It has been to the advantage of many microbial pathogens to acquire mechanisms for immune evasion. For example, an open reading frame encoding a sequence highly homologous to that of human and various monkey species of CD59 has been identified in the genome of herpesvirus saimiri (HVS), whose natural host is the squirrel monkey. It appears highly likely that the virus has captured this sequence from its host during the course of evolution. Preliminary studies indicate that the sequence does indeed encode a functional protein, so expression of this sequence by HVS could be considered as a virulence factor in aiding the virus to evade the detrimental effects of complement activation. Complement-inhibiting proteins that appear to have some antigenic relationship to CD59 have also been described in Entamoeba histolytica and Schistosoma mansoni. The E. histolytica protein is an integrin-like molecule consisting of two subunits, one of which shares very limited sequence homology with CD59. A cDNA for the S. mansoni protein has not yet been isolated. Since many pathogens are adept at avoiding destruction by the complement system, it is highly likely that other microbial proteins will emerge that are functionally, if not structurally, related to CD59 or the other human complement control proteins.
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