Complement Deficiencies and Pathogen Evasion
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p144
2025-07-23
574
Many genetic deficiencies of complement proteins have been described, and these generally lead to enhanced susceptibility to infectious disease (eg, C2 deficiency frequently leads to serious pyogenic bacterial infections). Deficiency in components of the MAC greatly enhances susceptibility to neisserial infections. Deficiencies in components of the alternative pathway are also known (eg, properdin deficiency is associated with greater susceptibility to meningococcal disease). There are also deficiencies in complement regulating proteins. For example, lack of the C1 inhibitor protein leads to hereditary angioedema.
The complement system is an important host protective system. However, some bacteria have evolved mechanisms to evade complement activity. For example, they can inter fere with opsonization or obstruct the insertion of the MAC. Complement activation can also be inhibited by the presence of microbial generated proteins, such as protein A and protein C, that bind IgG Fc. Finally, they can generate enzymes that degrade complement components. Organisms that possess these inhibitory properties are usually more pathogenic.
The complement system has also evolved strategies to attack cell-free virus and the virus-infected cells. In response, viruses have developed mechanisms to dodge complement attack. Some viruses, such as the smallpox virus, encode proteins that can inhibit host complement function. Other enveloped viruses, such as cytomegalovirus, can pick up some of the complement regulatory proteins as they mature by bud ding from the infected cell. These regulatory proteins (CD46, CD55, and CD59) on the virus envelope can downregulate complement activation. Finally, several viruses (Epstein-Barr virus [EBV], measles virus) use complement receptors to enter and infect cells.
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