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Articles - T gondii

13 important questions on Articles - T gondii

Explain which host cells are infected, and how T. gondii invades and disseminates in the host cell (e.g. intra/extracellular? type of cells; figure 1). Explain the biological characteristics of the parasite as is explained during the life cycle session.

In the gut the parasites invade enterocytes and replicate. They can also cross the epithelial barrier to reach the lamina propria, where they encounter macrophages, DCs and intraepithelial lymphocytes. The infection spreads to the lymph nodes, spleen and eventually all organs. In the host cell, T gondii resides in a parasitophorous vacuole (PV), which doesn't fuse with the endolysosomal system.

How does the parasite invade the host?

The parasite creates and enters a PV.
RONs (2,4,5) are secreted from the rhoprty neck to help mediate a moving junction.
ROPs are secreted from the bulb into the host cell cytosol and go the the nucleus (ROP16) and the surface of the PV (ROP2,5,18).
The PV cannot fuse with endosomes and lysosomes and also recrutes host mitochondria to the PV to get nutrients.
After multiple rounds of mytotic division, daughter parasites begin the invade neighbouring cells.

What does the extensive modification of the PV suggest?

It suggest that the parasite modulates many host cell functions to enhance the intracellular lifestyle

How are the lineages distributed around the world?

In North America and Europe 1-2-3, majority is 2.
In South America more diverse, which suggests more sexual recombination.

What is the first response of the immune system during an infection? Part a

T gondii GPI proteins are recognized by TLR2 and TLR4 of monocyte/macrophage, which induces the production of IL-12 and TNF.

Also, T gondii profilin interacts with TLR11 of DC, which stimulates IL-12 production.

Which innate and adaptive effectors are involved? Part b

NK cells (innate) produce IFNy
CD4+ and CD8+ (adaptive) also produce IFNy

IL-10 and IL-27 modulate these pathways and prevent the overproduction of Th1 type cytokines

How does the parasite control in a monocyte/marcophage work? Part c

IFNy propagates a signal through IFNyR (surface receptor) to activate STAT1 (transcription factor).
STAT1 activity makes macrophages and monocytes upregulate their production of NO and ROS.
NO and ROS contribute to the control of intracellular parasites.

INFy also upregulates IRGs (rupture PV) and GBPs (control), whose functions depend on autophagy protein 5 ATG5

In which 2 ways does the parasite alter host signalling/evase the immune system?

1. Defective STAT1 signaling -> cell unresponsive to IFNy -> blocked transcription factors STAT1 and NF-kB
2. Upregulation of anti-inflammatory pathways, including those involving SOC1, SOC3 and STAT3

Why can killing not be activited by the macrophages?

Macrophages need a second signal besides IFNy.
These signals are TNF and CD40, which both use the NF-kB signaling pathway.

In which strains is ROP16 present?

1&3, where it induces long term activation of STAT3 and STAT6

Which strain is only present in type 3 strains and what does it do?

ROP38, it downregulates the host's MAPK signaling pathway

What does GRA15 do? And in which strain(s)?

It stimulates the IL-12 response through activation of NF-kB.
Only in strain 2

Summarize the scheme with virulence factors per strain

ROP 15: high, high, low
ROP 5: Yes, no, no
ROP 16: yes, no, yes
GRA 15: no, yes, no

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Articles - T gondii

13 important questions on Articles - T gondii

Explain which host cells are infected, and how T. gondii invades and disseminates in the host cell (e.g. intra/extracellular? type of cells; figure 1). Explain the biological characteristics of the parasite as is explained during the life cycle session.

How does the parasite invade the host?

What does the extensive modification of the PV suggest?

How are the lineages distributed around the world?

What is the first response of the immune system during an infection? Part a

Which innate and adaptive effectors are involved? Part b

How does the parasite control in a monocyte/marcophage work? Part c

In which 2 ways does the parasite alter host signalling/evase the immune system?

Why can killing not be activited by the macrophages?

In which strains is ROP16 present?

Which strain is only present in type 3 strains and what does it do?

What does GRA15 do? And in which strain(s)?

Summarize the scheme with virulence factors per strain

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