Ricki Lewis

It's been a strange and busy 15 months for science journalists.

Each day, throughout the day, our inboxes overflow with the latest from the technical medical and science journals – tables-of-contents, abstracts, news releases, and the never-ending stream of article preprints. We jumpstart the journals by going straight to medRxiv and bioRxiv, aka "med-archive" and "bio-archive," where investigators post articles before peer review.

Where We Get Information

It's a deluge, an unrelenting barrage of new reports from the Science and Nature family of journals; the medical journals like JAMA, the Lancet group, and the NEJM; and publications that cover more basic science, like Cell and the journals from Public Library of Science, which has sponsored this blog since 2012. The journals send wrap-ups on the weekends, in case we've missed anything.

The clearinghouse for news releases for journalists, Eurekalert, provides information from a wide range of publications, government agencies, academic institutions, research centers, nonprofits, and companies, with quotes from experts and images and videos we can use. Eurekalert added a COVID tab to the topics menu early in the pandemic. Much appreciated!

As we try to stay ahead of our inboxes, we're invited to webinars, zooms, and podcasts, all wonderfully helpful in crafting our stories.

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

A year ago, the Director General of the World Health Organization, Tedros Adhanom Ghebreyesus, delivered the message that would divide time:

"WHO has been assessing this outbreak around the clock and we are deeply concerned both by the alarming levels of spread and severity, and by the alarming levels of inaction. We have therefore made the assessment that COVID-19 can be characterized as a pandemic."

What followed was a call to action to all. "We have rung the alarm bell loud and clear." And instantly, the redundant "global pandemic" ricocheted across the media, reverberating still.

The name of the enemy had changed quickly as 2020 began, from the "Wuhan coronavirus" to "2019 novel coronavirus" shortened to "2019-nCoV," and finally to SARS-CoV-2, acknowledging similarity to SARS, circa 2003-2004.

Whatever it's name, did SARS-CoV-2 have an older guise, perhaps in a lab?

The Bioweapon Hypothesis

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

Glimmers of hope are beginning to shine through the gloom of the past year. That was evident in a recent webinar that the Massachusetts Consortium on Pathogen Readiness (MassCPR) held to "demystify" the new viral variants. Each consists of several mutations.

Will the variants fuel "a novel stage of contagion, COVID 2.0?" opened George Daley, MD, PhD, dean of Harvard Medical School. "What has been unsettling is how many times mutations have cropped up independently in infected patients across the globe and in petri dishes. This is a consequence of Darwinian evolution by natural selection in real time," he added. The fact that the virus, SARS-CoV-2, has mutated in the same ways at different times and places suggests that the changes benefit the virus.

Also disturbing is that once variants appear, they proliferate. "That suggests the virus is more contagious, or replicates faster, so that it takes over the outbreak," said Jeremy Luban, MD, from the University of Massachusetts Medical School. Most mutations are neutral; we need to worry when they combine into "variants of concern," aka VOC. "They could permit the virus to escape immune control that's been established in a person from prior infection or from a vaccine," Luban added.

The "big three" variants of most concern now have hard-to-remember numerical names, which avoid stigmatizing a place: B.1.3.5.1 variant (South Africa), B.1.1.7 (UK), and P.1 (Brazil). The last one may be the worst to arise, so far. It first came to attention in Manaus, Amazonia. "Up to 70% of the population had been infected and they had developed what we'd consider herd immunity that would prevent new infection," Luban explained. The explosion of hospitalizations and deaths in December, a second wave, coincided with the appearance of the P.1 variant. "Many mutations in it raise concerns about whether the virus is resistant to the immune response against the first virus," he added.

Tackling variants requires asking three questions, Luban said:
• Do they enhance transmission?
• Do they permit reinfection?
• Do they decrease vaccine efficacy?

Fortunately, the vaccines so far are doing their job. Here are 6 pieces of good news.

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

Vaccines against COVID-19 were developed in record-smashing time, and now that the rollout has begun, attention is returning to herd immunity, in a real rather than hypothetical sense.

Herd immunity refers to the protection against an infectious disease that arises when a critical mass of individuals in a population becomes immune. The pathogen can't find welcoming bodies, and the epidemic dies out. Once herd immunity is attained, mitigation measures can be relaxed. But if society opens too soon, a second and even third wave of disease can ensue – as we've seen.

A vaccine, engineered to evoke a strong and diverse antibody response, is more likely to build herd immunity than is natural infection.

Establishing herd immunity against COVID-19 requires that a whole bunch of ducks align. The variables include:

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

Real life with COVID-19 is now scarier than anything a sci-fi writer could envision. So-called "escape mutations" that can turn the virus into an out-of-control shape-shifter that hides from the immune system are now a frightening reality. And they can't be totally stopped with masks or social distancing, lockdowns or travel restrictions. Even if we could keep all viruses out, the ones already here are mutating in a direction that keeps them infectious and deadly. The battle between us and this often-lethal virus has just jumped to a new level. 

While it may take awhile to see whether these escape mutations will evade the vaccines approved or in the pipeline, Tyler Starr from the Fred Hutchinson Cancer Research Center and colleagues report in a new study in Science an effect on two already available treatments — monoclonal antibodies. They've identified an escape mutation with a single glitch that enables the virus to evade Regeneron's double-antibody REGN-COV2 "cocktail" (which Trump took) and a third antibody in Eli Lilly's LY-CoV016. The researchers found the escapee using a new lab mapping technique that displays viruses contorted with mutation, and then they found it in a patient who was still testing positive, 145 days after the first test.

