The Toxoplasma gondii parasite, often called the “cat parasite,” infects roughly one in three people worldwide, lurking quietly in the brain and muscles for years without causing noticeable symptoms in most healthy individuals. For decades, scientists believed that during this chronic phase, the parasite simply goes dormant inside tiny protective cysts essentially “sleeping” to evade the immune system.
A major new study published in January 2026 in Nature Communications has turned that view upside down. Researchers at the University of California, Riverside, led by Professors Emma Wilson and Michael White, have uncovered surprising hidden activity and diversity inside these cysts. Far from being uniform sleeping bags of identical parasites, each cyst turns out to be a bustling microscopic community with specialized roles.
“If we want to really treat toxoplasmosis, the cyst is the place to focus.”
— Professor Emma Wilson, University of California, Riverside
The Silent Invader
Toxoplasma gondii spreads mainly through undercooked meat, contact with contaminated soil, or cat feces containing oocysts. In healthy adults, the initial (acute) infection usually passes unnoticed or causes only mild flu-like symptoms. The parasite then shifts gears, forming long-lived cysts filled with slow-growing forms called bradyzoites.
These cysts embed primarily in brain neurons and muscle tissue. For decades, researchers have considered them largely inactive—a dormant stage beyond the reach of current drugs.
This assumption creates a major clinical problem. In people with weakened immune systems, such as those with HIV/AIDS, organ transplant recipients, or cancer patients on chemotherapy, the cysts can reactivate. Bradyzoites then revert to fast-dividing tachyzoites. This shift triggers severe complications, including brain inflammation (toxoplasmic encephalitis) and eye damage that can progress to blindness. Congenital transmission during pregnancy can also harm developing fetuses.
Until now, the cyst stage has been a black box for drug developers no approved treatments eliminate established cysts.
Cracking Open the Cyst with New Evolving Tech
Studying cysts has always been tough. They’re small, slow-growing, wrapped in a tough wall, and hard to replicate reliably in lab dishes. Traditional cell cultures often produce incomplete or artificial versions of bradyzoites.
The UC Riverside team overcame these hurdles using a realistic mouse model of natural infection. They isolated parasites directly from brain cysts in living animals (in vivo) and applied single-cell RNA sequencing a powerful technique that reads the genetic activity of individual cells. This let them profile thousands of bradyzoites one by one, revealing their molecular identities.
The results were striking: instead of one uniform type of bradyzoite, each cyst contains at least five distinct subtypes. These aren’t minor random differences—they represent specialized populations with different gene expression profiles and likely different jobs.
“Each cyst turns out to be a bustling microscopic community with specialized roles not a passive shelter, but an active hub.”
— From the Nature Communications study
- Some subtypes appear geared toward long-term persistence and survival within the host.
- Others may support eventual transmission (e.g., if eaten by a new host).
- Certain ones seem “primed” for reactivation, ready to switch back to the aggressive tachyzoite form under the right conditions (like immune suppression).
The cyst, long imagined as a passive shelter, is actually an active hub. Within it, multiple parasite subtypes interact to sustain chronic infection.
A particularly important discovery emerged from this work. One major subtype dominates real, chronic mouse infections, yet it is completely absent from standard laboratory (in vitro) models of bradyzoite development. This mismatch likely explains a long-standing problem. Drugs that appear effective in petri dishes often fail in animals or humans because they are tested against an incomplete version of the parasite.
“What was once dismissed as dormancy now looks like a sophisticated, multi-role ecosystem.”
Physically, the cysts are up to about 80 microns across (visible under a microscope but tiny to the naked eye), each potentially harboring hundreds of these five-micron-long bradyzoites.
Why This Matters and What’s Next
This work reframes the cyst as the true “control center” of Toxoplasma‘s long-term strategy. By mapping the molecular signatures of these subtypes especially those prone to reactivation scientists can now design smarter, targeted therapies. These approaches focus on the vulnerable “trigger” populations that reside inside the cyst.
The findings also carry important implications for prevention and drug development. They could help reduce the risk of congenital toxoplasmosis. In addition, they highlight a critical flaw in current drug screening. Future tests must incorporate more realistic, in vivo–derived parasites to capture the full diversity present during chronic infection.
Reference
Ulu, A., Srivastava, S., Kachour, N., Le, B. H., White, M. W., & Wilson, E. H. (2026). Bradyzoite subtypes rule the crossroads of Toxoplasma development. Nature Communications.
