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Malaria is caused by mosquito-borne Plasmodium spp. parasites that must infect and survive within mosquito salivary glands (SGs) prior to host transmission. Recent advances in transcriptomics and the complete genome sequencing of mosquito vectors have increased our knowledge of the SG genes and proteins involved in pathogen infection and transmission. Membrane solute carriers are key proteins involved in drug transport and are useful in the development of new interventions for transmission blocking. Herein, we applied transcriptomics analysis to compare SGs mRNA levels in Anopheles stephensi fed on non-infected and P. berghei-infected mice. The A. stephensi solute carriers prestinA and NDAE1 were up-regulated in response to infection. These molecules are predicted to interact with each other, and are reportedly involved in the maintenance of cell homeostasis. To further evaluate their functions in mosquito survival and parasite infection, these genes were knocked down by RNA interference. Knockdown of prestinA and NDAE1 resulted in reduction of the number of sporozoites in mosquito SGs. Moreover, NDAE1 knockdown strongly impacted mosquito survival, resulting in the death of half of the treated mosquitoes. Overall, our findings indicate the importance of prestinA and NDAE1 in interactions between mosquito SGs and Plasmodium, and suggest the need for further research.Over the last 15 years, massive prevention measures and new treatment tools have greatly decreased the global malaria burden. However, despite these advances, about 214 million new malaria cases and 438,000 associated deaths were registered in 2015 alone 1 . Malaria is caused by mosquito-borne Plasmodium parasites. In particular, adult female mosquitoes of the genus Anopheles are efficient Plasmodium vectors in many diverse ecosystems 2, 3 . Anopheles stephensi is a competent vector for both Plasmodium falciparum and P. vivax, the most virulent malaria-associated species 3 , as well as for Plasmodium species that infect rodents and, thus, this mosquito species is widely used as a laboratory model. A. stephensi is found throughout the Indian subcontinent-with its territory extending from the Arabian Peninsula, Iran, and Iraq, to Bangladesh, southern China, Myanmar, and Thailand 4 .Malaria transmission from mosquitoes to vertebrate hosts occurs through the mosquito's salivary glands (SGs), and for this reason many studies have focused on this organ to develop new malaria control measures [5][6][7][8][9] . Sporozoite invasion of mosquito SGs is receptor-mediated, and involves several parasite and SG proteins 10,11 . Characterization of the salivary components involved in parasite infection and transmission would greatly enhance our understanding of the mosquito-host-pathogen interface, and potentially reveal candidate targets for malaria prevention and control.
Malaria is caused by mosquito-borne Plasmodium spp. parasites that must infect and survive within mosquito salivary glands (SGs) prior to host transmission. Recent advances in transcriptomics and the complete genome sequencing of mosquito vectors have increased our knowledge of the SG genes and proteins involved in pathogen infection and transmission. Membrane solute carriers are key proteins involved in drug transport and are useful in the development of new interventions for transmission blocking. Herein, we applied transcriptomics analysis to compare SGs mRNA levels in Anopheles stephensi fed on non-infected and P. berghei-infected mice. The A. stephensi solute carriers prestinA and NDAE1 were up-regulated in response to infection. These molecules are predicted to interact with each other, and are reportedly involved in the maintenance of cell homeostasis. To further evaluate their functions in mosquito survival and parasite infection, these genes were knocked down by RNA interference. Knockdown of prestinA and NDAE1 resulted in reduction of the number of sporozoites in mosquito SGs. Moreover, NDAE1 knockdown strongly impacted mosquito survival, resulting in the death of half of the treated mosquitoes. Overall, our findings indicate the importance of prestinA and NDAE1 in interactions between mosquito SGs and Plasmodium, and suggest the need for further research.Over the last 15 years, massive prevention measures and new treatment tools have greatly decreased the global malaria burden. However, despite these advances, about 214 million new malaria cases and 438,000 associated deaths were registered in 2015 alone 1 . Malaria is caused by mosquito-borne Plasmodium parasites. In particular, adult female mosquitoes of the genus Anopheles are efficient Plasmodium vectors in many diverse ecosystems 2, 3 . Anopheles stephensi is a competent vector for both Plasmodium falciparum and P. vivax, the most virulent malaria-associated species 3 , as well as for Plasmodium species that infect rodents and, thus, this mosquito species is widely used as a laboratory model. A. stephensi is found throughout the Indian subcontinent-with its territory extending from the Arabian Peninsula, Iran, and Iraq, to Bangladesh, southern China, Myanmar, and Thailand 4 .Malaria transmission from mosquitoes to vertebrate hosts occurs through the mosquito's salivary glands (SGs), and for this reason many studies have focused on this organ to develop new malaria control measures [5][6][7][8][9] . Sporozoite invasion of mosquito SGs is receptor-mediated, and involves several parasite and SG proteins 10,11 . Characterization of the salivary components involved in parasite infection and transmission would greatly enhance our understanding of the mosquito-host-pathogen interface, and potentially reveal candidate targets for malaria prevention and control.
