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Susceptibility of Anopheles stephensi to Plasmodium gallinaceum: a trait of the mosquito, the parasite, and the environment.

Hume JC, Hamilton H, Lee KL, Lehmann T - PLoS ONE (2011)

Bottom Line: Notably, the environment contributed 28%.These estimates are relevant only to the particular system under study, but this experimental design could be useful for other parasite-host systems.The prospects and limitations of the genetic manipulation of vector populations to render the vector resistant to the parasite are better considered on the basis of this framework.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.

ABSTRACT

Background: Vector susceptibility to Plasmodium infection is treated primarily as a vector trait, although it is a composite trait expressing the joint occurrence of the parasite and the vector with genetic contributions of both. A comprehensive approach to assess the specific contribution of genetic and environmental variation on "vector susceptibility" is lacking. Here we developed and implemented a simple scheme to assess the specific contributions of the vector, the parasite, and the environment to "vector susceptibility." To the best of our knowledge this is the first study that employs such an approach.

Methodology/principal findings: We conducted selection experiments on the vector (while holding the parasite "constant") and on the parasite (while holding the vector "constant") to estimate the genetic contributions of the mosquito and the parasite to the susceptibility of Anopheles stephensi to Plasmodium gallinaceum. We separately estimated the realized heritability of (i) susceptibility to parasite infection by the mosquito vector and (ii) parasite compatibility (transmissibility) with the vector while controlling the other. The heritabilities of vector and the parasite were higher for the prevalence, i.e., fraction of infected mosquitoes, than the corresponding heritabilities of parasite load, i.e., the number of oocysts per mosquito.

Conclusions: The vector's genetics (heritability) comprised 67% of "vector susceptibility" measured by the prevalence of mosquitoes infected with P. gallinaceum oocysts, whereas the specific contribution of parasite genetics (heritability) to this trait was only 5%. Our parasite source might possess minimal genetic diversity, which could explain its low heritability (and the high value of the vector). Notably, the environment contributed 28%. These estimates are relevant only to the particular system under study, but this experimental design could be useful for other parasite-host systems. The prospects and limitations of the genetic manipulation of vector populations to render the vector resistant to the parasite are better considered on the basis of this framework.

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Related in: MedlinePlus

Response of An. stephensi selected for susceptibility to P. gallinaceum based on mean oocyst load.The cumulative response to selection is regressed on the cumulative selection differential for the selected An. stephensi lines. Regression is forced through the origin.
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pone-0020156-g005: Response of An. stephensi selected for susceptibility to P. gallinaceum based on mean oocyst load.The cumulative response to selection is regressed on the cumulative selection differential for the selected An. stephensi lines. Regression is forced through the origin.

Mentions: Vector infection prevalence was the primary focus of our experiment, as truncation selection was applied against all mosquitoes with zero oocysts (see Materials and Methods). The estimated realized heritability of An. stephensi to its “vector susceptibility” (nVS), measured by infection prevalence, was high (mean value of 0.66, Table 1). As can be expected from the phenotypic response to selection (Figure 4), the realized heritability of the A line (0.83) was higher than that of the E line (0.49). Likewise, for oocyst load, h2r of line A (0.48, twice the slope coefficient [b] in Figure 5) was higher than that of line E (0.14, Figure 5) consistent with their differing responses to selection as illustrated in Figure 4. The average genetic contribution of the vector (nVS) to “vector susceptibility” (bVS) as measured by oocyst load was 0.31 (Table 1).


Susceptibility of Anopheles stephensi to Plasmodium gallinaceum: a trait of the mosquito, the parasite, and the environment.

Hume JC, Hamilton H, Lee KL, Lehmann T - PLoS ONE (2011)

Response of An. stephensi selected for susceptibility to P. gallinaceum based on mean oocyst load.The cumulative response to selection is regressed on the cumulative selection differential for the selected An. stephensi lines. Regression is forced through the origin.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3111409&req=5

pone-0020156-g005: Response of An. stephensi selected for susceptibility to P. gallinaceum based on mean oocyst load.The cumulative response to selection is regressed on the cumulative selection differential for the selected An. stephensi lines. Regression is forced through the origin.
Mentions: Vector infection prevalence was the primary focus of our experiment, as truncation selection was applied against all mosquitoes with zero oocysts (see Materials and Methods). The estimated realized heritability of An. stephensi to its “vector susceptibility” (nVS), measured by infection prevalence, was high (mean value of 0.66, Table 1). As can be expected from the phenotypic response to selection (Figure 4), the realized heritability of the A line (0.83) was higher than that of the E line (0.49). Likewise, for oocyst load, h2r of line A (0.48, twice the slope coefficient [b] in Figure 5) was higher than that of line E (0.14, Figure 5) consistent with their differing responses to selection as illustrated in Figure 4. The average genetic contribution of the vector (nVS) to “vector susceptibility” (bVS) as measured by oocyst load was 0.31 (Table 1).

Bottom Line: Notably, the environment contributed 28%.These estimates are relevant only to the particular system under study, but this experimental design could be useful for other parasite-host systems.The prospects and limitations of the genetic manipulation of vector populations to render the vector resistant to the parasite are better considered on the basis of this framework.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.

ABSTRACT

Background: Vector susceptibility to Plasmodium infection is treated primarily as a vector trait, although it is a composite trait expressing the joint occurrence of the parasite and the vector with genetic contributions of both. A comprehensive approach to assess the specific contribution of genetic and environmental variation on "vector susceptibility" is lacking. Here we developed and implemented a simple scheme to assess the specific contributions of the vector, the parasite, and the environment to "vector susceptibility." To the best of our knowledge this is the first study that employs such an approach.

Methodology/principal findings: We conducted selection experiments on the vector (while holding the parasite "constant") and on the parasite (while holding the vector "constant") to estimate the genetic contributions of the mosquito and the parasite to the susceptibility of Anopheles stephensi to Plasmodium gallinaceum. We separately estimated the realized heritability of (i) susceptibility to parasite infection by the mosquito vector and (ii) parasite compatibility (transmissibility) with the vector while controlling the other. The heritabilities of vector and the parasite were higher for the prevalence, i.e., fraction of infected mosquitoes, than the corresponding heritabilities of parasite load, i.e., the number of oocysts per mosquito.

Conclusions: The vector's genetics (heritability) comprised 67% of "vector susceptibility" measured by the prevalence of mosquitoes infected with P. gallinaceum oocysts, whereas the specific contribution of parasite genetics (heritability) to this trait was only 5%. Our parasite source might possess minimal genetic diversity, which could explain its low heritability (and the high value of the vector). Notably, the environment contributed 28%. These estimates are relevant only to the particular system under study, but this experimental design could be useful for other parasite-host systems. The prospects and limitations of the genetic manipulation of vector populations to render the vector resistant to the parasite are better considered on the basis of this framework.

Show MeSH
Related in: MedlinePlus