Complement Evasion: An Effective Strategy That Parasites Utilize to Survive in the Host

Abstract

Parasitic infections induce host immune responses that eliminate the invading parasites. However, parasites have evolved to develop many strategies to evade host immune attacks and survive in a hostile environment. The complement system acts as the first line of immune defense to eliminate the invading parasites by forming the membrane attack complex (MAC) and promoting an inflammatory reaction on the surface of invading parasites. To date, the complement activation pathway has been precisely delineated; however, the manner in which parasites escape complement attack, as a survival strategy in the host, is not well understood. Increasing evidence has shown that parasites develop sophisticated strategies to escape complement-mediated killing, including (i) recruitment of host complement regulatory proteins on the surface of the parasites to inhibit complement activation; (ii) expression of orthologs of host RCA to inhibit complement activation; and (iii) expression of parasite-encoded proteins, specifically targeting different complement components, to inhibit complement function and formation of the MAC. In this review, we compiled information regarding parasitic abilities to escape host complement attack as a survival strategy in the hostile environment of the host and the mechanisms underlying complement evasion. Effective escape of host complement attack is a crucial step for the survival of parasites within the host. Therefore, those proteins expressed by parasites and involved in the regulation of the complement system have become important targets for the development of drugs and vaccines against parasitic infections.

Toxoplasma gondii Recruits Factor H and C4b-Binding Protein to Mediate Resistance to Serum Killing and Promote Parasite Persistence in vivo

“…Parasites often target multiple complement pathways to achieve complement resistance (41). Both C4BP and FH contribute to protection against complement-mediated lysis by inactivating the classical/lectin and alternative pathways, respectively.…”

The Electrophoretic Pattern of Serum Proteins in Sheep with Naturally Acquired Gastrointestinal Nematode Infections

“…Some diagnostically important proteins were identifi ed in the β-globulin region, including transferrin, complement, as well as ferritin [43]. Higher concentrations of transferrin are usually associated with iron defi ciency anemia, resulting in a negative correlation between hemoglobin and transferrin [44]. In trichostrongyloides-infected cattle and sheep, severe normocytic anemia and symptoms of the depression of erythrogenesis have been reported previously [45].…”

Molecular characterization and induced expression analysis of the terminal complement component C9 in rohu,Labeo rohita

“…Probably, this parasite or its toxins might be indirectly influencing local inflammation by down‐regulating complement synthesis either in situ to make them more susceptible to infection. This action of parasite is indicative of its survival strategy by escaping to MAC at the site (Shao, Sun, Chen, Zhan, & Zhu, ) and making the fish more vulnerable to parasite or parasite‐induced pathology. Several toxins are being released by Argulus during the infection, which cause damage to the internal organs of the host.…”