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Unveiling the Malaria Parasite's Cloak of Invisibility?

Identification of a surface protein in Plasmodium falciparum reveals how it can escape detection by the mosquito immune system. [Also see Report by Molina-Cruz et al.] 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.