Ricki Lewis

One of the most terrifying aspects of the COVID-19 pandemic is that we don't know what makes one person die, another suffer for weeks, another have just a cough and fatigue, and yet another have no symptoms at all. Even the experts are flummoxed.

"I've been puzzled from the beginning by the sharp dichotomy of who gets sick. At first it was mostly older people with chronic disease, and then a young person with low risk would show up. It can be devastating and rapid in one individual but mild in another," said Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Disease on a media webinar.

What lies behind susceptibility to COVID-19? Gender? Genetics? Geography? Behavior? Immunity? All of these factors may be at play, and they overlap.

To continue reading, go to Genetic Literacy Project, where this post first appeared.

Daily life in the age of coronavirus has affected us in different ways. For science writers, it means that many of the physicians and scientists we would in normal times talk to are too busy saving lives. At the same time, the science and medical journals are spewing articles faster than we can keep up, peer review necessarily delayed.

For the first half of March, I wrote breaking news articles and quickly burnt out. No one was giving interviews as the publication cycle continually compressed, sometimes doubling back to correct errors as new information flooded in.

And then the webinars began, some for media, some for physicians. I've been doing as many as I can, from government agencies, patient advocacy groups, and the journals. This is my sixteenth piece on the novel coronavirus, thanks largely to these constant updates from the experts. My favorite webinar series is the Live Stream Q&A sessions from The Journal of the American Medical Association's editor-in-chief Howard Bauchner, MD.

I especially liked the webcast on April 2 with Frank Snowden, PhD, professor emeritus of history of medicine at Yale and the author of Epidemics and Society: From the Black Death to the Present, published fortuitously this past fall. Listening to him reminded me of my favorite books about plagues and pandemics, which I'll list at the end.

Dr. Anthony Fauci, who needs no introduction with his face plastered on tee shirts and donuts (I've joined his Facebook fan club), does the JAMA webinar regularly, most recently on April 8. So I'm going to pretend that both gentlemen are sitting here with me and my cats in my living room, briefing me on the past and future of COVID-19, and how it fits into the grand sweep of epidemiology.

To continue reading go to my DNA Science blog at Public Library of Science, where this post first appeared.

New York City has become a curious mosaic of crowds and barrenness, people packed into hospitals and homes, yet familiar favorite spaces eerily empty. The haunted cityscapes that accompany this article will fill again once we have a vaccine.

If all goes extremely well — with global cooperation, advances and insights to come, overlapping clinical trial phases, and a lot of luck — a year from now a vaccine or even vaccines against the novel coronavirus may exist. But that's a best-case scenario. Experts tend to be conservative.

"It's hard for me to see that we'd have a vaccine on this side of January. The process is designed to be slow, reflective, peer-reviewed and evidence-based. It takes a long time, not the science part nor to build the vaccine, but to conduct safety testing in enough people across enough time," said Gregory A. Poland, MD, director of the Mayo Clinic's Vaccine Research Group and editor-in-chief of the journal Vaccine.

To continue reading please go to Genetic Literacy Project, where this post first appeared.

Three otherwise healthy patients go to the emergency department with severe acute respiratory failure. Only one ventilator, required to sustain life until the worst of the coronavirus infection has passed, is available. Who gets the vent?

That's what "A Framework for Rationing Ventilators and Critical Care Beds During the COVID-19 Pandemic," a Viewpoint just published in the Journal of the American Medical Association (JAMA), addresses. Douglas White, MD, MAS, Endowed Chair for Ethics in Critical Care Medicine at the University of Pittsburgh School of Medicine and Bernie Lo, MD, from the University of California, San Francisco, wrote the Viewpoint, which links to a full policy document that's been in the works since 2009. It is being implemented in several states and can easily be adapted to any hospital, Dr. White said in a Webinar on March 27.

To continue reading go to Genetic Literacy Project, where this post first appeared.

How does the COVID-19 pandemic compare to other infamous viral infections that have plagued us in modern times? It's a question that's been asked repeatedly in social media circles in recent weeks as people struggle to gain a better understanding of what we are facing.

Recently, I received an answer that was terrifying.

The subject was raised during a March 18 webinar featuring Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases. He is the nation's top infectious disease expert, who was described recently by the Washington Post as the "grandfatherly captain of the corona­virus crisis".

Dr. Fauci was asked by the editor of the Journal of the American Medical Association to put the virus in historical context. His  response:

To continue reading, go to Genetic Literacy Project, where this article first appeared.

It's impossible to keep up with entries at ClinicalTrials.gov that include the search term "COVID-19."

Last week when I posted Can Existing Drugs Treat COVID-19? From Viagra to Thalidomide to Cough Syrup here at DNA Science, the number of studies was a tad over 100. Right now, it's at 158, a 50% increase. These are just registered studies – being listed doesn't imply approval, but rather intent to carry out an investigation.