Background: Entomological surveillance for malaria is inherently resource-intensive and produces crude population-level measures of vector exposure which are insensitive in low-transmission settings. Antibodies against Anopheles salivary proteins measured at the individual-level may serve as proxy biomarkers for vector exposure and malaria transmission, but their relationship is yet to be quantified. Methods: A systematic review of studies measuring antibodies against Anopheles salivary antigens (PROSPERO: CRD42020185449). Multilevel modelling estimated associations between seroprevalence with Anopheles human biting rate (HBR) and malaria transmission measures.Results: From 3981 studies identified in literature searches, 42 studies across 16 countries were included contributing 393 meta-observations of anti-Anopheles salivary antibodies determined in 42,764 samples. A positive non-linear association between HBR and seroprevalence was found; overall a 50% increase in HBR was associated with a 13% increase in odds of seropositivity (OR: 1.13, 95%CI: 1.06-1.20, p<0.001). The association between HBR and Anopheles salivary antibodies was strongest with concordant, rather than discordant Anopheles species. Seroprevalence was also significantly positively associated with established epidemiological measures of malaria transmission: entomological inoculation rate, Plasmodium spp. prevalence, and malarial endemicity class.Conclusions: Anopheles salivary antibody biomarkers can serve as a proxy measure for HBR and malaria transmission, and could monitor vectorial capacity and malaria receptivity of a population to sustain malaria transmission. Validation of Anopheles species-specific biomarkers are important given the global heterogeneity in the distribution of Anopheles species. Salivary biomarkers have the potential to transform surveillance by replacing impractical, inaccurate entomological investigations, especially in areas progressing towards malaria elimination.Funding: Australian National Health and Medical Research Council, Wellcome Trust.
Background Haemoglobin (Hb) variants such as sickle cell trait (SCT/HbAS) play a role in protecting against clinical malaria, but little is known about the development of immune responses against malaria parasite (Plasmodium falciparum surface protein 230 (Pfs230) and Plasmodium falciparum erythrocyte binding antigen 175 region-3 (PfEBA175-3R)) and vector (on the An. gambiae Salivary Gland Protein-6 peptide 1 (gSG6-P1)) antigens in individuals with variants Hb genotypes. This study assessed antibody (IgG) responses against malaria parasite, Pfs230 and PfEBA175-3R and vector, gSG6-P1 in febrile individuals with variant Hb genotypes. Methods The study was conducted on symptomatic malaria patients attending various healthcare facilities throughout Ghana. Microscopy and ELISA were used to determine the natural IgG antibody levels of gSG6-P1, PfEBA175-3R & Pfs230, and Capillarys 2 Flex Piercing was used for Hb variants determination. Results Of the 600 symptomatic malaria patients, 50.0% of the participants had malaria parasites by microscopy. The majority 79.0% (398/504) of the participants had Hb AA, followed by HbAS variant at 11.3% (57/504) and HbAC 6.7% (34/504). There were significantly (p < 0.0001) reduced levels of gSG6-P1 IgG in individuals with both HbAC and HbAS genotypes compared to the HbAA genotype. The levels of gSG6-P1 IgG were significantly (p < 0.0001) higher in HbAS compared to HbAC. Similarly, Pfs230 IgG and PfEBA-175-3R IgG distributions observed across the haemoglobin variants were significantly higher in HbAC relative to HbAS. Conclusion The study has shown that haemoglobin variants significantly influence the pattern of anti-gSG6-P1, Pfs230, and PfEBA-175 IgG levels in malaria-endemic population. The HbAS genotype is suggested to confer protection against malaria infection. Reduced exposure to infection ultimately reduces the induction of antibodies targeted against P. falciparum antigens.
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