Global study warns hepatitis B care must be overhauled to meet WHO 2030 elimination targets
University of Liverpool
The first global systematic review and meta-analysis of hepatitis B care has found critical patient losses at every step of care, calling for decentralised, integrated models to improve diagnosis, treatment, and patient retention.
Published in The Lancet Gastroenterology & Hepatology, the findings reveal that current hepatitis B service delivery models are failing to keep patients engaged in lifelong care — threatening the world’s ability to meet the World Health Organisation (WHO) 2030 hepatitis B elimination goals.
The WHO-commissioned review was conducted by researchers from the University of Liverpool and Imperial College London in collaboration with colleagues from The Gambia, India, the Philippines, the USA, and Vietnam. It analysed data from more than 1.7 million people with chronic hepatitis B across 50 countries and found significant drop-offs in diagnosis, treatment initiation, and long-term retention, even in the best-performing systems.
Key findings of the review show that:
- Specialist-led hospital care achieved the best results but still showed major gaps: fewer than 75% of patients were assessed for treatment eligibility; of those eligible, only 78% began therapy. Retention plummeted among those not receiving treatment.
- Primary care, co-managed care, and passive referral models fared worse, with lower rates of assessment, initiation of care, and retention once in care.
- Postpartum care for women diagnosed during antenatal care had particularly low follow-up rates.
- Community screening with active linkage to specialist care achieved high treatment initiation rates for eligible patients.
Lead author Dr Alexander Stockdale from the University of Liverpool, said: “This is the first global review to map our progress across the hepatitis B care pathway. Without urgent changes, millions will miss out on lifesaving treatment. Many patients are not being fully assessed or being started on antivirals when they could benefit, and far too many are lost to follow-up over time. Strengthening primary care in low- and middle-income countries is essential to prevent hepatitis B-related deaths — already estimated at 1.1 million in 2022.”
Senior author Professor Philippa Easterbrook (Imperial College London; formerly WHO Global Hepatitis Programme) added: “WHO’s 2024 guidelines were a major step forward, expanding treatment eligibility to nearly half of all people living with chronic hepatitis B. But simplifying criteria alone is not enough. Too many still lack access to services, and even where clinics exist, patients often fall through the cracks.
“We need simple, decentralised models — integrating hepatitis B into primary care or existing HIV and chronic disease services. The HIV response has proven that streamlined care can achieve over 90% diagnosis, treatment initiation, and retention. It’s time we applied those lessons to hepatitis B.”
Professor Easterbrook added: “An integrated approach is even more pressing given the recent reductions in funding through USAID and the US President’s Emergency Plan for AIDS Relief (PEPFAR) for health programmes in LMICs”
The researchers have made the following recommendations:
- Decentralise care into primary health facilities and integrate with HIV/non-communicable disease (NCD) clinics.
- Remove financial barriers by eliminating out-of-pocket costs for testing and treatment.
- Accelerate access through same-day assessment and treatment initiation.
- Improve long-term engagement using adherence and retention strategies from HIV care programmes.
Click here to read the full review.
Journal
The Lancet Gastroenterology & Hepatology
Method of Research
Meta-analysis
Subject of Research
People
New antibody therapy shows promise in reducing Zika virus in reproductive tissues
University of Alabama at Birmingham
A new study from the University of Alabama at Birmingham reveals that an antibody originally designed to fight dengue virus may also block the spread of Zika virus in vulnerable areas of the body — including the reproductive organs. The findings, published today in the Journal of Virology, offer new hope in the fight against a virus that has affected more than 80 countries since 2007 and poses serious risks to pregnant women and their babies.
What makes Zika especially dangerous is its ability to hide in protected areas of the body, including the brain, eyes and reproductive organs, where it can linger undetected. Even more troubling, Zika can be passed through sex or from a pregnant mother to her baby, potentially leading to severe birth defects.
In this new study, led by J. Victor Garcia, Ph.D., and Angela Wahl, Ph.D., in the Department of Microbiology at UAB, scientists tested the effectiveness of the C10 dengue virus antibody using a novel preclinical in vivo model. They found that a single dose of C10 administered before Zika virus exposure:
- Significantly suppressed viral replication in blood and tissues
- Prevented viral shedding in saliva and reproductive secretions
- Reduced viral levels in the brain, eyes and reproductive organs
- Improved survival rates in preclinical models
“Our work lays the foundation for deploying passive immunization strategies in high-risk populations,” Garcia said. “This could be a game-changer in outbreak response, especially in regions where Zika is endemic or resurging.”
Researchers evaluated the antiviral compound DFMA (7-deaza-2’-C-methyladenosine), which significantly reduced viremia and prolonged survival in a preclinical model.
“This study provides compelling evidence that antibody-based therapies can be used to reduce systemic infection and target the very tissues where Zika hides and causes the most damage,” Wahl said. “This is especially important for protecting pregnant individuals and preventing sexual transmission during future outbreaks.”
Currently, there are no approved treatments for Zika virus. This research marks a significant step toward developing effective countermeasures against future outbreaks.
Other collaborating institutions in this study include the University of North Carolina at Chapel Hill and Emory University.
Funding for this study was provided by the National Institutes of Health grant AI106695 (R.S.B.).
