Infection and immunity Flashcards
(17 cards)
What determines the clinical presentation of an infectious disease?
The dynamic interaction between the host’s immune system and the invading organism, including how the immune response and pathogen virulence factors interact.
What are the steps required for an infectious disease to occur?
- Reservoir, 2. Transmission, 3. Invasion of host, 4. Adherence via specific adhesins, 5. Multiplication, 6. Interference with host processes (e.g., immune evasion), 7. Exit and further transmission.
How do pathogens adhere to host tissues?
Pathogens express adhesins (proteins or structures like pili/fimbriae) that bind to host cell receptors (e.g., integrins, glycoproteins), allowing colonization.
What are superantigens and their mechanism of action?
Superantigens bind directly to MHC class II molecules and T-cell receptors (TCRs) outside the peptide-binding site, causing non-specific activation of up to 20% of T-cells, resulting in cytokine storm and potential toxic shock.
What are the basic functions of the innate immune system?
Includes physical barriers, phagocytic cells (macrophages, neutrophils), NK cells, pattern recognition receptors (e.g., TLRs), complement cascade, and pro-inflammatory cytokines like IL-1, TNF-α.
What is the role of antigen-presenting cells (APCs)?
APCs such as dendritic cells process pathogen peptides via the MHC II pathway, migrate to lymph nodes, and present antigens to naïve CD4+ T cells, initiating adaptive responses.
What are the main CD4+ T-helper subsets and their cytokines?
Th1 (IFN-γ): intracellular pathogens; Th2 (IL-4, IL-5): parasites; Th17 (IL-17, IL-22): fungi/bacteria; Treg (TGF-β, IL-10): immune suppression and tolerance.
What is antigenic variation and its molecular basis?
Antigenic variation includes genetic rearrangements, phase variation, and point mutations that alter surface antigen expression. Used by pathogens to evade immune detection.
Describe antigenic drift vs antigenic shift at a molecular level.
Drift: gradual accumulation of point mutations in genes like HA/NA in influenza. Shift: reassortment of gene segments between different viral strains leading to new antigens.
Why is HIV difficult to vaccinate against?
HIV mutates rapidly, especially in the env gene, and its glycan shield masks epitopes. It also infects CD4+ T cells, impairing immune coordination, and integrates into host DNA.
How do bacteria evade phagocytosis molecularly?
Via capsules (e.g., polysaccharide layers), secretion of anti-phagocytic proteins, or mimicking host molecules to avoid recognition by phagocytes.
List the six human pathogen groups.
- Prions (misfolded proteins), 2. Viruses (obligate intracellular), 3. Bacteria (prokaryotes), 4. Protozoa (unicellular eukaryotes), 5. Fungi (yeasts, molds), 6. Helminths (parasitic worms).
What is the molecular immune response to helminths?
Th2 cytokines stimulate IgE production and eosinophil recruitment. IgE binds mast cells, triggering degranulation and expulsion mechanisms like mucus secretion.
Describe phase variation in Neisseria spp.
Gene expression of pili proteins is switched on/off via slipped-strand mispairing or DNA recombination, altering surface structures and avoiding antibody binding.
How does Trypanosoma brucei perform antigenic variation?
It has hundreds of VSG genes but expresses only one at a time. Switching occurs via gene conversion or transcriptional control from telomeric VSG expression sites.
What is the immune response to intracellular protozoa like Toxoplasma or Leishmania?
Driven by Th1 responses, especially IFN-γ activation of macrophages, enabling killing of intracellular organisms via nitric oxide and reactive oxygen species.
How does the immune system respond to fungal infections molecularly?
Th1 and Th17 responses dominate; IL-17 recruits neutrophils. Pattern recognition via dectin-1 and TLRs on dendritic cells leads to cytokine release and inflammation.
