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Seasonal variation in infectious disease outbreaks may be related
to changes in host susceptibility mediated by the annual light/dark
cycle and patterns of melatonin secretion, according to a novel
theory proposed by Dr. Scott F. Dowell.
Dr. Dowell, of the Centers for Disease Control and Prevention in
Atlanta, poses the question, why do seasonal infectious disease
outbreaks seem to occur only in seasonal cycles? Is the human population
relatively immune the rest of the year?
He suggests that pathogens may be present in the population year-round,
and epidemics occur when the susceptibility
of the population increases enough to sustain them.
Dr. Dowell proposed as a possible mechanism changes in receptors
on the surface of epithelial cells, some of which may be expressed
more commonly in winter, some more in summer. Seasonal changes in
lymphocyte populations or blood cytokine levels could also be contributing
factors.
Many outbreaks, such as measles and influenza,
are similar in timing and duration from year to year.
Also supporting his theory is the simultaneous occurrence of pneumococcus
and influenza outbreaks in widely dispersed locations.
Latitude appears to be a critical determinant in the
timing and magnitude of peaks for polio, rotavirus and influenza.
Dr. Dowell offers an evolutionary perspective and suggests that
if you have a pathogen that is highly contagious and present year-round,
it would exhaust the population of those who are susceptible. Pathogens
that could sweep through for several months, then lie dormant until
the group of susceptible individuals is renewed, would be at an
evolutionary advantage.
Influenza rates drop by more than 90% for 9 months of the year.
If that's due to a down-regulated receptor in human nasopharyngeal
epithelium, and we could learn to modify
that receptor, it would open up broad new areas for treatment.
Emerging Infect Disease
May/June 2001;7:369-373
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