A Common Genetic Thread Between Humans and Macaques 

A rare form of inherited blindness that affects humans has now been identified in rhesus macaques at the California National Primate Research Center (CNPRC) at the University of California, Davis. Published in the Proceedings of the National Academy of Sciences, researchers found that some monkeys at the center naturally carry a mutation in a gene called OPA1, and that mutation causes eye changes remarkably similar to those seen in people with a disease called autosomal dominant optic atrophy, or ADOA. That shared biology could be a key to finding treatments that don’t yet exist. 

Understanding ADOA  

ADOA is a genetic condition that gradually damages the optic nerve, the cable that carries visual information from the eye to the brain. Over time, people with ADOA develop blind spots and can lose significant vision. It affects about 3 in 100,000 people worldwide, there is no treatment available, and many patients are diagnosed between the ages of 10 and 30, making it a notable cause of vision loss in young people. 

The disease traces back to a mutation in the OPA1 gene, which disrupts the normal function of mitochondria — the structures inside cells that produce energy. While every cell in the body relies on mitochondria, the long, delicate nerve fibers that run from the retina to the brain are especially sensitive to disruptions in energy supply. That’s why the eyes are the most affected. 

An Unexpected Discovery Born from a Pandemic Pivot 

This research came together in an unexpected way. Tracy Jaggers, then a veterinary student at Western University College of Veterinary Medicine, had planned a behavioral study at the primate center until the COVID-19 pandemic shut down her efforts. Her supervisor, Sara Thomasy, a professor of comparative ophthalmology at UC Davis, redirected her to something else: a large genetic dataset of nearly 1,800 animals at the center, compiled through a collaboration with Baylor College of Medicine. The OPA1 mutation had already been flagged in that data, but no one had yet connected it to eye disease. 

Thomasy admitted she wasn’t expecting much. “I actually expected it to be a negative study,” she said. “But Tracy was so tenacious with the data.” 

Connecting the Mutation to the Disease 

Using eye imaging tools borrowed from human medicine, Jaggers and Thomasy examined the monkeys more closely, and found that an animal showing eye abnormalities also carried a copy of the OPA1 mutation. That finding was enough to secure a grant from the National Eye Institute, allowing the team to dig deeper and establish a dedicated breeding colony to study the disease over time. 

Researchers could now observe how ADOA progresses across an animal’s lifetime and compare what happens in animals with one copy of the mutation versus two. 

A Model for Future Treatments 

Having a reliable animal model means researchers can now begin testing potential treatments and gene therapies in a way that simply wasn’t possible before. Thomasy and colleagues at UC Davis Health have also identified macaque versions of other inherited human eye diseases, including achromatopsia, which destroys the cells responsible for color vision and age-related macular degeneration.  

The study was supported by the National Institutes of Health and involved researchers from UC Davis, Baylor College of Medicine, the University of Wisconsin–Madison and the Legacy Devers Eye Institute in Portland, Oregon. This study brings hope for patients with ADOA by opening an avenue for treatment.  

New Concern for Newborns

Researchers from the University of Wisconsin–Madison, in collaboration with the National Primate Research Center (NPRC), found that Zika exposure during pregnancy may cause developmental problems even when babies are born without obvious symptoms. The research suggests that a healthy-looking newborn may still face hidden challenges later in infancy.

The Problems Zika Brings

Zika virus is known to cause severe birth defects such as brain damage and microcephaly. However, little is understood about why 30% of babies born without physical symptoms experience developmental problems, including vision and hearing loss. To close that gap, researchers studied pregnant rhesus macaque monkeys exposed to Zika virus early in pregnancy, and followed the resulting infants for one year through behavioral tests, vision and hearing assessments and social observations.

What the Study Found

Although the infant monkeys’ eyes appeared structurally normal, researchers found disruptions in how the eyes communicated with the brain — an issue known as cortical visual dysfunction. Early visual delays appeared as early as three months of age. However, those differences resolved by the time the infants were 12 months old. Researchers also found that hearing loss appeared more often in Zika-exposed infants than in unexposed animals, though the difference was not statistically significant. Together, these findings suggest that early sensory disruptions may be a signal worth watching, even when they don’t persist.

