Parasite Survival Strategies and Persistent Infections Flashcards
avoiding innate IR
antiphagocytic strategies
toxins prevention of oponisation prevention of contact inhibition of phagolysosome fusion escape into the cytoplasm resistance to killing
how is ciliary action avoided?
bordetella pertussis interferes with the cilia
how is the complement alternative pathway inhibited
outer surface (e.g. capsule) prevents either C activation or access to fixed C3b
bacterial membrane is resistant to MAC complex formation
Decoy proteins divert C components away from bacterial surface
what does Neisseria spp. produce in the host
produces iron-binding molecules -steal iron from transferrin
blocking interferons (INF)
host cells respond to dsRNA/RNA from infecting microbes by producing INF
some viruses are poor inducers of INF, (e.g. hapatitis B) or produce molecules that block action of INF in cells (e.g. HIV)
examples of how lymphocytes avoided (adaptive IR)
viruses, very good at avoiding immune defenses
no extensive tissue damage, better survival
latent viruses -remain hidden to resurface later
evasion strategies for adaptive IR
hit and run
concealment of antigens
antigenic variation
immunosuppression
Hit and run
microbe invades, multiplies and sheds within a few days
too quick for adaptive IR activation (e.g. rhinovirus, rotavirus)
concealment of antigens
hide in host cells
-prevent Ag presentation by MHC (adenovirus protein + class 1 MHC prevent its passage to cell surface)
hide at sites not exposed to circulating lymphocytes (skin. CNS, testis, placenta)
molecular mimicry -fragment similar to host cells
covering microbial surface with host molecules
hide at sites not exposed to circulating lymphocytes
IgA may interact but not enough to kill, only reduce disease
can hide in many glands
skin, intestinal lumen, secretions, testis, placenta, CNS
most privileged location=host DNA (occupied by retrovirus) -retroviral DNA
as long as viral products not expressed, remain undetected indefinitely (HIV)
molecular mimicry
microbial antigens look like host cells
streptococcal M-protein and human heart (streptococcal biogenis)
other variants of streptococci colonize local heart tissue
covering microbial surface with host molecules
antibodies can only attach in useless upside down position on the FC portion
antigenic variation
changing cell surface antigens -> escape immune system
during infection of single individual
during spread throughout population
eg relapsing fever, Borrelia spp
what the three molecular mechanisms for antigenic variation
mutation -nucleotide change
recombination -rearrangement of genes
gene switching -turn genes on and off
antigenic variation: mutation
e.g. influenza virus -spreads through population
genes encoding hemagglutinin and neuraminidase undergo mutation
leads to Ag change that makes them unrecognizable by B and T memory cells
=”antigenic drift”
also rhinovirus and enteroviruses
