Flashcards in Chapter 6 Deck (33):
How can a pathogen interfere with the complement pathway to avoid the innate immune response?
Using a capsule to prevent C activation or access to fixed C3b
Have bacterial membrane resistant to MAC complex formation
Use a decoy protein to divert C components away from the bacterial surface
What are some antiphagocytic strategies?
Prevention of opsonisation by covering constant chain
Prevention of contact using a capsule
Inhibition of phagolysosome
Escape in the cytoplasm
Resistance to killing by production of antioxidants
What uses iron binding molecules to avoid the innate immune response?
Neisseria produces its own iron-binding proteins to circumvent a shortage created by transferrin.
How can the blockage of interferons (INF) be used to avoid the innate immune response?
Some viruses are poor inducers of INF (hepatitis B)
Some produce molecules that block the action of INF in cells (HIV)
Why is the adaptive immune response more difficult to evade?
Due to lymphocytes.
B cells can recognize any shape (capsule and coat surface) to opsonize
T cells can recognize any amino acid sequence (even peptides from organisms presented with the MHC)
How can viruses avoid immune defenses?
They are intracellular and have no receptors.
They get into the genetic information of the host and replicates with it, can stay latent.
No damage=no signal to immune system
What is the hit and run evasion strategy?
When the microbe invades, multiplies and sheds within a few days.
Too quick for adaptive immune system activation
What viruses use the hit and run strategy?
Rhinovirus and rotavirus
What are some sites where pathogens can hide from circulating lymphocytes?
Skin, intestinal lumen and various secretions, CNS, joints, testes, placenta
What happens when pathogens hide in sites from circulating lymphocytes?
IgA can bind to the pathogen and reduce infectious potential, but not kill or control replication
What happens in sites with less circulating lymphocytes when the inflammatory process is induced?
Lymphocytes, antibodies and complement will rapidly appear on site.
What do retroviruses do?
Their retroviral RNA is reverse transcribed to DNA which becomes integrated into the host DNA
As long as viral products aren't expressed they aren't detected
What is the most privileged location in the body for pathogens?
The host DNA, occupied by retroviruses like HIV
How does molecular mimicry work?
Microbial antigens look like that of the host cell.
Doesn't prevent the host from making an antimicrobial or autoimmune response, may start attacking itself.
What pathogen uses molecular mimicry where?
Streptococcal M-protein in the human heart tissue to cause rheumatic heart disease
What happens when the microbial surface is covered with host molecules?
Immunoglobulin molecules of all specificities are bound in an upside down position so the variable chain is not available for detection.
Protein A on streptococcus aureus
What is antigenic variation?
The changing of cell surface antigens to escape the immune system so previous antibodies don't recognize it.
When can antigens change?
During infection in the host or when moving between hosts throughout a population
How does mutation in the influenza virus work?
Genes encoding hemagglutinin and neuraminidase undergo mutation which leads to antigen change that makes them unrecognizable by B and T memory cells from last flu infection
What is antigenic drift? In what does it occur?
Small changes in the antigenic structure (nucleotide bases) due to mutation
Occurs in influenza virus, rhinovirus, enteroviruses
What is genetic shift?
Large changes in the antigenic structure due to recombination that can create a completely new virus
How does the African trypanosome use gene switching?
It has genes for 1000 different surface molecules.
It can switch 1 gene for the next so that the surface antigens can change weekly. Fever disappears and reappears with each new antigen
Immune system is always playing catch up
What is the best example of recombination?
Influenza A virus, when human and avian strains combine after infecting the same host.
How does neisseria gonorrhoeae use gene switching?
It changes it's bacterial surface properties as the infection proceeds.
Initially it will express pili and outer membrane proteins that allow for attachment to the urethral epithelial cells. Once it is established, it may switch off so it's not sticky for phagocytes
Allows people to be reinfected multiple times, can be different between hosts.
What immune cells does HIV infect?
T Cells, Macrophages and Dendritic cells
How does the measles virus do immunosuppression?
Stops function of T cells
How does EBV do immunosuppression?
Stops function of B cells
How is the immune response interfered with?
Adenoviruses reduce MHC-1 expression
N. gonorrheoeae and S. pneumoniae are IgA protease
How can microbes persist?
Lower infectivity (adenovirus in tonsils)
Stay in a continuously infectious form (hepatitis B virus in blood)
Go into a non-infectious form (latent virus, HSV)
What can latent infections do?
Associate with chronic infections (HIV with AIDS)
Associate with cancer (HBV with liver cancer)
Persistance in the community
When does reactivation usually occur?
Typically during periods of immunocompromise (disease, cancer, tissue transplant, elderly, pregnancy)
What are the 2 stages of reactivation?
Stage A: Stimulus
Stage B: Spread and replication