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Background  The cattle tick  Rhipicephalus (Boophilus) microplus  is involved in the transmission of the protozoan  Babesia bovis , the etiological agent of bovine babesiosis. Interactions between ticks and protozoa are poorly understood and the investigation of tick genes that affect tick fitness and protozoan infection can set the stage for dissecting the molecular interactions between the two species.    Results  In this study, RNA interference was used to silence  R. microplus  genes that had been previously shown to be up-regulated in response to  B. bovis  infection. The silencing of a putative immunophilin gene ( Imnp ) in female ticks fed on a calf acutely infected with  B. bovis  decreased the hatching rate and survival of larval progeny. Interestingly,  Imnp  was up-regulated significantly in ovaries of  R. microplus  in response to  B. bovis  infection and its silencing in female ticks significantly increased the infection rate of the protozoan in larval progeny. The results also showed that the silencing of a putative Kunitz-type serine protease inhibitor ( Spi ) gene and a putative lipocalin ( Lpc ) gene decreased the fitness of  R. microplus  females, but had no significant effect on the infection rate of  B. bovis  in larval progeny.    Conclusion  The silencing of the  Imnp ,  Spi  or  Lpc  genes decreased the fitness of  R. microplus  females fed on a calf during acute  B. bovis  infection. The  Imnp  gene data suggest that this putative immunophilin gene is involved in the defense system of  R. microplus  against  B. bovis  and may play a role in controlling the protozoan infection in tick ovaries and larval progeny.

parasites and vectors

Silencing of a putative immunophilin gene in the cattle tick Rhipicephalus (Boophilus) microplus increases the infection rate of Babesia bovis in larval progeny