Such a fascinating, albeit terrifying study! In case you didn't see it, the study was also covered in @theconversation.com

theconversation.com/a-common-par...

Thanks Jean. I'm glad that you like it ☺️

7/ Why does this matter? Shows T. gondii can rapidly invade male reproductive organs reveals a novel mechanism of sperm damage and raises questions about potential impacts on male fertility. Is it interesting? check out the above link #Toxoplasma #ReproductiveHealth#Microbiology #Parasitology

6/ Surprisingly, ROS levels did not increase, and the acrosome reaction (key for fertilization) was unaffected. This suggests T. gondii damages sperm via direct mechanical disruption and mitochondrial dysfunction.

5/ Is this damage caused by direct contact or secreted molecules? We ruled out soluble factors—only direct parasite contact induced sperm decapitation. Extracellular vesicles (exosomes) also had no effect and no DNA fragmentation. But apoptosis & necrosis increased. MMP dropped sharply.

4/ Scanning electron microscopy (SEM) revealed: Parasites attaching to sperm heads/tails Twisted, coiled tails. Holes in sperm heads (!) and Some heads were completely emptied of content

3/ Next, we tested how T. gondii affects human sperm. After just 5 minutes of exposure: 22% of sperm lost their heads (vs. 1.6% in controls). By 15 min, headless sperm increased 8-fold!.

2/ But are these parasites still infectives? Yes. We extracted infected tissues, injected them into healthy mice, and confirmed new infections via PCR. The parasites remain viable and infectious!.

1/ T. gondii effects on male reproduction are poorly understood, and here we reveals how T.g invades testes, epididymis, and even damages. After 2 days tachyzoites were detected in both testes and epididymis with immune cell infiltration and structural damage in seminal tubules.

👌🏽

Congratulations Francesca!🎉

Congratulations! Well deserved it

Finally, I would like to thank all authors,
@ivanconejeros.bsky.social, and
@moritztreeck.bsky.social for allowing us to work with T.g. HCE1 and MYR1 mutants.

5/Host cells activate the ATM DNA damage response mechanism despite DNA damage. Other genome instability signs found were cytokinesis failure and micronuclei formation, which were observed early during infection. Interestingly, these effects proved independent of MYR1 or HCE1.
#CellBiology

4/ Strikingly, T. gondii-induced DNA damage begins just 15 minutes post-infection. This damage, marked by γH2AX foci, predominantly affects cells in the S-phase and is independent of reactive oxygen species (ROS).
#GenomeInstability

3/ MYR1 drives the translocation of parasite effectors into the host nucleus, leading to cell cycle arrest and a MYR1-dependent DNA damage response. These findings highlight MYR1's central role in parasite-host manipulation.
#DNAResearch #Parasitology

2/ Within 15 minutes of infection, T. gondii causes host cells to arrest in the S-phase of the cell cycle. This rapid effect, seen in endothelial cells, relies on the parasite’s MYR1 protein but not HCE1.
#CellCycle #HostPathogenInteractions