Why Standard Screening May Not Be Enough

One of the study’s most significant findings was what didn’t predict risk. Maternal virus levels, placental infection and antibody responses did not predict which infants experienced developmental differences, suggesting that common maternal biomarkers are poor indicators of a child’s long-term risk. As study co-author and UW–Madison pediatrics professor Emma Mohr put it, “We couldn’t predict those outcomes from the mother’s infection characteristics, which is a problem if we’re trying to identify which babies need closer follow-up.”

What This Means for Families

One of the biggest takeaways is that babies exposed to Zika may need long-term developmental monitoring, even if they seem healthy at birth. Routine checkups may not catch the subtle problems that can affect learning, behavior and social development later on in life. Early screening can help families and doctors identify concerns sooner and connect children with support.

Why Prevention Still Matters

There is no vaccine for Zika, so prevention remains the best defense. Avoiding mosquito bites, using repellent, wearing protective clothing and reducing mosquito breeding sites are still important steps. For pregnant people and families planning a pregnancy, those precautions matter even more.

Even after the fever and cough are gone, some people continue to feel unwell following a case of COVID-19 or seasonal flu.  Tulane National Biomedical Research Center (NBRC) scientist Dr. Xuebin Qin and colleagues set out to understand which long-term effects are shared between COVID-19 and the flu, and which may be unique to COVID-19.

The Study

Their new study, published in Frontiers in Immunology, compared how SARS-CoV-2 (the virus that causes COVID-19) and influenza affect the body after the acute infection has resolved. Using a carefully controlled mouse model, the team examined lung and brain tissue weeks after infection to identify what kind of biological “footprint” each virus leaves behind. While animal models cannot capture every aspect of human disease, they allow researchers to closely examine biological changes that are difficult to study in patients. The findings may help explain why both COVID-19 and the flu can leave behind lasting lung problems, while long COVID is more often linked to neurological symptoms such as brain fog, fatigue and mood changes.

When researchers studied the lungs, they saw a similar pattern after both infections. Immune cells remained more active than normal instead of fully standing down, and there was an increased buildup of collagen, a protein associated with scarring. These changes can stiffen lung tissue and make breathing feel harder, offering a potential biological explanation for why some people have persistent shortness of breath after respiratory infections.

What Was Discovered

A key difference emerged when the team examined how the lungs were trying to heal. After influenza, the lungs showed signs of switching into repair mode: specialized cells moved into damaged areas to rebuild the lining of the airways. After COVID-19, that repair response appeared to be limited. This suggests that SARS-CoV-2 may interfere with the lung’s natural healing process, potentially setting the stage for longer recovery and lasting respiratory symptoms.

The most striking findings came from the brain. Even though neither virus was detectable in brain tissue at the time of analysis, mice that had recovered from COVID-19 still showed signs of ongoing brain inflammation. The researchers also observed small areas of bleeding earlier in the infection, pointing to potential damage to tiny blood vessels.

Gene expression analysis revealed that inflammatory signaling remained elevated, and that key pathways related to serotonin and dopamine regulation were disrupted. These chemical systems are closely tied to mood, cognition and energy levels, which are frequently affected in people with long COVID. In contrast, brains from influenza-infected animals showed far fewer of these persistent changes.

“In both infections, we observed lasting lung injury,” Qin noted. “But long-term effects in the brain were unique to SARS-CoV-2. That distinction is critical to understanding long COVID.”

Connecting Infection, Blood Vessels and The Brain

The findings suggest that inflammation and damage to small blood vessels in the brain may play a role in long-lasting neurological symptoms. Even without the virus present, these changes can affect how brain cells communicate.

By clearly defining these biological changes, researchers at Tulane NBRC are helping to create a roadmap for future clinical studies. The patterns they identified could guide how clinicians monitor patients after infection, which biomarkers to track, and which pathways might be most promising for new therapies aimed at preventing or reducing lasting damage.

Why This Matters for Patients and Future Therapies

By directly comparing COVID-19 with flu in the same experimental framework, Tulane NBRC investigators provide a clearer picture of which long-term issues are shared across severe respiratory infections, and which are specific to SARS-CoV-2. That knowledge can help clinicians and scientists focus their efforts on where they are most likely to make a difference for patients still waiting to feel fully recovered.

Measles is Making a Comeback

Measles was declared eliminated in the U.S. in 2000, but that progress is now at risk. As vaccination rates have dropped, measles cases have risen, with the country seeing the highest levels since 1991. The disease remains highly contagious and can lead to serious complications, especially for young children.

