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How coronavirus’s genetic code can help control outbreaks

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The six British patients seemed to have little in common besides this: Each was dealing with kidney failure, and each had tested positive for the coronavirus.

They were among scores of virus-stricken people showing up at Addenbrooke’s Hospital in Cambridge in the early weeks of April. Had they lived in the United States instead of the United Kingdom, the link that allowed the contagion to spread among them might have slipped by unnoticed.

But the U.K. had done something in the early days of the pandemic that the United States and many other nations had not. It funded a national push to repeatedly decode the coronavirus genome as it made its way across the country. The process reveals tiny, otherwise invisible changes in the virus’s genetic code, leaving a fingerprint that gives scientists valuable glimpses into how the disease is spreading. It’s a cutting-edge technique that was not widely available in prior global pandemics but that researchers believe can help hasten the end of this one.

[The code: How genetic science helped expose a secret coronavirus outbreak]

Experts cite this practice, known as “genomic epidemiology,” as one more tool the United States has failed to fully employ in the fight against the virus. Though it first sequenced the 3 billion-base-pair human genome 20 years ago and spends more on basic biomedical research than almost any other nation, the United States has yet to muster the kind of well funded and comprehensive national effort that could produce a more precise accounting of how covid-19 is infiltrating communities around the country.

In the case of the six British patients, sequencing revealed they had been infected by almost identical sub-strains of SARS-CoV-2, the virus that causes covid-19. Epidemiologists soon determined that all six had visited the same outpatient dialysis clinic on the same day of the week. Many had ridden in the same small transport van that regularly brought patients for treatment from across the surrounding area.

Officials promptly put in place new safety measures, including mandatory masks and intense cleaning of the van and the chairs at the dialysis clinic.

“And, you know, we’ve had no further cases,” said Estée Török, an infectious-disease expert at the University of Cambridge who helped decipher the outbreak. Studying the virus’s genome “helps to highlight cryptic or hidden transmission. That’s the real power of it — you can detect outbreaks and act while they’re happening.”

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Estée Török, an infectious-disease expert at the University of Cambridge, and her colleagues have sequenced and catalogued thousands of viral genomes since the spring. (Photos by Anastasia Taylor-Lind for The Washington Post)

Already, the United Kingdom has sequenced at least 72,529 coronavirus genomes, nearly as many as the rest of the world combined. By contrast, U.S. labs have produced less than half as many sequences as their British counterparts, based on data from the GISAID Initiative, a global database of coronavirus genomes. That’s despite the fact that the United States is battling an epidemic that’s massively larger.

The Health 202: Genetic tracing could show how coronavirus spread through White House

White House spokesman Judd Deere said tracing has been done for people who had contact with Trump. But it’s the kind recommended by the Centers for Disease Control and Prevention, which involves merely tracking people who were nearby those known to be infected.

“Contact tracing has been done by the White House Medical Unit consistent with CDC guidelines,” Deere said, though The Post has reported many of the hundreds of people potentially exposed to the president found out via media reports of his diagnosis.

Coding coronavirus samples would give a clear picture of whether recent White House events were so-called “superspreaders.”

This is an approach researchers have tried around the country.

They’ve watched the virus accumulate a catalogue of mutations as it moved through Zip codes in the Houston area. They’ve used genetic sequencing to trace how the virus spread outward from a conference in Boston, infecting people from Alaska to Senegal to Luxembourg.

And as detailed by my colleagues Sarah Kaplan, Desmond Butler, Juliet Eilperin, Chris Mooney and Luis Velarde, tumor geneticist Paraic Kenny sequenced samples taken from people in the small town of Postville, Iowa. By looking at variants in their genetic coding, he was able to identify a cluster of cases that all originated from one meatpacking plant.

“Infectious particles swabbed from a patient’s nose carry small but distinctive differences in its genome that can be used, like a molecular bar code, to track where the virus came from and how it had been transmitted,” my colleagues write. “By reading the virus’s RNA, Kenny could unveil how cases were connected to one another, exposing the secret spread of the disease.”

Genetic tracing could play a critical role in seeing how the virus spread – and even whether Trump himself played a role in spreading it. 

They include senior policy adviser Stephen Miller, who tested positive along with several others who helped Trump prepare for last week’s debate. Former New Jersey Gov. Chris Christie, who checked himself into the hospital after testing positive, has said masks were not worn while prepping the president. 

NBC News’s Kelly O’Donnell:

A Coast Guard aide is also infected. Jennifer Jacobs, senior White House reporter for Bloomberg News:

Others who have contracted the virus also include assistant press secretary Jalen Drummond, who attended a Sept. 26 Rose Garden event where Trump announced Amy Coney Barrett as his Supreme Court nominee. While others who attended that event – including Republican Sens. Mike Lee and Thom Tillis – later tested positive, several White House press aides are also infected. 

From the New York Times’s Maggie Haberman:

The Rose Garden event has prompted speculation it may have turned into a so-called “superspreader event” where the virus was transmitted to many people. While that’s less likely to happen outdoors, part of the event was held indoors — and many guests were not wearing masks and were pictured hugging, shaking hands and talking closely together. And during the time they were outside, they were seated close to one

Penn Medicine researchers discover a rare genetic form of dementia

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IMAGE: Abnormal neurofibrillary tangles (NFTs) — a buildup of tau protein in parts of the brain — helped Edward Lee, MD, PhD, an assistant professor of Pathology and Laboratory Medicine, and…
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Credit: Edward Lee

PHILADELPHIA — A new, rare genetic form of dementia has been discovered by a team of Penn Medicine researchers. This discovery also sheds light on a new pathway that leads to protein build up 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 today in Science.

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) gene 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,” 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.”

The researchers noted that the tau protein they observed building up looked very similar to the tau protein aggregates seen in Alzheimer’s disease. With these similarities, they aimed to uncover how this VCP mutation is causing this new disease — to aid in finding treatments for this disease and others. Rare genetic causes of diseases can very often offer insight into more prevalent ones.

The researchers first examined the proteins themselves, in addition to studying cells and an animal model, and found that the tau protein buildup is, in fact, due to the VCP mutation.

“What we found in this study is a pattern we’ve never seen before, together with a mutation that’s never been described before,” Lee said. “Given that this mutation inhibits VCP activity, that suggest the converse might be true — that if you’re able to boost VCP activity, that could help break up the protein aggregates. And if that’s true, we may be able to break up tau aggregates not only for this extremely rare disease, but for Alzheimer’s disease and other diseases associated with tau protein aggregation.”

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Lee led this work with first author, Nabil Darwich, MD/PhD student in the Neuroscience Graduate Group at Penn.

These findings describe a new biologic function of VCP, define a