Introduction to Avoiding Host Defense Mechanisms: Videos & Practice Problems

Pathogens can hide within host cells to evade immune detection by entering and residing in cells where they are less accessible to immune defenses. This intracellular lifestyle allows them to avoid extracellular immune components like antibodies and complement proteins. Some pathogens, such as viruses, naturally replicate inside host cells. Others, like certain bacteria, have evolved mechanisms to invade and survive within host cells. For example, Mycobacterium tuberculosis can inhibit phagosome-lysosome fusion in macrophages, allowing it to survive and replicate within these immune cells. By hiding within host cells, pathogens can effectively evade the host's immune surveillance and establish persistent infections.

Pathogens employ several strategies to avoid phagocytosis, including:

• Capsules: Many bacteria produce a polysaccharide capsule that inhibits phagocytosis by preventing recognition and binding by phagocytes.
• Fc Receptors: Some pathogens express Fc receptors that bind the Fc region of antibodies, preventing opsonization and subsequent phagocytosis.
• Preventing Encounter: Pathogens can secrete enzymes or toxins that kill phagocytes or inhibit their chemotaxis.
• Surviving Inside Phagocytes: Some pathogens can survive and replicate within phagocytes by inhibiting phagosome-lysosome fusion or resisting the toxic environment of the phagolysosome.

These mechanisms help pathogens evade the immune system and establish infections.

Pathogens can avoid the complement system through various mechanisms:

• Capsules: Capsules can prevent complement activation by inhibiting the binding of complement proteins to the bacterial surface.
• Complement Regulatory Proteins: Some pathogens mimic host complement regulatory proteins, which inhibit complement activation.
• Proteases: Pathogens can produce proteases that degrade complement proteins, preventing their activation and function.

By evading the complement system, pathogens can avoid opsonization, inflammation, and cell lysis, enhancing their ability to cause disease.

Antigenic variation is a mechanism by which pathogens alter their surface proteins to evade the host's immune response. By changing the antigens that are recognized by the immune system, pathogens can avoid detection and destruction by antibodies and immune cells. This variation can occur through genetic mutations, recombination, or gene conversion. For example, the malaria parasite Plasmodium falciparum frequently changes its surface proteins to avoid immune recognition. Antigenic variation allows pathogens to persist in the host, cause chronic infections, and evade vaccine-induced immunity.

IgA proteases are enzymes produced by certain pathogens that specifically cleave IgA antibodies. IgA is a critical component of the mucosal immune system, providing the first line of defense against pathogens at mucosal surfaces. By producing IgA proteases, pathogens can degrade IgA antibodies, reducing their ability to neutralize and opsonize the pathogen. This allows the pathogen to colonize mucosal surfaces and evade the host's immune response. Examples of pathogens that produce IgA proteases include Neisseria gonorrhoeae and Haemophilus influenzae.