On March 18, Dr. Anthony Fauci, who no longer needs introduction, mentioned chloroquine as an example of a drug that might possibly be repurposed against the novel coronavirus, and that several clinical trials are already evaluating its safety and efficacy against the new disease. Dr. Fauci said this at a webinar series that the Journal of the American Medical Association holds regularly for media. The drug has been used for years to treat malaria, rheumatoid arthritis, lupus, and other conditions.

To continue reading, go to DNA Scienced, where this post first appeared.

As the number of cases of COVID-19 continues to mount, so do entries at clinicaltrials.gov for potential treatments, reaching into the existing pharmacopeia for repurposing candidates.

Clinical trials for COVID-19 treatments range from 10 people to nearly 600, and most are happening in China. But a caveat: ClinicalTrials.gov is a clearinghouse of proposals, not requiring approval. The entries are from all over the world.

Normally – and these are far from normal times – a clinical trial is optimally designed to assess the safety and efficacy of a new treatment on two groups of people, one taking the drug, the other a placebo. Or, in a crossover design, participants take courses of both treatment and placebo at different times but don't know which is when.

The standard, scientific approach to evaluating drugs takes time. Lots of it. And right now, people are hesitant to sign up for a clinical trial knowing that they face a 50:50 chance of being assigned to a placebo group.

To continue reading, go to my DNA Science blog at Public Library of Science. 

As the world sought to cope with the growing coronavirus outbreak, there was a common refrain uttered by those failing to grasp the severity of this health crisis: "Oh, it's just a bad flu." In fact, they couldn't have been more wrong. Thinking that a novel virus is exactly like a familiar one is like assuming that a guinea pig is the same as a rat.

The confusion arises from using "flu" to denote the familiar litany of respiratory misery, fever and fatigue. These symptoms are mostly due to the response of the immune system to infection. But the specific illness "influenza" is actually due to infection from an influenza virus (not to be further confused with the tiny bacterium Hemophilus influenzae).

The Director-General of the World Health Organization (WHO), Tedros Adhanom Ghebreyesus, puts it succinctly. "This virus is not SARS, it's not MERS, and it's not influenza. It is a unique virus with unique characteristics."

To continue reading, go to Genetic Literacy Project, where this post first appeared.

As epidemiologists try to stay ahead of the spread of new coronavirus COVID-19, vaccine developers, like Sanofi and Johnson & Johnson, are focusing on the "spike" proteins that festoon viral surfaces. Following clues in genomes is critical to disrupting the tango of infectivity as viruses meet and merge with our cells.

Vaccine developers look specifically to the molecular landscapes where viruses impinge upon our respiratory and immune system cells. Targeting COVID-19 is especially challenging, because efforts to develop a vaccine against its relative, the SARS coronavirus (SARS-CoV), elicit only partial responses. But those steps are now serving as jumping off points for pharma.

The relationship between viruses and humans can seem like a science fiction plot. The viruses that make us sick may be little more than snippets of genetic material borrowed, long ago, from human genomes. Packaged with their own proteins, viruses return to our bodies, taking over to make more of themselves.

To continue reading, go to my DNA Science weekly blog at Public Library of Science, where this post first appeared.

While COVID-19, the novel coronavirus, dominates health news headlines, less exotic viral foes are still around: influenza, the rhinovirus, adenovirus, and respiratory syncytial virus behind the common cold, norovirus outbreaks aboard cruise ships, and always hepatitis and HIV.

What these viruses share is RNA as their genetic material, a nucleic acid less familiar than DNA. Among the RNA viruses are also West Nile, chikungunya, and those behind Ebola and Marburg hemorrhagic fevers, dengue, rabies, and yellow fever.

When science writer David Quammen made the media rounds recently to discuss COVID-19, he skipped the RNA part – "don't worry about that right now." But his excellent book Spillover: Animal Infections and the Next Human Pandemic, which charts the predictions of the current situation starting nearly a decade ago, details the significance of RNA viruses.

RNA is a nucleic acid like its cousin DNA, but has uracil in place of thymine as one of the four nitrogen-containing bases that carry each molecule's encrypted information. RNA's sugar – ribose – has an oxygen atom in a place that DNA's deoxyribose doesn't. DNA is the same in every cell of an individual, whereas shorter and shorter-lived RNA molecules carry out the specific DNA instructions that sculpt different cell types and functions.

The inability of RNA to repair itself, as DNA can, allows mutations to accrue in RNA viruses, enabling them to replicate wantonly and spread explosively. And our bodies help them. New viral particles spew from coughs and sneezes, are propelled in vomit, and ooze from blood and diarrhea, often before our immune systems begin to respond.

To continue reading, go to Genetic Literacy Project, where this post first appeared.