Mosquito immune responses and compatibility between Plasmodium parasites and anopheline mosquitoes.
BACKGROUND
Functional screens based on dsRNA-mediated gene silencing identified several Anopheles gambiae genes that limit Plasmodium berghei infection. However, some of the genes identified in these screens have no effect on the human malaria parasite Plasmodium falciparum; raising the question of whether different mosquito effector genes mediate anti-parasitic responses to different Plasmodium species.


RESULTS
Four new An. gambiae (G3) genes were identified that, when silenced, have a different effect on P. berghei (Anka 2.34) and P. falciparum (3D7) infections. Orthologs of these genes, as well as LRIM1 and CTL4, were also silenced in An. stephensi (Nijmegen Sda500) females infected with P. yoelii (17XNL). For five of the six genes tested, silencing had the same effect on infection in the P. falciparum-An. gambiae and P. yoelii-An. stephensi parasite-vector combinations. Although silencing LRIM1 or CTL4 has no effect in An. stephensi females infected with P. yoelii, when An. gambiae is infected with the same parasite, silencing these genes has a dramatic effect. In An. gambiae (G3), TEP1, LRIM1 or LRIM2 silencing reverts lysis and melanization of P. yoelii, while CTL4 silencing enhances melanization.


CONCLUSIONS
There is a broad spectrum of compatibility, the extent to which the mosquito immune system limits infection, between different Plasmodium strains and particular mosquito strains that is mediated by TEP1/LRIM1 activation. The interactions between highly compatible animal models of malaria, such as P. yoelii (17XNL)-An. stephensi (Nijmegen Sda500), is more similar to that of P. falciparum (3D7)-An. gambiae (G3).
Jaramillo-Gutierrez
Giovanna
G
Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 29892, USA. gutierrgi@niaid.nih.gov
Rodrigues
Janneth
J
Ndikuyeze
Georges
G
Povelones
Michael
M
Molina-Cruz
Alvaro
A
Barillas-Mury
Carolina
C
D000818:Animals; D000852:Anopheles / Q000235:genetics / Q000276:immunology* / Q000469:parasitology; D005260:Female; D020868:Gene Silencing; D017344:Genes, Insect; D005982:Glutathione Transferase / Q000235:genetics; D006790:Host-Parasite Interactions / Q000276:immunology*; D007303:Insect Vectors / Q000235:genetics / Q000276:immunology / Q000469:parasitology; D051379:Mice; D008807:Mice, Inbred BALB C; D010962:Plasmodium berghei / Q000276:immunology / Q000502:physiology*; D010963:Plasmodium falciparum / Q000276:immunology / Q000502:physiology*; D010967:Plasmodium yoelii / Q000276:immunology / Q000502:physiology*; D013045:Species Specificity
C413545:glutathione S-transferase T1; D005982:Glutathione Transferase