infant DHF'.
This study was supported by National Institutes of Health grant U01 AI065654.
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