Steroid Hormone Function Controls Non-competitive Plasmodium Development in Anopheles.

Autor:	Werling K; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA., Shaw WR; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA., Itoe MA; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA., Westervelt KA; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA., Marcenac P; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA., Paton DG; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA., Peng D; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA., Singh N; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA., Smidler AL; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA; Wyss Institute for Biologically Inspired Engineering, Boston, MA 02115, USA., South A; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA., Deik AA; Broad Institute, Cambridge, MA 02142, USA., Mancio-Silva L; Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02142, USA., Demas AR; Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02142, USA., March S; Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02142, USA., Calvo E; Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, NIH, Rockville, MD 20852, USA., Bhatia SN; Broad Institute, Cambridge, MA 02142, USA; Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA; Koch Institute for Integrative Cancer Research, Cambridge, MA 02142, USA; Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA., Clish CB; Broad Institute, Cambridge, MA 02142, USA., Catteruccia F; Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA. Electronic address: fcatter@hsph.harvard.edu.
Jazyk:	angličtina
Zdroj:	Cell [Cell] 2019 Apr 04; Vol. 177 (2), pp. 315-325.e14. Date of Electronic Publication: 2019 Mar 28.
DOI:	10.1016/j.cell.2019.02.036
Abstrakt:	Transmission of malaria parasites occurs when a female Anopheles mosquito feeds on an infected host to acquire nutrients for egg development. How parasites are affected by oogenetic processes, principally orchestrated by the steroid hormone 20-hydroxyecdysone (20E), remains largely unknown. Here we show that Plasmodium falciparum development is intimately but not competitively linked to processes shaping Anopheles gambiae reproduction. We unveil a 20E-mediated positive correlation between egg and oocyst numbers; impairing oogenesis by multiple 20E manipulations decreases parasite intensities. These manipulations, however, accelerate Plasmodium growth rates, allowing sporozoites to become infectious sooner. Parasites exploit mosquito lipids for faster growth, but they do so without further affecting egg development. These results suggest that P. falciparum has adopted a non-competitive evolutionary strategy of resource exploitation to optimize transmission while minimizing fitness costs to its mosquito vector. Our findings have profound implications for currently proposed control strategies aimed at suppressing mosquito populations. (Copyright © 2019 Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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