Lecture 4 – Host-Parasite Coevolution I: Immune Evasion & host manipulation
Parasites maximize their fitness in two main ways: evading the host’s defenses and transmitting
propagules
I. Immune Evasion – ability of parasite to escape immune detection or minimize immune effectors.
A. Hide away – parasite hides in immune-privileged tissues (e.g. central nervous system, testes,
placenta or eye). Examples: Loa loa nematode (aka the eye worm) and Toxoplasma
gondii
B. Invisibility – Parasite can cap or shed antigenic surface components (PAMPs – parasite
associated molecular patterns) once recognized by the host immune system. Examples:
some bacteria modify lipid A portion of LPS to become less recognizable. Enveloped
viruses coat themselves in host cellular membrane.
C. Change Identity – continuously changing surface epitopes, prolonging infection. Examples:
Trypanosoma bruci stores a “library” of surface epitopes. HIV continually mutates
surface epitopes.
D. Latency – parasite stops activity and ceases to invoke an immune response.
1. Episomal latency – viral genome floats naked in cytoplasm and does not evoke an
immune response (e.g. Herpes virus).
2. Proviral latency – viral genes integrated into host genome (e.g. HIV)
E. Macrophage neutralization – parasites can actively inhibit the immune cells that hunt them.
1. Alter macrophage cytoskeleton (e.g. Yops proteins secreted by Yersinia pestis)
2. Induce apoptosis (e.g. shigella)
3. Block parasite transport into lysozymes
4. Lysozyme escape via pore proteins (e.g. Listeria)
5. Interfere with MHC presentation (e.g. tuberculosis)
F. Network signaling interference – many parasites inhibit paracrine signaling molecules (e.g.
cytokines, interferons and chemokines). Example: Yersinia pestis Yop proteins inhibit
TNF-α
G. Antigen presentation interference – antigen presenting cells (MHC II) and infected cells (MHC
I) kept from actively presenting parasite epitopes.
H. Minimize immune effectors – immune effectors are soluble compounds that effect and
immune response (e.g. antimicrobial peptides, ROS, antibodies)
1. Degrade effectors (e.g. Pseudomonas aeruginosa secretes proteases that cleave
antibodies)
2. Reduce efficiency of effectors (e.g. staphylococcus reduces negative charge of their
cell membranes, reducing opsonization).
Lecture 4 – Host-Parasite Coevolution I: Immune Evasion & host manipulation
3. Catabolize effectors (e.g. some tapeworms can utilize antibodies as nutrients)
II. Host manipulation – parasite modifies host behavior or morphology to improve transmission to
another host.
A. Change in host behavior – parasite manipulates host to move to an appropriate site for
transmission. Examples: Lambornella clarki causes infected mosquitos to forgo a blood
meal and spread parasite in waters containing mosquito larvae. Nematode causes
cricket to commit suicide by jumping in water, allowing the nematode to escape.
B. Change in host morphology- parasite modifies host morphology to improve transmission
1. Horizontal transmission
a. Change in coloration
b. Castration
3. Vertical transmission
a. increase host fecundity
b. distort sex ratio
1. induce parthenogenesis
2. male feminization
3. eliminate uninfected females
4. eliminate uninfected males
III. Co-evolution
A. Hosts clear parasites; parasites evade / manipulate hosts. Who wins?
1. Winner take all - Sometimes host, sometimes parasite wins
2. Compromise – parasite inflicts minimal damage prior to transmission (low parasite
virulence)
3. Mafia strategy – as host immune response increases, parasite virulence increase
forcing a compromise of tolerance.