Viral hepatitis is an inflammatory liver disease caused by infection with any of the known hepatitis viruses—A, B, C, D, and E. Most of the global viral hepatitis burden is from hepatitis B and C, which affect 354 million people and result in 1.1 million deaths annually. The Centers for Disease Control and Prevention estimates that in 2020 there were 14,000 and 50,300 new acute infections of hepatitis B and C in the United States, respectively, while at least 880,000 people in the country were living with chronic (long-term) hepatitis B and 2.4 million people had chronic hepatitis C. About half of those with viral hepatitis are unaware of their infection. Chronic and persistent inflammation from the disease can lead to liver failure, cirrhosis, or liver cancer. Viral hepatitis affects all ages and there are pronounced inequities in disease outcomes in the United States. Hepatitis B and C disproportionately affect people living with HIV, and HIV increases the rate of complications and death in people with viral hepatitis.

On this World Hepatitis Day, the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, shares a snapshot of its investments in basic (laboratory), preclinical (laboratory/animal), and clinical (human) research to improve screening, prevention and treatment for hepatitis B and C. Scientists in the Hepatic Pathogenesis and Structural Virology sections of NIAID’s Laboratory of Infectious Diseases conduct basic and translational research to better understand hepatitis B and C disease progression, clarify the role of hepatitis viruses in liver cancer, and inform discovery of new vaccines, medicine and technologies. Both NIAID’s Division of AIDS (DAIDS) and the Division of Microbiology and Infectious Disease (DMID) support scientific programs focused on hepatitis B and C research and curative strategies, reflecting the widespread impact of viral hepatitis and the urgent need for safe and effective interventions.

Finding a hepatitis B cure.

More often than not, studies of human biology are conducted when the body is under duress from infection or disease. Now, as part of a larger effort to delineate what “healthy” looks like, two Stanford Medicine teams have unfurled detailed molecular maps of healthy human intestinal and placental tissues. The maps, which capture cell types, cell quantity and other cellular nuances, are just two of a collection of maps that will establish a cellular baseline for the majority of the human body, including where cells in certain tissues congregate, how tissues develop during pregnancy and how cell-to-cell interactions drive human biology.

The studies, which published in Nature on July 19, are part of a larger effort spearheaded by the Human Biomolecular Atlas Program — called HuBMAP — funded by the National Institutes of Health. It aims to fill gaps in our knowledge of how the human body works when it’s in tip-top shape. Dozens of teams from the United States and Europe contribute to the HuBMAP consortium.

“In research, we have a habit of studying things that are abnormal without really understanding what normal looks like,” said Michael Angelo, MD, PhD, an assistant professor of pathology who is also the co-chair of the HuBMAP steering committee. “That’s created a big gap in our knowledge. HuBMAP is the only effort that is systematically focusing on the spatial architecture of these tissues.”

Researchers have found that people with obstructive sleep apnea have an increased cardiovascular risk due to reduced blood oxygen levels, largely explained by interrupted breathing. Obstructive sleep apnea has long been associated with increased risk of cardiovascular issues, including heart attack, stroke, and death, but the findings from this study, published in the American Journal of Respiratory and Critical Care Medicine, show the mechanism mostly responsible for the link.

“These findings will help better characterize high-risk versions of obstructive sleep apnea,” said Ali Azarbarzin, Ph.D., a study author and director of the Sleep Apnea Health Outcomes Research Group at Brigham and Women’s Hospital and Harvard Medical School, Boston. “We think that including a higher-risk version of obstructive sleep apnea in a randomized clinical trial would hopefully show that treating sleep apnea could help prevent future cardiovascular outcomes.”

Researchers reviewed data from more than 4,500 middle-aged and older adults who participated in the Osteoporotic Fractures in Men Study (MrOS) and the Multi-Ethnic Study of Atherosclerosis (MESA), and sought to identify features of obstructive sleep apnea that could explain why some people were more likely than others to develop cardiovascular disease or related death.

Reduction in blood oxygen levels, largely attributed to blocked airways, emerges as a leading factor.

Researchers have found that people with obstructive sleep apnea have an increased cardiovascular risk due to reduced blood oxygen levels, largely explained by interrupted breathing. Obstructive sleep apnea has long been associated with increased risk of cardiovascular issues, including heart attack, stroke, and death, but the findings from this study, partially supported by the National Institutes of Health and published in the American Journal of Respiratory and Critical Care Medicine, show the mechanism mostly responsible for the link.

“These findings will help better characterize high-risk versions of obstructive sleep apnea,” said Ali Azarbarzin, Ph.D., a study author and director of the Sleep Apnea Health Outcomes Research Group at Brigham and Women’s Hospital and Harvard Medical School, Boston. “We think that including a higher-risk version of obstructive sleep apnea in a randomized clinical trial would hopefully show that treating sleep apnea could help prevent future cardiovascular outcomes.”