Host – Pathogen Interaction: Immune Evasion

Successful pathogens have evolved sophisticated mechanisms to evade host immune defenses. Antigenic variation: influenza undergoes antigenic drift (point mutations — annual epidemics) and antigenic shift (genome reassortment — pandemics); Trypanosoma brucei cycles through ~1,000 variant surface glycoproteins; HIV has extremely high mutation rate generating diverse quasispecies. Intracellular survival: M. tuberculosis inhibits phagosome-lysosome fusion; Listeria escapes the phagosome using listeriolysin O and spreads cell-to-cell via actin polymerization; Toxoplasma creates its own parasitophorous vacuole. Complement evasion: S. aureus protein A binds IgG Fc preventing opsonization; Strep pyogenes M protein prevents complement deposition. Superantigens (TSST-1, erythrogenic toxin) cross-link MHC-II and TCR non-specifically, causing polyclonal T-cell activation and cytokine storm (toxic shock syndrome). Molecular mimicry: Group A Strep M protein mimics cardiac myosin → rheumatic fever; Campylobacter LOS mimics gangliosides → Guillain-Barré syndrome. Immune suppression: HIV destroys CD4+ T cells; measles causes immune amnesia by destroying memory cells.