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Archive - Oct 5, 2020

Caltech Researcher Unveils Low-Cost Device That Detects SARS-CoV-2 Virus, Anti-Virus Antibodies, and Inflammatory Molecules in Under 10 Minutes; Device Designed for Home Use & Detects Virus in Infected, But Still Pre-Symptomatic Individuals

One feature of the COVID-19 virus that makes it so difficult to contain is that it can be easily spread to others by a person who has yet to show any signs of infection. The carrier of the virus might feel perfectly well and go about his/her daily business--taking the virus with him/her to work, to the home of a family member, or to public gatherings. A crucial part of the global effort to stem the spread of the pandemic, therefore, is the development of tests that can rapidly identify infections in people who are not yet symptomatic. Now, Caltech researchers have developed a new type of multiplexed test (a test that combines multiple kinds of data) with a low-cost sensor that may enable the at-home diagnosis of a COVID infection through rapid analysis of small volumes of saliva or blood, without the involvement of a medical professional, in less than 10 minutes. The research was conducted in the lab of Wei Gao, PhD, Assistant Professor in the Andrew and Peggy Cherng Department of Medical Engineering at Caltech. Previously, Dr. Gao and his team have previously developed wireless sensors that can monitor conditions such as gout, as well as stress levels, through the detection of extremely low levels of specific compounds in blood, saliva, or sweat. Dr. Gao's sensors are made of graphene, a sheet-like form of carbon. A plastic sheet etched with a laser generates a 3D graphene structure with tiny pores. Those pores create a large amount of surface area on the sensor, which makes it sensitive enough to detect, with high accuracy, compounds that are only present in very small amounts. In this sensor, the graphene structures are coupled with antibodies, immune system molecules that are sensitive to specific proteins, like those on the surface of a COVID virus, for example.

2020 Nobel Prize for Physiology or Medicine Awarded Jointly to Three Scientists for Discovery of Hepatitis C Virus

On October 5, 2020, it was announced that this year’s Nobel Prize in Physiology or Medicine has been awarded jointly to three scientists who have made a decisive contribution to the fight against blood-borne hepatitis, a major global health problem that causes cirrhosis and liver cancer in people around the world. Harvey J. Alter, MD, Michael Houghton, PhD, and Charles M. Rice, PhD, made seminal discoveries that led to the identification of a novel virus, Hepatitis C. Prior to their work, the discovery of the Hepatitis A and B viruses had been critical steps forward, but the majority of blood-borne hepatitis cases remained unexplained. The discovery of Hepatitis C virus revealed the cause of the remaining cases of chronic hepatitis and made possible blood tests and new medicines that have saved millions of lives. Liver inflammation, or hepatitis, a combination of the Greek words for liver and inflammation, is mainly caused by viral infections, although alcohol abuse, environmental toxins, and autoimmune disease are also important causes. In the 1940’s, it became clear that there are two main types of infectious hepatitis. The first, named hepatitis A, is transmitted by polluted water or food and generally has little long-term impact on the patient. The second type is transmitted through blood and bodily fluids and represents a much more serious threat because it can lead to a chronic condition, with the development of cirrhosis and liver cancer. This form of hepatitis is insidious, as otherwise healthy individuals can be silently infected for many years before serious complications arise. Blood-borne hepatitis is associated with significant morbidity and mortality, and causes more than a million deaths per year world-wide, thus making it a global health concern on a scale comparable to HIV-infection and tuberculosis.

Researchers Discover Rare Genetic Form of Dementia; Mutation in VCP Gene Associated with Pathologic Buildup of Tau Proteins; Results Suggest That Restoring VCP Function Might Be Helpful in Neurological Protein Aggregation Diseases Like Alzheimer’s

A new, rare genetic form of dementia has been discovered by a team of University of Pennsylvania School of Medicine (Penn Medicine) researchers. This discovery also sheds light on a new pathway that leads to protein buildup in the brain--which causes this newly discovered disease, as well as related neurodegenerative diseases like Alzheimer's Disease--that could be targeted for new therapies. The study was published online on October 1, 2020 in Science. The article is titled “Autosomal Dominant VCP Hypomorph Mutation Impairs Disaggregation of PHF-tau.” Alzheimer's disease (AD) is a neurodegenerative disease characterized by a buildup of proteins, called tau proteins, in certain parts of the brain. Following an examination of human brain tissue samples from a deceased donor with an unknown neurodegenerative disease, researchers discovered a novel mutation in the valosin-containing protein (VCP) (image) ene in the brain, a buildup of tau proteins in areas that were degenerating, and neurons with empty holes in them, called vacuoles. The team named the newly discovered disease “vacuolar tauopathy” (VT)--a neurodegenerative disease now characterized by the accumulation of neuronal vacuoles and tau protein aggregates. "Within a cell, you have proteins coming together, and you need a process to also be able to pull them apart, because otherwise everything kind of gets gummed up and doesn't work. VCP is often involved in those cases where it finds proteins in an aggregate and pulls them apart," said Edward Lee, MD, PhD, an Assistant Professor of Pathology and Laboratory Medicine in the Perelman School of Medicine at the University of Pennsylvania. "We think that the mutation impairs the proteins' normal ability to break aggregates apart."