Abstract
Frequency matters: How successive feeding episodes by blood-feeding insect vectors influences disease transmission.
Highlights
Earlier and more efficient virus dissemination. Modelling these changes in virus dissemination kinetics revealed that the shortened extrinsic incubation period (EIP) associated with additional blood meals could significantly increase the basic reproductive number, R0 [17]. These findings demonstrate the real-world implications that multiple blood meals can have on the epidemiology and epidemic potential of mosquito-borne arboviruses
While previous studies have demonstrated that mosquito complement does not contribute to Plasmodium oocyst killing in traditional single-feed experiments [27,28], additional feeding and subsequent degradation of the midgut basal lamina enables thioestercontaining protein 1A(TUE:PP1)leraesceongontiettihoantTanEdPk1ihllaisnbgeoefndPe. fbineregdhaesitoeloocmysetrsa[s2e6p]r.oMteoinrceomvepro, nsiemnti-1initsfirstm lar experiments in An. gambiae infected with human malaria parasites demonstrate that TEP1 does not recognize P. falciparum oocysts [26], suggesting that successfully invading P. falciparum ookinetes that initially evaded TEP1 and mosquito complement recognition [29,30,31] are protected during the oocyst stage
When an additional blood meal is provided at 12 days postinfection, metacyclic promastigotes undergo conversion into retroleptomonad promastigotes [34] (Fig 3). This newly described stage denoted by a large cell body, short flagella, and low motility enables the further amplification of parasite numbers in the sandfly midgut before differentiation back into metacyclic promastigotes, dramatically increasing metacyclic numbers and blockage of the stomodeal valve to further promote Leishmania parasite transmission [34] (Fig 3)
Summary
While previous studies have demonstrated that mosquito complement does not contribute to Plasmodium oocyst killing in traditional single-feed experiments [27,28], additional feeding and subsequent degradation of the midgut basal lamina enables thioestercontaining protein 1A(TUE:PP1)leraesceongontiettihoantTanEdPk1ihllaisnbgeoefndPe. fbineregdhaesitoeloocmysetrsa[s2e6p]r.oMteoinrceomvepro, nsiemnti-1initsfirstm lar experiments in An. gambiae infected with human malaria parasites demonstrate that TEP1 does not recognize P. falciparum oocysts [26], suggesting that successfully invading P. falciparum ookinetes that initially evaded TEP1 and mosquito complement recognition [29,30,31] are protected during the oocyst stage.
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