MICROBIAL ANTICOMPLEMENTARY MECHANISMS
In general, complement-mediated phagocytosis is the most effective mechanism for elimination of infectious microorganisms. However, pathogenic organisms have evolved several mechanisms to circumvent either effective complement activation or effective complement deposition on their outer surface. These evasion strategies are most efficient during the early stages of an infection, when the levels of specific antibody are low.
In some cases, microorganisms (e.g., Candida) have on their surface a structural pro-tein that mimics the protective effect of DAF or other complement regulators. Interestingly, HIV appears to adsorb Factor H from serum and also acquires membrane DAF upon leaving the infected host cell. In these situations, a reduced deposition of complement components on the surface of the microorganism leads to a less effective neutralization/elimination. How-ever, the role of the complement system in immunity to HIV has not been established.
Other less sophisticated complement-restrictive mechanisms that different microor-ganisms have acquired include the shedding of MAC-coated pili, destruction of C3b by proteases on the bacterial surface, and protection of the cytoplasmic membrane from the dissolving effect of the MAC by slime layers, peptidoglycan layers, polysaccharide cap-sules, etc. In the presence of sufficient antibody levels, these protective mechanisms are usually overridden, and the microorganisms are properly phagocytosed, although some bacteria have acquired antiphagocytic capsules that further complicate the job of the immune system .
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