Why Explore a Treatment?

The MMR vaccine is highly effective and remains the best protection against measles, and it is still highly effective. With increasing cases, researchers are exploring a treatment option for people who are infected.

What Researchers are Testing

At Texas Biomedical Research Institute in San Antonio, researchers will test a potential measles treatment using monoclonal antibodies. This lab-made protein is designed to interfere with the virus before it can enter cells and spread.

Unlike many antiviral drugs which target viruses after they have already entered cells, monoclonal antibodies can block infection earlier in the process. They attach to specific parts of the virus and stop it from getting into the body’s cells. Monoclonal antibodies may also help reduce viral load and support the immune response after infection has begun.

Next Steps

The antibody being studied, called mAb 77, was developed by researchers at the La Jolla Institute for Immunology and Columbia University. It showed promise in lab and rodent studies, and Texas Biomed will now test it in juvenile rhesus monkeys. If those results are consistent, the treatment could eventually move into human clinical trials.

Will this Treatment Replace Vaccines?

Measles once caused millions of deaths each year before the vaccine became widely available. Today, the vaccine can prevent most cases after two doses. Researchers say a treatment could be helpful especially for those who are immunocompromised or too young to be vaccinated, but the larger lesson is clear: vaccination remains the simplest and most effective way to stop measles from spreading in the first place.

Cytomegalovirus (CMV) is one of the most common viruses people encounter, often causing mild or unnoticeable symptoms in healthy adults and children. However, when a person contracts a first-time CMV infection during pregnancy, the virus can cross the placenta and pose serious risks to the developing fetus, including lifelong hearing loss and neurodevelopmental problems. CMV is the world’s most commonly transmitted mother-to-child infection, yet the mechanisms of how this happens across pregnancy have been poorly understood. 

To shed light on this critical gap, researchers at the Tulane National Biomedical Research Center (Tulane NBRC) conducted a study using a nonhuman primate model that closely mirrors human pregnancy. This model allows scientists to observe how the virus interacts with the immune system and the placenta in a living system – something that can’t be replicated in a non-animal model (NAM). Researchers followed pregnancies in animals that encountered the virus for the first time in the second trimester, monitoring maternal health, placental tissues and fetal development over time. 

The research team led by Dr. Amitinder Kaur found that CMV did not behave the same way in every pregnancy. Some pregnancies showed brief or low‑level signs of infection, while others had more extensive viral involvement. Across almost all cases, however, the virus was detected in the placenta, even when fetal tissues showed little or no virus. Notably, pregnancies with higher levels of virus in placental tissues tended to have smaller fetuses at birth, suggesting that the virus may affect fetal growth even without direct fetal infection.  

By comparing immune markers in mothers and fetuses, the researchers also identified patterns that may predict a higher risk of transmission. Elevated levels of certain inflammatory signals and changes in other immune factors were linked to cases where the virus crossed the placenta more readily. These potential biomarkers could one day help clinicians identify which pregnancies need closer monitoring or targeted interventions.  

Why it matters: Congenital CMV is a major public health concern because there is currently no approved vaccine to prevent it, and existing strategies can’t reliably stop transmission. By mapping how CMV crosses the placenta and influences fetal outcomes, this work from Tulane NBRC lays crucial groundwork for identifying at-risk pregnancies and informing the development of vaccines or other preventive approaches in the future. 

A new investigational treatment for Parkinson’s disease is showing early promise in its first human clinical trial, thanks in part to foundational work at the University of Wisconsin–Madison and the Wisconsin National Primate Research Center (WNPRC).  

Parkinson’s disease gradually kills dopaminergic neurons that produce the chemical messenger dopamine, disrupting communication between brain regions that control movement. Standard treatments such as L‑DOPA can boost dopamine levels and reduce symptoms, but their effectiveness often wanes over time, and they do not replace the lost cells. 

In the Phase 1/2a ASPIRO trial, run by biotechnology company Aspen Neuroscience, patients receive transplants of dopamine-producing neurons grown from their own cells, which are then delivered to affected areas of the brain. 

Aspen Neuroscience recently announced that it will enroll a third patient cohort after reporting that participants are safely tolerating the treatment and showing encouraging improvements in Parkinson’s symptoms. According to the company, early data from the first four patients indicate that intracranial delivery of these cells is safe and well tolerated, with both patient-reported and clinician-reported measures showing positive results. Unlike typical organ transplants, because the neurons are derived from each patient’s own induced pluripotent stem cells—a fully autologous approach—no long-term immunosuppressive drugs are required. 

