scholarly journals Genetic changes of Plasmodium vivax tempers host tissue-specific responses in Anopheles stephensi

Author(s):  
Seena Kumari ◽  
Charu Chauhan ◽  
Sanjay Tevatiya ◽  
Deepak Singla ◽  
Tanwee Das De ◽  
...  
2019 ◽  
Author(s):  
Sanjay Tevatiya ◽  
Seena Kumari ◽  
Charu Chauhan ◽  
Deepak Singla ◽  
Tanwee Das De ◽  
...  

AbstractIn our preceding study (Sharma et al., 2019; BioRxiv) we showed that in the gut lumen Plasmodium vivax follows a unique strategy of immuno-suppression by disabling gut flora proliferation. Here, we further demonstrate that post gut invasion, a shrewd molecular relationship with individual tissues such as midgut, hemocyte, salivary glands, and strategic changes in the genetic makeup of P. vivax favors its survival in the mosquito host. A transient suppression of ‘metabolic machinery by early oocysts, and increased immunity’ against late oocysts suggested a unique mechanism of gut homeostasis restoration and Plasmodium population regulation. Though a hyper immune response of hemocyte was a key to remove free circulating sporozoites, but a strong suppression of salivary metabolic activities, may favor successful survival of invaded sporozoites. Finally, genetic alteration of P. vivax ensures evasion of mosquito responses. Conclusively, our system-wide RNAseq analysis provides first genetic evidences of direct mosquito-Plasmodium interaction and establishes a functional correlation.Author SummaryMalaria transmission dynamics is heavily influenced by mosquito –parasite interaction. When passing through tissue specific barriers, Plasmodium have to compromise by losing its own population, but genetic relation is unknown. To win the developmental race Plasmodium need to overcome two important immuno-physiological barriers. First one accounts an indirect 24-30hr long pre-invasive gut-microbe-parasite interaction in the gut lumen. And second one follows a direct post gut invasive 14-18 days interaction with midgut, hemocyte and salivary glands. During pre-invasive phase of interaction, we showed Plasmodium vivax follows immuno-suppression strategy by restricting microbial growth in the gut lumen. Here, we demonstrate that switch of parasite from one stage to another stage within mosquito vector is accompanied by genetic changes of parasite. Our data suggests genetic makeup change enables the parasite to manipulate the metabolism of mosquito tissues. This strategy not only clear off multifaceted mosquito’s tissue specific immune responses, but also favors Plasmodium own survival and transmission. Comprehending this tissue specific interaction between host and parasite at molecular level could provide new tool to intervene the plasmodium life cycle within vector.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Ajeet Kumar Mohanty ◽  
Charles de Souza ◽  
Deepika Harjai ◽  
Prathamesh Ghavanalkar ◽  
Mezia Fernandes ◽  
...  

Abstract Background Efforts to study the biology of Plasmodium vivax liver stages, particularly the latent hypnozoites, have been hampered by the limited availability of P. vivax sporozoites. Anopheles stephensi is a major urban malaria vector in Goa and elsewhere in South Asia. Using P. vivax patient blood samples, a series of standard membrane-feeding experiments were performed with An. stephensi under the US NIH International Center of Excellence for Malaria Research (ICEMR) for Malaria Evolution in South Asia (MESA). The goal was to understand the dynamics of parasite development in mosquitoes as well as the production of P. vivax sporozoites. To obtain a robust supply of P. vivax sporozoites, mosquito-rearing and mosquito membrane-feeding techniques were optimized, which are described here. Methods Membrane-feeding experiments were conducted using both wild and laboratory-colonized An. stephensi mosquitoes and patient-derived P. vivax collected at the Goa Medical College and Hospital. Parasite development to midgut oocysts and salivary gland sporozoites was assessed on days 7 and 14 post-feeding, respectively. The optimal conditions for mosquito rearing and feeding were evaluated to produce high-quality mosquitoes and to yield a high sporozoite rate, respectively. Results Laboratory-colonized mosquitoes could be starved for a shorter time before successful blood feeding compared with wild-caught mosquitoes. Optimizing the mosquito-rearing methods significantly increased mosquito survival. For mosquito feeding, replacing patient plasma with naïve serum increased sporozoite production > two-fold. With these changes, the sporozoite infection rate was high (> 85%) and resulted in an average of ~ 22,000 sporozoites per mosquito. Some mosquitoes reached up to 73,000 sporozoites. Sporozoite production could not be predicted from gametocyte density but could be predicted by measuring oocyst infection and oocyst load. Conclusions Optimized conditions for the production of high-quality P. vivax sporozoite-infected An. stephensi were established at a field site in South West India. This report describes techniques for producing a ready resource of P. vivax sporozoites. The improved protocols can help in future research on the biology of P. vivax liver stages, including hypnozoites, in India, as well as the development of anti-relapse interventions for vivax malaria.


2019 ◽  
Author(s):  
Punita Sharma ◽  
Jyoti Rani ◽  
Charu Chauhan ◽  
Seena Kumari ◽  
Sanjay Tevatiya ◽  
...  

AbstractBlood feeding-enriched gut-microbiota boosts mosquitoes’ anti-Plasmodium immunity. Here, we ask how Plasmodium vivax alters microbiota, anti-Plasmodial immunity and impact tripartite Plasmodium-mosquito-microbiota interactions in the gut lumen. Using a metagenomics analysis, we predominantly detect Elizabethkingia meningitis and Pseudomonas sps. in naïve mosquitoes. Naïve blood fed gut shows a heightened presence of Elizabethkingia, Pseudomonas and Serratia. A parallel RNAseq analysis of blood-fed midguts identify Elizabethkingia-transcripts, which may have role in iron metabolism. Post, a Plasmodium vivax infected blood-meal, however, we do not detect bacterial until circa 36 hours. Intriguingly, transcriptional expression of a selected array of antimicrobial arsenal cecropins 1-2, defensin-1 and gambicin remains low during the first 36 hours–a time frame when ookinietes/early oocysts invade gut. We conclude during the preinvasive phase, Plasmodium vivax outcompetes midgut-microbiota. Suppression of important immune factors, likely due to altered microbiota, may enhance Plasmodium vivax survival. Additional finding of a novel Wolbachia association warrants further research to design ‘paratransgenesis’ tools for malaria control.Author SummarySuccessful malaria transmission relies on the competitive interactions of Plasmodium and mosquito’s tissue specific immune potential. Within 24hrs of blood meal gut-microbiota grows exponentially and lead to robust enhancement of mosquito immune response, which is detrimental to parasite survival and development. But the mechanism how Plasmodium manages to evade this pre-invasive immune barrier is not well known. We investigated the influence of tripartite gut-microbiome-parasite interaction on human malaria parasite Plasmodium vivax in its natural/native vector Anopheles stephensi. Surprisingly we found that infectious blood meal lead to dramatic suppression in gut-bacteria population, a plausible strategy of P. vivax ookinetes to avoid immune responses. Our study suggests that for its own survival Plasmodium vivax causes early suppression of bacterial population, possibly by scavenging Fe from the blood meal which is indispensable for bacterial growth. Disruption and manipulation of this gut-microbe-interaction may help to design new ‘paratransgenesis’ molecular tool for malaria control.


2018 ◽  
Vol 17 (1) ◽  
Author(s):  
Ajeet Kumar Mohanty ◽  
Praveen Balabaskaran Nina ◽  
Shuvankar Ballav ◽  
Smita Vernekar ◽  
Sushma Parkar ◽  
...  

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