Vl 1 Trypanosoma brucei I

Question 1

Describe the molecular and immunological basis for the

fluctuation of Trypanosoma brucei parasites in the peripheral blood.

Answer 1

1 or more always switch their vsg expression⇒ only when good immune system is present

switch always 1 week faster than immune system

immune system needs 1 week to build up antibodies⇒ all that dont switch vsg get killed

-vsg exchange via:
gene conversion, telomere exchange, transcriptional switch

have to switch vsg, because they are extracellular

Question 2

How are VSGs embedded in and realeased from the T. brucei plasma membrane?

Answer 2

via gpi anchors, which can be cut by phospholipases

Question 3

How can T. brucei switch its surface coat?

Answer 3

expression of new coats and phospholipases, which cut the vsg coats prior to switching

3 mechanisms of VSG switching:

1) Gene conversion (same transcription site, but expression site of old VSG cut out and replaced by copy and paste of a new expression site of another VSG)
2) Telomere exchange (same reading/ transcription site, but telomere parts between chromosomes are exchanged)
3) Transcriptional switch (just reading a VSG-gen from another site)

Question 4

Describe the life cycle of Trypanosoma brucei. How does the parasite adapt
to acquired immunity in the vertebrate host?

Answer 4

1) Tsetse fly injects metacyclic trypomastigotes into skin tissue
2) parasites enter lymphatic system and pass into bloodstream
3) bloodstream trypomastigotes multiply by binary fission (slender form)
4) tsetse fly infected during bloodmeal (stumpy form)
5) develop to procyclic trypomastigotes in gut
6) migrate to salivary glands, transform to epimastigotes (continue multiplying)
7) transform to metacyclic trypomastigotes ⇒ injected in host

entire lifecycle represented by extracellular stages

cycle in the fly takes approximately 3 weeks

long slender form has vsg-switching ⇒ adaption to aquired immunity via antigen variation