Although UW–Madison is not a clinical site for ASPIRO, scientists at the university and WNPRC played a key role in getting the therapy ready for first-in-human testing. In 2024, a team led by UW–Madison medical physics professor and WNPRC investigator Marina Emborg, M.D., Ph.D., successfully transplanted human progenitor cells into the brains of macaque monkeys. These progenitors were programmed to become dopamine-producing neurons, the same type of cells lost in Parkinson’s disease. Aspen supplied the human cell lines and specialized delivery equipment, while the Emborg lab optimized the surgical approach in nonhuman primates. 

Aspen scientists and WNPRC researchers refined a delivery method that uses MRI-guided neurosurgical techniques to place very small volumes of cells—just a few microliters at a time—into the areas of the brain where they are needed. The 2024 study in macaques focused on demonstrating that Aspen’s human cells could be delivered safely and effectively with fewer surgical passes, reducing risk while still reaching the target area of the brain. Results from this work, published in the Journal of Neurosurgery, supported Aspen’s successful application to begin the ASPIRO trial. 

The ASPIO trial research builds on earlier successes at UW–Madison, where Dr. Emborg and Wisconsin School of Medicine and Public Health scientist Su‑Chun Zhang, M.D., Ph.D., previously reversed Parkinson’s-like symptoms in nonhuman primates using an autologous cell graft approach. Together, these studies helped validate the concept that individualized cell replacement can restore function in a Parkinson’s model and informed critical details such as cell preparation, quality control and surgical logistics. 

For Dr. Emborg and her colleagues at the Wisconsin National Primate Research Center, seeing the first human patients receive the therapy has been a powerful milestone. Years of iterative work in nonhuman primates—testing cell lines, refining delivery tools and optimizing postoperative care—directly shaped how the ASPIRO trial is conducted today. The early human results offer hope that this carefully developed approach could one day provide people with Parkinson’s disease a new option that goes beyond symptom management to address the underlying cell loss. 

As the ASPIRO trial progresses, the partnership between Aspen Neuroscience, UW–Madison and WNPRC underscores how translational nonhuman primate research can help bridge the gap between laboratory discoveries and first-in-human therapies, particularly for complex neurological diseases. 

Today the NPRCs led a coordinated response to voice concerns about a recent CDC plan to transfer approximately 160 macaques to the Born Free USA Primate Sanctuary.

In collaboration with more than 20 scientific, veterinary and biomedical research organizations, institutions and others, the NPRCs sent a letter to Centers for Disease Control and Prevention Director Dr. Jay Bhattacharya requesting a transparent retirement plan that prioritizes the welfare, safety, behavioral stability and long-term quality of life for the macaques. The current CDC plan is inconsistent with best practices for introducing adult macaques into a large social group setting, putting their welfare at risk.

The letter also calls into question the sanctuary’s staffing and expertise to safely carry out a transition of this magnitude and complexity. In addition, the signatories raise additional concerns regarding the validity and accuracy of the CDC’s sole source justification for selecting Born Free as the only qualified retirement option.

The signatories emphasize the welfare of these macaques must be the overriding priority in any retirement decision.

Read the full letter here.

A study published in Nature may point to a promising new path in the fight against pediatric HIV. Led by Mauricio A. Martins, PhD, and Amir Ardeshir, DVM, MPVM, PhD, with key work conducted at the California National Primate Research Center and contributions from Tulane National Biomedical Research Center, researchers showed that a single gene therapy injection given at birth could provide long-term protection against HIV by taking advantage of a unique window when a newborn’s immune system is more tolerant.

The study used an adeno-associated virus, or AAV, to deliver genetic instructions for producing broadly neutralizing antibodies, which are powerful antibodies capable of recognizing multiple strains of HIV. The therapy essentially turns muscle cells into antibody-producing “micro-factories,” offering a potential way to provide lasting protection without repeated treatments or boosters.

Timing proved critical. Infant rhesus macaques treated at birth maintained antibody expression for more than three years and were protected in models that mimic HIV transmission through breastfeeding and sexual exposure. Older recipients were less protected, underscoring the importance of early intervention and the role of the newborn immune system’s natural window of tolerance.

