UCLA researchers have developed miniature organ models from human stem cells to investigate how hantaviruses infect the body and to search for potential treatments. The study, published in PLOS Pathogens, used organoids—3D models of lungs, hearts, and brains—to observe how different hantavirus strains behave in human tissues.
Hantaviruses are rare but can be deadly. They are spread by rodents and have been responsible for outbreaks worldwide since the 1950s. Mortality rates vary widely depending on the strain. Recent deaths in New Mexico and California have renewed concerns about these viruses.
Dr. Vaithi Arumugaswami, senior author of the study and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, said, “Hantaviruses pose a serious threat to public health, yet we know little about how they attack the human body. By creating human organoid systems, we can finally see how these viruses behave in lung, heart and brain tissue — and start to identify ways to stop them.”
Traditional studies often use animal models such as hamsters, but strict safety requirements make this challenging for hantaviruses. The UCLA team used stem cell-derived organoids to overcome these obstacles.
The research found that Andes virus—the only hantavirus known to spread between people—can infect all tested cell types: lung epithelial and endothelial cells, cardiomyocytes (heart muscle cells), and astrocytes (brain cells). Hantaan virus showed more selective infection patterns, while Sin Nombre virus was mainly limited to lung endothelial cells.
Arunachalam Ramaiah, co-senior author of the study, stated, “This is the first evidence that Andes virus can replicate efficiently in human lung organoids. It shows just how versatile — and dangerous — this virus can be.”
The study also revealed that Andes virus disrupts normal cellular metabolism. Infected lung cells experienced inflammation and injury along with disrupted cholesterol processing. In heart models, infection interfered with cell structure and normal rhythmic beating.
“The virus reprograms cell metabolism to favor its own survival,” said Arumugaswami. “That disruption may contribute to the severe lung and heart damage seen in patients.”
There are currently no approved treatments or vaccines for hantavirus infections. The UCLA team tested several compounds using their organoid system. Urolithin B—a natural substance found in some fruits and nuts—and favipiravir—an antiviral drug approved in Japan for influenza—both blocked Andes virus infection in lab tests.
“Two compounds, urolithin B and favipiravir, showed real promise in blocking Andes virus,” said Nikhil Chakravarty, a co-author of the study. “It’s early work, but it points us toward the possibility of new therapies where none currently exist.”
Although infections remain uncommon in the United States, experts warn that climate change could increase risk by bringing rodents into closer contact with humans.
Arjit Vijey Jeyachandran, first author of the paper at UCLA’s David Geffen School of Medicine, noted: “The impacts of climate change may bring people into more frequent contact with hantavirus carriers. That makes it even more important to understand how these viruses spread — and how we can stop them.”
The research received support from the National Institutes of Health.
