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CQ for P. vivax CQR P. falciparum SPR P. falciparum Θ = Genetic Variation LD = Neutral Linkage = Transmission MI = Multiple Infections = Asymptomatic LD Θ MI LD Θ MI LD Θ MI CQR SPR CQ SP CQR SPR CQR SPR

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CQ for P. vivax

CQR P. falciparumSPR P. falciparum

Θ = Genetic Variation

LD = Neutral Linkage

= Transmission

MI = Multiple Infections

= Asymptomatic

LDΘMI

LDΘMI

LDΘMI

CQRSPR

CQSP

CQRSPR

CQRSPR

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Sample

Populat ion

SamplingEvolut ionar

yProcess

Mig ration

SelectionMutationDriftRecombinationDemog raphy

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LD between A and B

DemographicHistory

Drug Selection

Effective Pop Size (Ne)Recombination (r)Population Structure

sB

Ch j

Ch i

sA

A

B

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• Population ecology models: The frequency of theresistant mutant is modeled from generation togeneration without regard to stochasticfluctuations due to changes in the effectivepopulation size.

• Epidemiological models where the proportion ofhosts infected (Census population size) ismodeled alongside the resistant allele's relativefrequency.

• These approaches provide an overall theoreticalframework, however, the models were not meantto be real experimental designs with parametersthat actually could be defined in the field andestimated.

• However, we need to incorporate the evolutionarydynamic of mutations in the context of thepopulations demographic history

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•Theory that allow analyzing data of several allelessweeping simultaneously in populations withcomplex demographic histories•The STRs high density in the P. falciparumgenome, together with their high mutation ratemakes them a good choice for characterizing thedynamics of sensitive versus resistant alleles•There are robust attempts for developingexperimental and theoretical methods for SNPs (is agood proxy for human genetic diseases).•We need to understand the dynamic of STRs(mutation models) and how they relate with SNPsunder complex demographic models

Evolutionary Biology

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•Complexity of infection as measured by a set ofgenetic markers instead of intra-host dynamics•Immunity defined in terms of specific antigens•Contribution of the clinical and sub clinicalinfections into malaria transmission•Gene flow among populations (parasites/mosquitoes/ humans)•Transient linkage (inbreeding) as it effects the riskof multi-drug resistant lineages

Disease Ecology

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