This approach could help address mother-to-child HIV transmission, which remains a major global health challenge, especially in regions where access to follow-up care and long-term treatment can be limited. A one-time intervention given at birth could offer a more practical and scalable prevention strategy for infants at risk.

More research is needed before this approach can be tested in humans, including studies to determine how it may work against different HIV strains. Still, the findings offer hope for a cost-effective, long-lasting strategy to help reduce pediatric HIV and may eventually inform similar approaches for other infectious diseases, including malaria.

Oregon Health & Science University (OHSU) is shedding light on how vitamin C supplementation during pregnancy could help protect babies from some of the harmful effects of maternal smoking. 

The Problem: Smoking and Pregnancy 

Smoking during pregnancy is known to harm fetal development, particularly the lungs, brain, kidneys, and blood vessels. Nicotine crosses the placenta, directly impacting the growing fetus and often leading to long-term respiratory issues for children born to mothers who smoke. 

The Study: Can Vitamin C Help? 

Researchers at OHSU, led by Dr. Eliot Spindel and Dr. Cindy McEvoy, conducted a clinical trial involving pregnant women who were unable to quit smoking. All participants received a standard prenatal vitamin with 60 mg of vitamin C, but one group also received an additional 500 mg of vitamin C daily. 

Key Findings: Improved Placental Blood Flow 

Using Doppler ultrasound, the team measured blood flow in the umbilical cord. They found that vitamin C supplementation improved placental blood flow in smokers, bringing it closer to the levels seen in nonsmokers. Examining placentas after birth, researchers also observed improved blood vessel development and overall placental function in babies whose mothers received extra vitamin C. 

“It is clear that placental development is abnormal in women who smoke. …In this human clinical trial, it is important to note that some, but not all, abnormalities were prevented by vitamin C intake,” said Dr. Spindel. 

Long-Term Benefits for Babies 

Follow-up studies showed that children born to mothers who took extra vitamin C had better lung function at 3 months, 12 months, and even at age 5 compared to those whose mothers did not receive the supplement. 

Limitations and Continued Risks 

While vitamin C supplementation improved some aspects of placental and fetal health, it did not prevent all the negative effects of smoking during pregnancy. Risks such as premature birth, reduced brain development, and stunted growth remain, and vitamin C does not address these issues. 

Why Not Just Quit Smoking? 

Despite public health efforts, more than half of women who smoke continue during pregnancy. Nicotine is highly addictive, and genetic factors can make quitting especially difficult for some individuals. Importantly, the study also notes that nicotine from vaping and other products likely poses similar risks to fetal development. 

What’s Next? 

Vitamin C supplementation during pregnancy may help mitigate some of the harm caused by smoking, particularly by improving placental blood flow and supporting better lung function in children. However, quitting smoking remains the best way to protect both maternal and fetal health.

Texas Biomedical Research Institute (Texas Biomed) has uncovered new insights into the lifespan of nonhuman primates in captivity. Dr. Hillary F. Huber and her team, including collaborators from Wake Forest University, have compiled the largest database to date on primate lifespans, challenging long-held assumptions and providing crucial information for future research. 

The study, which included data from 12 primate species across 15 institutes, including all seven National Primate Research Centers, revealed that the median lifespan for many primates used in biomedical research is lower than previously reported. For example, baboons, often thought to live up to 37.5 years, were found to have a maximum observed lifespan of 30 years in research settings, with a median age at death of just 11.5 years. 

This discrepancy highlights the importance of using median age rather than maximum lifespan when considering animal models for human aging research. As Dr. Huber points out, “Having a more accurate understanding of how long nonhuman primates live in captivity is essential for researchers to correctly correlate health and disease observations in primates to humans.” 

The study’s strict methodology—limited to animals with known birth dates and death dates who died naturally or were humanely euthanized after developing a serious disease such as cancer—ensures robust data. This approach provides a more accurate picture of primate health span – the length of healthy life free from major diseases – which aligns closely with current geroscience research focusing on improving quality of life throughout the human lifespan. 

The Southwest National Primate Research Center at Texas Biomed played a critical role in this study, contributing valuable data and expertise. This collaborative effort underscores the commitment of National Primate Research Centers to improve animal care, medical treatments and research methods – all supporting the broader goal of advancing animal and human health.