Abstract
Many parasites and pathogens cause silent/covert infections in addition to the more obvious infectious disease-causing pathology. Here, we consider how assumptions concerning superinfection, protection and seasonal host birth and transmission rates affect the evolution of such covert infections as a parasite strategy. Regardless of whether there is vertical infection or effects on sterility, overt infection is always disadvantageous in relatively constant host populations unless it provides protection from superinfection. If covert infections are protective, all individuals will enter the covert stage if there is enough vertical transmission, and revert to overt infections after a 'latent' period (susceptible, exposed, infected epidemiology). Seasonal variation in transmission rates selects for non-protective covert infections in relatively long-lived hosts with low birth rates typical of many mammals. Variable host population density caused by seasonal birth rates may also select for covert transmission, but in this case it is most likely in short-lived fecund hosts. The covert infections of some insects may therefore be explained by their outbreak population dynamics. However, our models consistently predict proportions of covert infection, which are lower than some of those observed in nature. Higher proportions of covert infection may occur if there is a direct link between covert infection and overt transmission success, the covert infection is protective or the covert state is the result of suppression by the host. Relatively low proportions of covert transmission may, however, be explained as a parasite strategy when transmission opportunities vary. © 2009 The Royal Society.
| Original language | English |
|---|---|
| Pages (from-to) | 2217-2226 |
| Number of pages | 10 |
| Journal | Proceedings of the Royal Society B: Biological Sciences |
| Volume | 276 |
| Issue number | 1665 |
| DOIs | |
| Publication status | Published - 22 Jun 2009 |
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Keywords
- Covert
- Disease
- Evolution
- Latent
- Model
- Vertical transmission
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The evolution of covert, silent infection as a parasite strategy. / Sorrell, Ian; White, Andrew; Pedersen, Amy B.; Hails, Rosemary S.; Boots, Mike.
In: Proceedings of the Royal Society B: Biological Sciences, Vol. 276, No. 1665, 22.06.2009, p. 2217-2226.Research output: Contribution to journal › Article
TY - JOUR
T1 - The evolution of covert, silent infection as a parasite strategy
AU - Sorrell, Ian
AU - White, Andrew
AU - Pedersen, Amy B.
AU - Hails, Rosemary S.
AU - Boots, Mike
PY - 2009/6/22
Y1 - 2009/6/22
N2 - Many parasites and pathogens cause silent/covert infections in addition to the more obvious infectious disease-causing pathology. Here, we consider how assumptions concerning superinfection, protection and seasonal host birth and transmission rates affect the evolution of such covert infections as a parasite strategy. Regardless of whether there is vertical infection or effects on sterility, overt infection is always disadvantageous in relatively constant host populations unless it provides protection from superinfection. If covert infections are protective, all individuals will enter the covert stage if there is enough vertical transmission, and revert to overt infections after a 'latent' period (susceptible, exposed, infected epidemiology). Seasonal variation in transmission rates selects for non-protective covert infections in relatively long-lived hosts with low birth rates typical of many mammals. Variable host population density caused by seasonal birth rates may also select for covert transmission, but in this case it is most likely in short-lived fecund hosts. The covert infections of some insects may therefore be explained by their outbreak population dynamics. However, our models consistently predict proportions of covert infection, which are lower than some of those observed in nature. Higher proportions of covert infection may occur if there is a direct link between covert infection and overt transmission success, the covert infection is protective or the covert state is the result of suppression by the host. Relatively low proportions of covert transmission may, however, be explained as a parasite strategy when transmission opportunities vary. © 2009 The Royal Society.
AB - Many parasites and pathogens cause silent/covert infections in addition to the more obvious infectious disease-causing pathology. Here, we consider how assumptions concerning superinfection, protection and seasonal host birth and transmission rates affect the evolution of such covert infections as a parasite strategy. Regardless of whether there is vertical infection or effects on sterility, overt infection is always disadvantageous in relatively constant host populations unless it provides protection from superinfection. If covert infections are protective, all individuals will enter the covert stage if there is enough vertical transmission, and revert to overt infections after a 'latent' period (susceptible, exposed, infected epidemiology). Seasonal variation in transmission rates selects for non-protective covert infections in relatively long-lived hosts with low birth rates typical of many mammals. Variable host population density caused by seasonal birth rates may also select for covert transmission, but in this case it is most likely in short-lived fecund hosts. The covert infections of some insects may therefore be explained by their outbreak population dynamics. However, our models consistently predict proportions of covert infection, which are lower than some of those observed in nature. Higher proportions of covert infection may occur if there is a direct link between covert infection and overt transmission success, the covert infection is protective or the covert state is the result of suppression by the host. Relatively low proportions of covert transmission may, however, be explained as a parasite strategy when transmission opportunities vary. © 2009 The Royal Society.
KW - Covert
KW - Disease
KW - Evolution
KW - Latent
KW - Model
KW - Vertical transmission
UR - http://www.scopus.com/inward/record.url?scp=66749146235&partnerID=8YFLogxK
U2 - 10.1098/rspb.2008.1915
DO - 10.1098/rspb.2008.1915
M3 - Article
VL - 276
SP - 2217
EP - 2226
JO - Proceedings of the Royal Society B: Biological Sciences
JF - Proceedings of the Royal Society B: Biological Sciences
SN - 0962-8452
IS - 1665
ER -