Transmission blocking vaccines to control insect-borne diseases: a review

Coutinho-Abreu, Iliano V.; Ramalho-Ortigão, Marcelo

doi:10.1590/s0074-02762010000100001

Cited by 51 publications

(29 citation statements)

References 53 publications

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“…To this end, use has been made of experimental models that mimick the intestinal microenvironment of the host, such as cultures of intestinal epithelial cells, macrophages and dendritic cells 411, 415, 416. Our results showed that the initial ability to invade the intestinal cell is similar between EIEC and Shigella , but that the expression of virulence genes ( ipaABCD , icsA , icsB , virF , virB ), capacity to escape from the phagosome, intracellular proliferation and dissemination of EIEC, as well as the ability to cause cell damage during the infection, are much lower than with S. flexneri 411 .…”

Section: Enteroinvasive E Colimentioning

confidence: 99%

Diarrheagenic Escherichia coli

Gomes

Elias

Scaletsky

et al. 2016

Brazilian Journal of Microbiology

433

353

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Most Escherichia coli strains live harmlessly in the intestines and rarely cause disease in healthy individuals. Nonetheless, a number of pathogenic strains can cause diarrhea or extraintestinal diseases both in healthy and immunocompromised individuals. Diarrheal illnesses are a severe public health problem and a major cause of morbidity and mortality in infants and young children, especially in developing countries. E. coli strains that cause diarrhea have evolved by acquiring, through horizontal gene transfer, a particular set of characteristics that have successfully persisted in the host. According to the group of virulence determinants acquired, specific combinations were formed determining the currently known E. coli pathotypes, which are collectively known as diarrheagenic E. coli. In this review, we have gathered information on current definitions, serotypes, lineages, virulence mechanisms, epidemiology, and diagnosis of the major diarrheagenic E. coli pathotypes.

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Section: Enteroinvasive E Colimentioning

confidence: 99%

Diarrheagenic Escherichia coli

Gomes

Elias

Scaletsky

et al. 2016

Brazilian Journal of Microbiology

433

353

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“…In malaria studies, transmission-blocking vaccines (TBVs) had been reported by several laboratories (66)(67)(68). Mosquito proteins related to virus infection were selected as immunogens and showed a role in blocking dengue virus infection.…”

Section: Fig 6 Anti-mosgctl-7 Serum Inhibits Jev Infection In Vivo Anmentioning

confidence: 99%

mosGCTL-7, a C-Type Lectin Protein, Mediates Japanese Encephalitis Virus Infection in Mosquitoes

Liu

Qian

Jung

et al. 2017

J Virol

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Japanese encephalitis virus (JEV) is an arthropod-borne flavivirus prevalent in Asia and the Western Pacific and is the leading cause of viral encephalitis. JEV is maintained in a transmission cycle between mosquitoes and vertebrate hosts, but the molecular mechanisms by which the mosquito vector participates in transmission are unclear. We investigated the expression of all C-type lectins during JEV infection in Aedes aegypti. The C-type lectin mosquito galactose-specific C-type lectin 7 (mosGCTL-7) (VectorBase accession no. AAEL002524) was significantly upregulated by JEV infection and facilitated infection in vivo and in vitro. mosGCTL-7 bound to the N-glycan at N154 on the JEV envelope protein. This recognition of viral N-glycan by mosGCTL-7 is required for JEV infection, and we found that this interaction was Ca 2ϩ dependent. After mosGCTL-7 bound to the glycan, mosPTP-1 bound to mosGCTL-7, promoting JEV entry. The viral burden in vivo and in vitro was significantly decreased by mosPTP-1 double-stranded RNA (dsRNA) treatment, and infection was abolished by anti-mosGCTL-7 antibodies. Our results indicate that the mosGCTL-7/mosPTP-1 pathway plays a key role in JEV infection in mosquitoes. An improved understanding of the mechanisms underlying flavivirus infection in mosquitoes will provide further opportunities for developing new strategies to control viral dissemination in nature.IMPORTANCE Japanese encephalitis virus is a mosquito-borne flavivirus and is the primary cause of viral encephalitis in the Asia-Pacific region. Twenty-four countries in the WHO Southeast Asia and Western Pacific regions have endemic JEV transmission, which exposes Ͼ3 billion people to the risks of infection, although JEV primarily affects children. C-type lectins are host factors that play a role in flavivirus infection in humans, swine, and other mammals. In this study, we investigated C-type lectin functions in JEV-infected Aedes aegypti and Culex pipiens pallens mosquitoes and cultured cells. JEV infection changed the expression of almost all C-type lectins in vivo and in vitro, and mosGCTL-7 bound to the JEV envelope protein via an N-glycan at N154. Cell surface mosPTP-1 interacted with the mosGCTL-7-JEV complex to facilitate virus infection in vivo and in vitro. Our findings provide further opportunities for developing new strategies to control arbovirus dissemination in nature.

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“…The emergence of insecticide resistance as well as the lack of other efficient insecticidal tools to control disease vectors imply that new methodologies need to be developed in order to reduce vector-borne disease transmission [1]. For this, the study of vector-pathogen interaction pinpointing factors underlying vector competence can reveal new molecular targets to be disrupted, preventing pathogen transmission [2], [3].…”

Section: Introductionmentioning

confidence: 99%

Targeting the Midgut Secreted PpChit1 Reduces Leishmania major Development in Its Natural Vector, the Sand Fly Phlebotomus papatasi

et al. 2010

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BackgroundDuring its developmental cycle within the sand fly vector, Leishmania must survive an early proteolytic attack, escape the peritrophic matrix, and then adhere to the midgut epithelia in order to prevent excretion with remnants of the blood meal. These three steps are critical for the establishment of an infection within the vector and are linked to interactions controlling species-specific vector competence. PpChit1 is a midgut-specific chitinase from Phlebotomus papatasi presumably involved in maturation and degradation of the peritrophic matrix. Sand fly midgut chitinases, such as PpChit1, whether acting independently or in a synergistic manner with Leishmania-secreted chitinase, possibly play a role in the Leishmania escape from the endoperitrophic space. Thus, we predicted that silencing of sand fly chitinase will lead to reduction or elimination of Leishmania within the gut of the sand fly vector.Methodology/Principal FindingsWe used injection of dsRNA to induce knock down of PpChit1 transcripts (dsPpChit1) and assessed the effect on protein levels post blood meal (PBM) and on Leishmania major development within P. papatasi. Injection of dsPpChit1 led to a significant reduction of PpChit1 transcripts from 24 hours to 96 hours PBM. More importantly, dsPpChit1 led to a significant reduction in protein levels and in the number of Le. major present in the midgut of infected P. papatasi following a infective blood meal.Conclusion/SignificanceOur data supports targeting PpChit1 as a potential transmission blocking vaccine candidate against leishmaniasis.

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Transmission blocking vaccines to control insect-borne diseases: a review

Abstract: Insect

Cited by 51 publications

References 53 publications

Diarrheagenic Escherichia coli

Diarrheagenic Escherichia coli

mosGCTL-7, a C-Type Lectin Protein, Mediates Japanese Encephalitis Virus Infection in Mosquitoes

Targeting the Midgut Secreted PpChit1 Reduces Leishmania major Development in Its Natural Vector, the Sand Fly Phlebotomus papatasi

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