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Polymorphism in sexual versus non-sexual disease transmission
 

Summary: Polymorphism in sexual versus non-sexual disease
transmission
PETER H. THRALL AND JANIS ANTONOVICS
Department of Botan , Duke Uni ersit , Durham, orth arolina 27708, USA
SUMMARY
Pathogens causing sexually transmitted diseases (STDs) often consist of related strains that cause non-
sexually transmitted, or `ordinary infectious', diseases (OIDs). We use differential equation models of
single populations to derive conditions under which a genetic variant with one (e.g. sexual) transmission
mode can invade and successfully displace a genetic variant with a different (e.g. non-sexual) transmission
mode. Invasion by an STD is easier if the equilibrium population size in the presence of an OID is smaller;
conversely an OID can invade more easily if the equilibrium size of the population with the STD is larger.
Invasion of an STD does not depend on the degree of sterility caused by the infection, but does depend
on the added mortality caused by a resident OID. In contrast, the ability of an OID to invade a
population at equilibrium with an STD decreases as the degree of sterility caused by the STD increases.
When equilibrium population sizes for a population infected with an STD are above the point at which
non-sexual contacts exceed sexual contacts (the sexual­social crossover point) and when equilibrium
population sizes for an OID are below this point, there can be a stable genetic polymorphism for
transmission mode. This is most likely when the STD is mildly sterilizing, and the OID causes low or
intermediate levels of added mortality. Because we assume the strains are competitively equivalent and
there are no heterogeneities associated with the transmission process, the polymorphism is maintained by

  

Source: Antonovics, Janis - Department of Biology, University of Virginia

 

Collections: Biology and Medicine