Journal
Journal of Virology
Article Title
Envelope-dimer epitope 1 (EDE1) antibody (C10) treatment significantly reduces Zika virus replication in the male and female reproductive tracts
Article Publication Date
18-Aug-2025
Study reveals how HPV reprograms immune cells to help cancer grow
Using animal models, researchers from the USC Norris Comprehensive Cancer Center at the Keck School of Medicine of USC uncovered how cervical and throat cancers linked to the human papillomavirus evade the immune system, opening the door to new treatment
The most common cancer-causing strain of human papillomavirus (HPV), HPV16, undermines the body’s defenses by reprogramming immune cells surrounding the tumor, according to new research from the Keck School of Medicine of USC. In mice, blocking this process boosted the ability of experimental treatments for HPV to eliminate cancer cells. The results were just published in the Journal for ImmunoTherapy of Cancer.
HPV16 causes more than half of cervical cancer cases and roughly 90% of HPV-linked throat cancers. It can be neutralized with the preventive vaccine Gardasil-9, but only if vaccination occurs prior to HPV exposure.
Researchers are now working to develop “therapeutic vaccines,” which can be taken after HPV exposure—for instance, following an abnormal pap smear or cancer diagnosis—to trigger an immune response against infected cells by T-cells, a type of “fighter” cell that helps defend the body from disease. But these vaccines, now in clinical trials, have limited effectiveness—and the new study helps explain why.
The research, funded in part by the National Institutes of Health, focuses on a signaling protein in the immune system with inflammatory properties called Interleukin-23 or IL-23. While IL-23 was previously implicated in cervical and throat cancers, its exact role was unclear. In a series of tests in mice and cell cultures, USC researchers found that two HPV proteins, E6 and E7, prompt nearby cells to release IL-23, which in turns prevents the body’s T-cells from attacking the tumor.
“In order to eliminate the cancer, T-cells need to proliferate and destroy infected cells. But IL-23 stops them from working effectively, so the tumor keeps growing,” said the study’s senior author, W. Martin Kast, PhD, professor of molecular microbiology & immunology, obstetrics & gynecology, and otolaryngology and Walter A. Richter Cancer Research Chair at the Keck School of Medicine.
Kast and his colleagues found that blocking IL-23 made an HPV therapeutic vaccine more effective because it let T-cells do their job: find and kill cancer. Antibodies that inhibit IL-23 are already FDA-approved for treating psoriasis and other conditions, offering a clear and potentially quick path to use in cancer treatment when they are combined with therapeutic vaccines.
“The fact that these antibodies are already FDA-approved for something else makes this approach promising—and it also allows for rapid translation into the clinic,” said Kast, who also co-leads the Tumor Microenvironment Program at the USC Norris Comprehensive Cancer Center.
The role of IL-23
Researchers used a combination of cell cultures, mouse studies and genomic analyses to uncover IL-23’s role in cancers caused by HPV16.
First, they implanted mice with HPV16 tumors, then delivered a therapeutic vaccine that caused the mice to develop specialized T-cells for fighting the tumor. They extracted these T-cells, then combined them with IL-23. When IL-23 was present, the T-cells had reduced capacity to multiply and destroy cancerous cells.
The researchers then gave IL-23 neutralizing antibodies to mice with HPV16 tumors. Blocking IL-23 increased the number of T-cells around the tumor that could recognize and kill cancer. When combined with the HPV therapeutic vaccine, this approach triggered a stronger immune response and led to longer survival than either treatment on its own.
Researchers also analyzed the RNA and chromatin (the DNA and proteins that control gene activity) of tumor cells to reveal precisely how HPV’s E6 and E7 proteins increase IL-23 production. Understanding the biological mechanism is a key step toward better treatments for HPV-linked cancers, Kast said.
New strategies for treatment
The study offers insight into why therapeutic vaccines for HPV, now in clinical trials, have had limited success.
“Therapeutic vaccines do prompt the immune system to create HPV-specific T-cells, but they don’t work well—and now we have an idea why,” Kast said.
Combining experimental vaccines with IL-23 neutralizing antibodies could significantly increase their effectiveness, he added. He and his team are now developing their own therapeutic vaccine, which they will test in combination with antibodies that block IL-23.
The findings may have implications for cancers not related to HPV, such as testicular and bladder cancers, where IL-23 is also found at high levels. Further research is needed to clarify what role IL-23 plays in those diseases, the researchers said.
About this research
In addition to Kast, the study’s other authors are Ruben Prins, Daniel Fernandez and Omid Akbari from the Department of Molecular Microbiology and Immunology and the USC Norris Comprehensive Cancer Center, Keck School of Medicine of USC, University of Southern California; and Diane Da Silva from the Department of Obstetrics & Gynecology and the USC Norris Comprehensive Cancer Center, Keck School of Medicine of USC, University of Southern California.
This work was supported by the National Institutes of Health [R01 CA074397], the American Association of Immunologists, R.F. Brennan, S. Bloch and I.Y. Khandros.
Journal
Journal for ImmunoTherapy of Cancer
Method of Research
Experimental study
Subject of Research
Animals
Article Title
HPV16 E6 AND E7 EXPRESSING CANCER CELLS SUPPRESS THE ANTI-TUMOR IMMUNE RESPONSE BY UPREGULATING KLF2 MEDIATED IL-23 EXPRESSION IN MACROPHAGES
Article Publication Date
19-Aug-2025
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