The dynamics of interactions between Plasmodium and the mosquito: a study of the infectivity of Plasmodium berghei and Plasmodium gallinaceum, and their transmission by Anopheles stephensi, Anopheles gambiae and Aedes aegypti

Alavi, Yasmene; Arai, Meiji; Mendoza, Jacqui; Bayona, Marta Tufet; Sinha, Ria; Fowler, Karen B.; Billker, Oliver; Franke-Fayard, Blandine; Janse, Chris J.; Waters, Andrew P.; Sinden, Robert E.

doi:10.1016/s0020-7519(03)00112-7

Cited by 143 publications

(98 citation statements)

References 59 publications

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“…There is evidence that H 2 O 2 causes the death of P. berghei ookinetes (Herrera-Ortiz et al 2004) but it is unclear whether this death equates to the apoptotic-like death observed in ookinetes in vivo and in vitro (Al-Olayan, Williams and Hurd, 2002). However, what is certain is that very few of the thousands of mosquito stages that begin their development in this hostile environment survive to become oocysts (Vaughan, Hensley and Beier, 1994 a ;Vaughan, Noden and Beier, 1994 b;Alavi et al 2003). Data for the reduction in numbers of P. falciparum, P. yoelii and P. vivax as they pass through different stages in development has been tabulated in Ghosh et al (2000).…”

Section: P a R A S I T E D E A T Hmentioning

confidence: 99%

Apoptosis-like death as a feature of malaria infection in mosquitoes

2006

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Malaria parasites of the genus Plasmodium make a hazardous journey through their mosquito vectors. The majority die in the process, many as a result of the action of mosquito defence mechanisms. The mosquito too is not unscathed by the encounter with these parasites. Tissue damage occurs as a result of mid-gut invasion and reproductive fitness is lost when many developing ovarian follicles are resorbed. Here we discuss some of the mechanisms that are involved in killing the parasite and in the self-defence mechanisms employed by the mosquito to repair the mid-gut epithelium and to manipulate resources altering the trade-off position that balances reproduction and survival. In all cases, cells die by apoptotic-like mechanisms. In the midgut cells, apoptosis-induction pathways are being elucidated, the molecules involved in apoptosis are being recognised and Drosophila homologues sought. The death of ookinetes in the mosquito mid-gut lumen is associated with caspase-like activity and, although homologues of mammalian caspases are not present in the malaria genome, other cysteine proteases that are potential candidates have been discussed. In the ovary, apoptosis of patches of follicular epithelial cells is followed by resorption of the developing follicle and a subsequent loss of egg production in that follicle.

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Section: P a R A S I T E D E A T Hmentioning

confidence: 99%

Apoptosis-like death as a feature of malaria infection in mosquitoes

2006

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“…Recent detailed laboratory-based analysis of the population dynamics of avian, murine and human malaria parasites in different vector species has identified a strong developmental bottleneck during the transition of ookinetes to oocysts coinciding with the transition of the parasite through the midgut epithelium (2). This bottleneck was also observed by using field isolates of Plasmodium falciparum (3).…”

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confidence: 97%

Increased melanizing activity in Anopheles gambiae does not affect development of Plasmodium falciparum

Michel

Suwanchaichinda

Morlais

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Serpins are central to the modulation of various innate immune responses in insects and are suspected to influence the outcome of malaria parasite infection in mosquito vectors. Three Anopheles gambiae serpins (SRPN1, -2, and -3) were tested for their ability to inhibit the prophenoloxidase cascade, a key regulatory process in the melanization response. Recombinant SRPN1 and -2 can bind and inhibit a heterologous phenoloxidase-activating protease and inhibit phenoloxidase activation in vitro. Using a reverse genetics approach, we studied the effect of SRPN2 on melanization in An. gambiae adult females in vivo. Depletion of SRPN2 from the mosquito hemolymph increases melanin deposition on foreign surfaces such as negatively charged Sephadex beads. As reported, the knockdown of SRPN2 adversely affects the ability of the rodent malaria parasite Plasmodium berghei to invade the midgut epithelium and develop into oocysts. Importantly, we tested whether the absence of SRPN2 from the hemolymph influences Plasmodium falciparum development. RNAi silencing of SRPN2 in an An. gambiae strain originally established from local populations in Yaoundé , Cameroon, did not influence the development of autochthonous field isolates of P. falciparum. This study suggests immune evasion strategies of the human malaria parasite and emphasizes the need to study mosquito innate immune responses toward the pathogens they transmit in natural vector-parasite combinations.innate immunity ͉ malaria ͉ mosquito ͉ serpin

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“…stephensi, but it is not transmissible through Ae. aegypti (Alavi et al 2003;Abraham and Jacobs-Lorena 2004). The mosquito midgut is one of the major impediments between the parasite and the mosquito.…”

Section: Discussionmentioning

confidence: 99%

Amplified Fragment Length Polymorphism Mapping of Quantitative Trait Loci for Malaria Parasite Susceptibility in the Yellow Fever Mosquito Aedes aegypti

Zhong

Menge

Temu³

et al. 2006

Genetics

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The yellow fever mosquito Aedes aegypti has been the subject of extensive genetic research due to its medical importance and the ease with which it can be manipulated in the laboratory. A molecular genetic linkage map was constructed using 148 amplified fragment length polymorphism (AFLP) and six singlestrand conformation polymorphism (SSCP) markers. Eighteen AFLP primer combinations were used to genotype two reciprocal F 2 segregating populations. Each primer combination generated an average of 8.2 AFLP markers eligible for linkage mapping. The length of the integrated map was 180.9 cM, giving an average marker resolution of 1.2 cM. Composite interval mapping revealed a total of six QTL significantly affecting Plasmodium susceptibility in the two reciprocal crosses of Ae. aegypti. Two common QTL on linkage group 2 were identified in both crosses that had similar effects on the phenotype, and four QTL were unique to each cross. In one cross, the four main QTL accounted for 64% of the total phenotypic variance, and digenic epistasis explained 11.8% of the variance. In the second cross, the four main QTL explained 66% of the variance, and digenic epistasis accounted for 16% of the variance. The actions of these QTL were either dominance or underdominance. Our results indicated that at least three new QTL were mapped on chromosomes 1 and 3. The polygenic nature of susceptibility to P. gallinaceum and epistasis are important factors for significant variation within or among mosquito strains. The new map provides additional information useful for further genetic investigation, such as identification of new genes and positional cloning.

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The dynamics of interactions between Plasmodium and the mosquito: a study of the infectivity of Plasmodium berghei and Plasmodium gallinaceum, and their transmission by Anopheles stephensi, Anopheles gambiae and Aedes aegypti

Cited by 143 publications

References 59 publications

Apoptosis-like death as a feature of malaria infection in mosquitoes

Apoptosis-like death as a feature of malaria infection in mosquitoes

Increased melanizing activity in Anopheles gambiae does not affect development of Plasmodium falciparum

Amplified Fragment Length Polymorphism Mapping of Quantitative Trait Loci for Malaria Parasite Susceptibility in the Yellow Fever Mosquito Aedes aegypti

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