WS 18/19 1. Termin Flashcards
Describe the molecular and immunological basis for the
fluctuation of Trypanosoma brucei parasites in the peripheral blood.
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 austausch: über transkriptionsswitch, telomeraustausch oder reinkopieren vsg expressionsstelle
have to switch vsg, because they are extracellular
Describe the mechanism of trans-splicing in Trypanosoma brucei
combines two separate pre-mRNA molecules to form a chimeric non-co-linear RNA⇒ may exert a function distinct from its original molecules.
- splice leader RNA helps cutting out the Introns from the pre-mRNA and fuse them with the Exon.
⇒ all mRNA in Trypanosoma have the same 39-nt sequence on the 5´end.
- Trans-spliced RNAs may encode novel proteins or serve as noncoding or regulatory RNAs⇒ increase the complexity of the proteome and provide new regulatory mechanisms for gene expression.
How does Trypanosoma cruzi invade its host cells?
induzierte Phagocytose/Endocytose über PIP3 oder rekrutierte Lysosomen
- viele Liganden auf oberfläche (besonders wichtig Fibronectin zum binden an Zellen)
What are the main virulence factors in Entamoeba histolytica and how do they work?
Gal/GalNAc lectin:
- bindet an Wirtszelle, resistent durch hohen Cysteingehalt, bewirkt Ca2+ Influx⇒ Tod der Wirtszelle
- auch bei Enzystierung wichtig
Gal/GalNAc binding proteins: hgl, lgl, igl
amoebapore:
kann Zellmembranen zerstören
- sehr unspezifisch
- lagern sich in targetzellemembran ein und machen Löcher
cysteine proteasen:
zum precessieren von Enzymen
- hilft bei zerstörung der extrazell. matrix
What is the molecular basis of the RTS,S/ASO1 anti-malaria vaccine candidate?
genes from repeat + T-cell epitope from CSP and a viral envelope protein of hepatitis B virus + adjuvant to increase immune response
infection prevented by inducing humoral and cellular immunity with high antibody titers -> block parasite from infecting the liver
Describe erythrocyte remodeling by Plasmodium falciparum.
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 various tissues
knobs also temporary storage of multiple parasitic proteins that are to be secreted on the host cells surface, and building a parasitophorous duct, connecting the parasite to the outside, and building nutrient channels into the erythrocyte surface to get better nourished
What are the immunological hallmarks of helminth infections and auto-immune diseases?
TH2 immune response: IgE immune response and eosinophily (T-cells: IL-5 - B-cells: IL-4, IL-13 important)
other immune responses have problems due to overlaps
What factors determine the disease spectrum in patients with Ochocerca volvulus infections?
3 different patterns, leading to different clinical pictures:
- adequate immune response ⇒ resistant “putatively immune” (Mf-negative)
- hyporeacative (cellular supression)⇒ little pathology (Mf-positive)⇒ contribute to infection
- hyperreactive⇒ strong pathology (Mf-negative)⇒ go blind
Describe the complications of an Echinococcus infection. Which pathogens cause the disease?
both in liver
granulosus: one big cyst - easy to get out via surgery
multilocularis: infection branched - chemotherapy or transplant only viable treatments
The pathogens are eggs
Describe the temporal development of immune responses to a Schistosoma spp. infection.
cercaria: TH1 response (adult parasites in liver/bladder can hide via protective coat of host specific proteins)
Eggs: trigger TH2 response
adults can induce cancer in liver/bladder
Which host cells are invaded by Leishmania, and how does host cell invasion occur? Describe the course of infection after transmission by an infected Phlebotomus sandfly.
-macrophages
-2 ways:
- via receptors
- via intake of neutrophiles (trojan horse) ⇒ prolonging
the lifetime of the neutrophiles
+ lifecycle
Describe the mechanism of Toxoplasma tachyzoite locomotion and host cell invasion.
- locomotion via gliding motility, (actin-myosin contractions) + secretion of “Schleimspur”
- active invasion of host cells by SAG1 of parasite, binding to host cell surface⇒ mediates moving junctions and dressing up in host cells membrane without it’s proteins to form a clean parasitophorous vacuole (screws into the cell)
Describe the Avexis approach to identify erythrocyte ligands for merozoite invasion
known: erythrocyte surface ligands bind to parasite surface proteins or other
Avexis: approach with pentamer “antibodies”⇒ strengthened protein interaction can be verified⇒ they are tested independently in a screening plate
