New research from the University of Pittsburgh School of Medicine and La Jolla Institute for Immunology has made a groundbreaking discovery in understanding the mechanism by which cytomegalovirus (CMV), a herpes virus that infects millions worldwide, enters cells lining the blood vessels and contributes to vascular disease.

The study, published in Nature Microbiology, reveals that CMV employs an alternative molecular “key” called GATE (gH-UL116-UL141 complex) to sneak through a side door and evade the body’s natural immune defenses. This finding may explain why efforts to develop prophylactic treatments against CMV have been unsuccessful.

In the United States, approximately one in every 200 babies is born with congenital CMV infection, which can result in birth defects such as hearing loss or long-term health challenges. For most adults, CMV infections are asymptomatic, but a CMV infection during pregnancy presents significant health risks to the unborn child and could be deadly for people who are immunosuppressed.

The researchers suggest that targeting the GATE complex could become a potential vaccine target for CMV and other herpes viruses, which have also been linked to various diseases. This breakthrough has far-reaching implications for developing antiviral drugs and vaccines to combat CMV infection and its consequences.

“If we don’t know what weapons the enemy is using, it’s hard to protect against it,” said senior author Jeremy Kamil, Ph.D., associate professor of microbiology and molecular genetics at Pitt. “We found a missing puzzle piece that represents one possible reason why immunization efforts against CMV have been unsuccessful.”

The research was supported by the National Institutes of Health and ARPA-H APECx contract. Other authors of this study include researchers from the University of Toronto, Louisiana State University Health Shreveport, and La Jolla Institute for Immunology.

This discovery has the potential to revolutionize our understanding of CMV infection and its impact on human health, leading to the development of more effective treatments and a better chance at combating this widespread virus.

The discovery of an “off switch” enzyme that can help prevent heart disease and diabetes is a significant breakthrough in the medical field. Scientists at The University of Texas at Arlington have identified an enzyme called IDO1, which plays a crucial role in inflammation regulation. By blocking this enzyme, researchers believe they can control inflammation and restore proper cholesterol processing.

Inflammation is a natural response to stress, injury, or infection, but when it becomes abnormal, it can lead to chronic diseases such as heart disease, cancer, diabetes, and dementia. The team found that IDO1 becomes activated during inflammation, producing a substance called kynurenine that interferes with how macrophages process cholesterol.

When IDO1 is blocked, however, macrophages regain their ability to absorb cholesterol, suggesting a new way to prevent heart disease by keeping cholesterol levels in check. The researchers also discovered that another enzyme linked to inflammation, nitric oxide synthase (NOS), worsens the effects of IDO1.

The findings are crucial because they suggest that understanding how to prevent inflammation-related diseases could lead to new treatments for conditions like heart disease, diabetes, cancer, and others. The research team plans to further investigate the interaction between IDO1 and cholesterol regulation, with the goal of finding a safe way to block this enzyme and develop effective drugs to combat chronic diseases.

The discovery is supported by grants from the National Institutes of Health (NIH) and the National Science Foundation (NSF), indicating the importance of this research in advancing our understanding of inflammation-related diseases. With further study, it’s possible that we may see a new era in disease prevention and treatment, giving hope to millions of people affected by these conditions.

The discovery of ancient DNA in human bones has revolutionized our understanding of diseases that have plagued humans for centuries. Recently, researchers have uncovered evidence that leprosy, also known as Hansen’s Disease, had a presence in the Americas long before European colonization. This finding challenges the common assumption that leprosy was introduced to the continent by European settlers.

Leprosy is a chronic disease caused by either Mycobacterium leprae or Mycobacterium lepromatosis. While M. leprae is the more commonly known pathogen, M. lepromatosis has been found in a rare form of the disease. The discovery of ancient DNA from 4000-year-old skeletons in Chile suggests that M. lepromatosis was present in the Americas thousands of years ago.

This finding is significant because it reveals a previously unknown chapter in leprosy’s history. Historically, leprosy has been documented in Europe and Asia for thousands of years, but its presence in the Americas before European colonization had gone undetected. The discovery of ancient DNA from M. lepromatosis in Chile provides evidence that this disease was present in the Americas at least 4000 years ago.

The study of ancient DNA has become a valuable tool for researchers to uncover the history of diseases that have affected humans over time. By analyzing ancient bone samples, researchers can identify the presence of pathogens and reconstruct their evolutionary history. In this case, the discovery of M. lepromatosis in Chile provides a fascinating example of how ancient DNA can shed new light on the history of a disease.

Further research is needed to understand the full extent of leprosy’s history in the Americas. The discovery of M. lepromatosis in Chile has opened up new avenues for research, and it is likely that more cases will be identified in the coming years. By studying ancient DNA from other time periods and contexts, researchers can gain a better understanding of how leprosy was transmitted and evolved over time.

Ultimately, the discovery of M. lepromatosis in Chile highlights the importance of studying ancient DNA to uncover the history of diseases that have affected humans for centuries. By doing so, we can gain a deeper understanding of how these diseases were transmitted and evolved over time, and perhaps even find new ways to prevent or treat them.