Week 4 - Immune Evasion 1 Flashcards
What strategies may a parasite employ to evade the host?
Mimicry - They may produce proteins or coats that look like host.
Immuno-suppression - They may secrete cytokine-like molecules.
Hiding - They may hide in tissue with little protection or inside other cells.
Keeping ahead - They may constantly change the identity of their surface proteins.
What does HAT stand for?
Human African trypanosomiasis.
By what is HAT transmitted?
Human African trypanosomiasis is transmitted by the tsetse fly.
How many subspecies of ‘Trypanosoma brucei’ are there?
There are three subspecies of ‘Trypanosoma brucei’
T. b. brucei
T. b. gambiense.
T. b. rhodesiense
What disease does ‘T. b. brucei; cause?
‘T. b. brucei’ is a bloodstream parasite and causes nagana, a disease of antelopes but also livestock.
What species of Trypanosome cause HAT?
‘T. b. gambiense’ and ‘T. b. rhodesiense’ are the etiological agents of African sleeping sickness.
‘T. b. gambiense’ causes a chronic form of the disease.
‘T. b. rhodesiense’ caises a more acute infection.
Describe the Lifecycle of HAT.
- The Tsetse fly takes a blood meal of a human and injects metacyclic trypomastigotes.
- The injected metacyclic trypomastigotes transform into bloodstream trypmastigotes, which are carried to other sites.
- Trypomastigotes multiply by binary fission in various body fluids (blood, lymph and spinal fluid).
- The trpomastigotes are then present in blood.
- The Tsetse fly takes a blood meal and bloodstream trypomastigotes are ingested.
- The bloodstream trypomastigotes transform into pro cyclic trypomastigotes in the tsetse fly’s midgut. Procyclic trypomastigotes multiply by binary fission.
- The pro cyclic trypomastigotes leave the midgut and transform into epimastigotes.
- The epimastigotes multiply in salivary gland. They transform into metacyclic trypomastigotes.
Describe the cell surface of ‘Trypanosoma brucei’.
The bloodstream-form trypanosome is covered in a coat of variant surface glycoprotein (VSG).
How is antigenic variation employed as a pathogen survival strategy?
A survival strategy common to many bacterial, viral and eukaryotic pathogens, comprising the most rapidly evolving arms race between pathogen and host, is antigenic variation.
Over the course of the infection, the host mounts specific immune responses against a major pathogen surface antigen, but these are unable to eradicate the entire pathogen population, as some individuals have already switched to express different variants of the antigen.
What powers antigenic variation?
Antigenic variation is powered by diversity in expressed antigens across the pathogen population over the course of infection, and reinfection of partially immune or already infected hosts.
What are VSGs?
VSGs are variant surface glycoproteins. They enshroud bloodstream trypanosomes in a dense, highly immunogenic coat.
These VSG homodimers conceal invariant surface molecules of the parasite and are a major target of the host immune response.
What is the structure of VSG?
Each VSG monomer is a homodimer, consisting of a membrane-proximal C-terminal domain (CTG) that is inaccessible to antibodies, anchored to the surface by GPI (glycosyl phosphatidyl inositol).
The N-terminal domain (NTD) is exposed and contains the biologically relevant epitopes, there is a signal peptide at this end.
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