‘Mind-control’ parasite Toxoplasma hides from the immune system with 2 key genes

A new study could help scientists find a cure to lifelong infections caused by the parasite Toxoplasma gondii.  

The parasite Toxoplasma gondii hides in up to half of humans, although it rarely causes symptoms. But when it infects mice, the single-cell organism can exert a kind of “mind control” to change the rodents’ behavior and help itself spread.

Now, researchers report being one step closer to curing T. gondii infections in humans, which can be lifelong due to the parasite’s ability to morph into a dormant, defensive state. Two transcription factors — proteins that switch genes “on” and “off” — lie at the root of this metamorphosis, and the discovery opens avenues to block the process.

Often dubbed the “mind-control parasite,” T. gondii takes over the minds of infected mice and steers them towards cats to become their next meal. This enables the parasites to jump into our feline friends, the only known hosts in which they can reproduce sexually.

Scientists remain unsure whether the parasite can similarly control the human brain; some studies suggest it could contribute to aggression, impulsive behavior and schizophrenia, while other studies dispute these effects. Most people carrying T. gondii don’t develop any symptoms, but more rarely, the infection can trigger mild, flu-like symptoms or even severe illness. Developing fetuses, newborns, and people with weak immune systems are most vulnerable to severe toxoplasmosis, which can damage the eyes and brain and sometimes be fatal.  (See link for article)



  • Similarly to Lyme, T. gondii burrows into tissues and morphs into a different form when it’s threatened making it hard to find.  Also, similar to Lyme, current therapies do not cure the infection because the chronic stages are resistant.
  • Researchers have previously discovered a protein that is essential for morphing.
  • Now, a new study in Nature Microbiology, found another transcription factor that regulates morphing.
  • By deleting this gene, mice that had 100 copies of T. gondii injected into them did not appear to develop cysts in their brains 45 days later.

The team determined that T. gondii cells maintain a supply of this mRNA, but they can only make the BFD1 protein when BFD2 binds to the mRNA and thus triggers protein synthesis. This binding only happens when the cell is under stress.

By perpetuating each other’s activity, the two transcription factors can commit tachyzoites to morphing into bradyzoites by “locking the cell into this developmental trajectory,” said M. Haley Licon, parasitologist and lead author of the study. Future research could unravel what factors switch “off” this self-perpetuating loop, she added, enabling bradyzoites to revert to tachyzoites when stressful conditions elapse.

Hakimi argued that scientists are a long way from developing such drugs. “It’s very hard to target transcription factors,” and aside from select drugs used in cancer treatment, “very few drugs” do, he said.

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