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. Author manuscript; available in PMC: 2017 Jul 21.
Published in final edited form as: Sci Immunol. 2017 Jan 20;2(7):eaal1505. doi: 10.1126/sciimmunol.aal1505

Fig. 5. Proposed model of the role of HdMv on mosquito complement activation.

Fig. 5

Ookinete invasion causes irreversible cell damage; activates a nitration response that involves the induction of nitric oxide synthase (NOS), NOX5, and HPX2; and attracts hemocytes to the basal surface of the midgut. Contact of hemocytes with the nitrated surface of the basal lamina triggers the release of HdMv. Activation of circulating full-length TEP1 (TEP1-full) requires a proteolytic cleavage to generate TEP1-cut that deposits on the parasite’s surface (3, 25). Because HdMv release is necessary to activate the mosquito complement system, we propose that HdMv may contain a factor or factors (such as a convertase and/or a convertase cofactor) that promote TEP-1 activation.