Medical Bulletin 25/December/2025

The Nipah virus is a highly lethal zoonotic disease first identified in 1999 in Malaysia and now causes annual outbreaks across South and Southeast Asia, including India. Transmitted from animals such as fruit bats to humans—and sometimes between people—it can cause severe respiratory distress and brain inflammation. The World Health Organization lists Nipah as a high-priority pathogen needing urgent research because no approved vaccines or antiviral treatments currently exist.

To evaluate safety and immune performance, researchers conducted a randomized, double blind, placebo-controlled trial involving 192 healthy adults aged 18 to 49 years. Participants were divided into groups receiving single or double doses of HeV sG V at varying strengths, or placebo, with doses spaced 28 days apart. Researchers measured neutralizing antibody titers—a key sign of protection—alongside adverse reactions in the weeks following vaccination.

The results were encouraging. All dose regimens were safe and well tolerated, with only mild to moderate injection site pain reported and no serious side effects or hospitalizations. More importantly, participants who received two doses of the 100 microgram formulation developed the strongest antibody response, showing a dramatic rise in neutralizing antibodies within one month, which persisted long after the second dose. A single shot, however, produced only limited immunity.

Experts from India’s ICMR–National Institute of Virology, writing in an accompanying commentary, called the study a “milestone” in Nipah vaccine development and urged larger phase 2 trials to confirm protection levels.

If subsequent trials prove successful, the HeV sG V candidate could become the first weapon against a virus that has repeatedly triggered deadly outbreaks across Asia—offering a real chance to prevent future health emergencies before they begin.

REFERENCE: Frenck, Robert W et al.; Safety and immunogenicity of a Nipah virus vaccine (HeV-sG-V) in adults: a single-centre, randomised, observer-blind, placebo-controlled, phase 1 study; The Lancet, Volume 406, Issue 10521, 2792 – 2803; doi: 10.1016/S0140-6736(25)01390-X

Fixing disrupted body clock rhythms found to lower cancer risk: Study

Cancer doesn’t just grow—it disrupts the body’s natural rhythm. A groundbreaking study from Cold Spring Harbor Laboratory, led by Dr. Jeremy Borniger, has found that tumors in mice can disturb the body’s daily hormone cycles, and that restoring these rhythms can dramatically shrink tumor growth. The findings, published in Nature Metabolism, point to a fascinating new approach to cancer therapy: treating the body’s internal clock, not just the tumor itself.

Every cell in the body follows a circadian rhythm, a 24 hour biological cycle that aligns behavior, metabolism, and hormone production with day and night. This rhythmic balance is controlled by a communication network called the hypothalamic pituitary adrenal (HPA) axis, which regulates secretion of the stress hormone corticosterone (the counterpart of cortisol in humans). Chronic disruption of these cycles—through stress, poor sleep, or diet—has long been associated with metabolic and immune dysfunction.

To explore how cancer interferes with this system, the researchers developed a mouse model of breast cancer and closely monitored corticosterone levels around the clock. Within just three days of inducing the cancer, even before tumors were physically detectable, corticosterone rhythms were cut in half, showing blunted day night variation. When the scientists examined the brain’s hypothalamus, they found that crucial rhythm generating neurons had become hyperactive yet low output, disrupting their ability to send proper timing signals.

Using chemogenetic technology, the team selectively stimulated these hypothalamic neurons at different times of day. Remarkably, when they activated the neurons at a specific circadian window—just before the light to dark transition—the mice’s hormonal rhythms returned to normal. This re synchronization of corticosterone release strengthened anti cancer immune responses, increasing tumor infiltrating T cells and causing tumors to shrink significantly. But when neuron activity was restored at the wrong time of day, the effect disappeared, underscoring how tightly linked circadian timing is to cancer control.

The results suggest that synchronizing biological clocks—through “chronotherapy” or timed treatment—could enhance existing cancer treatments while lowering their toxicity. Future research will explore exactly how tumors disrupt circadian communication and whether similar strategies can be adapted for human cancers.

REFERENCE: Sahar, S., Sassone-Corsi, P. Metabolism and cancer: the circadian clock connection. Nat Rev Cancer 9, 886–896 (2009). https://doi.org/10.1038/nrc2747

Father’s microplastic exposure linked to metabolic disorders in offspring, study finds

Plastic pollution may be changing more than our environment—it could be altering the health of future generations. A new study from the University of California, Riverside, published in the Journal of the Endocrine Society, reveals for the first time that a father’s exposure to microplastics (MPs) can disrupt metabolism in his offspring. Conducted with laboratory mice, the research shows that fathers exposed to microscopic plastic particles can pass on a higher risk of diabetes and metabolic disorders, even without any changes in their own diet.

Microplastics—tiny fragments less than 5 millimeters wide—form when consumer products and industrial waste break down. They’ve already been found in human organs and reproductive systems, raising alarm about their potential health effects. But while previous studies focused mostly on maternal exposure, this work led by Dr. Changcheng Zhou of UCR’s School of Medicine extends concern to fathers.

In the experiment, male mice were first exposed to environmentally relevant levels of MPs while being fed a normal diet. These males were then bred with unexposed females, and their offspring (F1 generation) were given a high fat diet to mimic modern eating habits and reveal hidden metabolic traits. Although the fathers showed no signs of illness, their female offspring developed diabetic like symptoms, while male offspring experienced reduced fat mass but no diabetes.

Detailed genetic analysis of liver tissue from the affected females showed increased activity of inflammatory and pro diabetic genes, patterns previously linked to type 2 diabetes in humans. To understand how these effects were transmitted, the researchers used an advanced screening tool known as PANDORA seq, a next generation sequencing platform developed at UCR. They found that microplastic exposure had changed the non coding RNA content of sperm, particularly tRNA derived and rRNA derived small RNAs—molecular messengers that regulate gene expression during early development.

The findings suggest that microplastics can leave a molecular “fingerprint” in sperm, priming the next generation for disease. Although the study was done in animals, Zhou believes the implications for humans are significant.

REFERENCE: Seung Hyun Park, Jianfei Pan, Xudong Zhang, Ting-An Lin, Sijie Tang, Xiuchun Li, Sihem Cheloufi, Qi Chen, Tong Zhou, Changcheng Zhou, Paternal microplastic exposure alters sperm small non-coding RNAs and affects offspring metabolic health in mice, Journal of the Endocrine Society, 2025;, bvaf214, https://doi.org/10.1210/jendso/bvaf214