Vl 9 Plasmodium III

Question 1

Describe erythrocyte remodeling by Plasmodium falciparum.

Answer 1

alters morphology ⇒ causes adhesive knobs
⇒ parasite derived surface proteins (PfEMP1) on erythrocyte membrane (exported through PTEX)⇒ bind to receptors on human cells⇒ clinging of infected erythrocytes on blood vessels and other erythrocytes

also:

• knot is temporary storage of multiple parasitic proteins that are to be secreted on host cells surface
• builds parasitophorous duct and nutrient channels ⇒ connect parasite to outside and nourish it

Question 2

What are the main clinical complications of a Plasmodium falciparum infection? Explain.

Answer 2

• high fever due to synchronized proliferation and antigen excretion
• anemia due to rupture of erythrocytes as only host cell type
• cerebral malaria by clogging up blood vessels in brain region
• multiple organ failure

Question 3

How can we interpret the slow acquisition of natural immunity against malaria disease?

Answer 3

• takes long and constant exposure to all 60 PfEMP1 variants for the immune system to recognize and react to them all ⇒ not possible in young children
• natural immunity can be lost⇒ b-cell response vanishes after some time

Question 4

How could one identify signatures of naturally acquired immunity against malaria?

Answer 4

by screening for antigens of all PfEMP1 variations

Question 5

What are the prospects of malaria eradication? Explain.

Answer 5

eradication of the greatest death cause for children, because the most severe and highest mortalities are in children under age 5