Open AccessWolbachia depletion blocks transmission of lymphatic filariasis by preventing chitinase-dependent parasite exsheathment
Author(s) -
Shan Quek,
Darren Cook,
Yang Wu,
Amy E. Marriott,
Andrew Steven,
Kelly L. Johnston,
Louise Ford,
John Archer,
Janet Hemingway,
Stephen A. Ward,
Simon C. Wagstaff,
Joseph D. Turner,
Mark J. Taylor
Publication year - 2022
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2120003119
Subject(s) - wolbachia , lymphatic filariasis , biology , parasite hosting , brugia malayi , chitinase , filariasis , immunology , helminths , host (biology) , ecology , enzyme , biochemistry , world wide web , computer science
Significance Lymphatic filariasis caused byWuchereria bancrofti ,Brugia malayi , andBrugia timori affects 51 million people, leading to severe physical and mental disabilities. A mutualistic symbiosis between these filarial nematodes andWolbachia bacteria has been exploited as a new curative treatment. Epidemiological modeling of anti-Wolbachia treatment assumes that transmission persists due to the lag phase before microfilariae (mf) become removed from circulation. Here, we show thatWolbachia -depleted mf cannot develop within the mosquito vector—a phenotype associated with down-regulation ofB. malayi mf-specific chitinase, an enzyme essential for exsheathment. Our findings add to the broad range of host biological processes dependent onWolbachia and suggest that anti-Wolbachia treatment mediates a more accelerated impact on elimination of lymphatic filariasis than currently predicted.