Unveiling the malaria parasite's cloak of invisibility?

Several insects, particularly mosquitoes, are responsible for the transmission of many viral, protozoan, and even worm infections. Previously, insects were considered passive pathogen carriers. But sophisticated cross-talk exists between the pathogen effectors and the immune system of the insect vector. As in vertebrates, the insect's first line of defense is a sophisticated innate immune response (IIR), employing pattern recognition molecules to detect pathogens and shape the antipathogen response. IIR involves humoral and cellular responses ( 1 ), including phagocytic cells and complement-like systems, which result in the activation of effector molecules—for example, thioester-containing protein 1 (TEP1) ( 2 )—that cause lysis or encapsulation of the parasite through melanization. IIR may also trigger free-radical release, causing lethal damage to the pathogen. Despite a fairly detailed picture of how a mosquito responds to pathogen infection ( 3 , 4 ), parasite targets and mechanisms of mosquito immune evasion by parasites are largely unknown. On page 984 of this issue, Molina-Cruz et al. ( 5 ) identify a gene in the human malarial parasite, Plasmodium falciparum , that mediates evasion of the mosquito IIR.