What does this mean? The discovery of escape mutations derailing antibody treatments means that the companies' initial tests hadn't caught them all. And the escape mutations — the new mapping revealed three others — are already in circulation.

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

When a new variant of the COVID-19 virus appeared in the UK as 2020 drew to a close, I didn't think it would show up a half hour's drive from my home soon after. The first cases were near Denver and in San Diego, and then traced to a jewelry store on Broadway in Saratoga Springs. We've felt rather insulated and isolated here, hours from New York City.

The Legacy of Caffe Lena

This week began with an email from Sarah Craig, executive director of Caffe Lena, the oldest coffeehouse in the US. Don McLean debuted "American Pie" there, Arlo Guthrie first tried out "Alice's Restaurant," and Bob Dylan and many others have commanded the iconic tiny stage in the small, homey establishment that opened in 1960.

The café is now in "Safe Mode," with even the fabulous online events it has held throughout the pandemic too risky to record. The one-month shutdown follows the death January 12 from COVID of Matt McCabe, owner of Saratoga Guitar and frequent performer at the coffeehouse. The opening image captures his final show, in December.

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

Early on in the pandemic, a worse clinical scenario for the male of the species emerged. A study published mid-May from Italian researchers offered early statistics from the WHO and Chinese scientists: a death rate of 1.7% for women and 2.8% for men. Then Hong Kong hospitals reported that 15% of females and 32% of males with COVID-19 needed intensive care or had died.

In July a Perspective published in Nature Reviews Immunology from researchers at Johns Hopkins University and the University of Montreal noted a similar "male bias" for other viral infections, including SARS and MERS. By then, the wide community testing in South Korea and data from the U.S. indicated 1.5-fold higher mortality for men for COVID-19. The pattern repeated in 38 countries, for patients of all ages.

Now a new study published in Nature Communications expands the increased risk for those who have only one X chromosome

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

It's hard to imagine anything worse than the horrors at our hospitals right now. But in a recent JAMA webinar, Nicholas Christakis, Yale Sterling Professor, put the fatality rate of COVID-19 into historical perspective:

"Bad as it is, the fatality rate, at .5-.8%, isn't as bad as bubonic plague, which would kill 50% of a population in a few months. Or Ebola at 80%. Or smallpox at 95%. It could have been so much worse." He's a physician, scientist, public health expert, and sociologist.

It's an unusual viewpoint to downplay the horror of this moment in time, but Dr. Christakis's new book, "Apollo's Arrow: The Profound and Enduring Impact of Coronavirus on the Way We Live," takes a broader look. He said at the webinar:

"This way we're living right now seems alien and unnatural, but plagues aren't new to our species, just new to us. People have struggled with plagues for thousands of years. The Iliad opens with a plague on the Greeks and Apollo reigns down, the Bible, Shakespeare. What's different about our current experience is our time in the crucible happens to be occurring when we can create a vaccine in real time. The fact that we have the technological capability to respond within a year with phase 3 trials of active agents is mind-boggling."

We aren't the only species subject to unseen pathogens, including the viruses that aren't even cells or technically alive, just borrowed bits of our own genomes turned against us. With Dr. Christakis's wider view in mind, I noticed a new article about an infectious cancer in Tasmanian devils. It combines two terrors.

A Transmissible Cancer

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

Science and medical writers have been under an avalanche of information for nearly a year now, as we translate technical information about COVID-19 for the public. Links to the latest journal articles overload our inboxes, but, at the beginning and now during another surge, tracking down experts to interview has been difficult. They're simply too busy saving lives.

A critical resource for me has been the series of JAMA Live Q+A webinars for the media hosted by Howard Bauchner, editor-in-chief of the Journal of the American Medical Association. It is wonderful to hear the top clinicians and researchers speak freely, at length, and in context, or meander – a nice contrast to the echoing soundbites of mainstream media.

JAMA webinar speakers have included the career scientists who've already led us through the waters of HIV/AIDS, hepatitis, influenza, Ebola, zika, SARS, and other epidemics and pandemics. Anthony Fauci is a frequent guest – I wrote up his talk with FDA's Peter Marks here.

The webinars also feature the young clinicians battling our new enemy. Early on, Maurizio Cecconi's session, "Coronavirus in Italy: Report From the Front Lines," brought me to tears. The head of the Anaesthesia and Intensive Care Department at Humanitas Research Hospital in Milan, Dr. Cecconi described, at the webinar and in a report (both accessible here), the admission of "patient zero" to the ICU in Lombardy, on February 20, 2020, and how his infection was traced to a local friend who'd had contact with an infected person from China. The 38-year-old was initially not very ill and partied a lot. And the rest is medical history.

Recently Dr. Bauchner spoke with Paul Offit, who directs the Vaccine Education Center and is an attending physician in the Division of Infectious Diseases at Children's Hospital of Philadelphia. He's on the FDA Advisory panel that will meet December 10 to discuss Pfizer's COVID-19 vaccine and on the 17th to consider Moderna's.

Dr. Offit is best known for co-inventing a vaccine against rotavirus, a diarrheal disease that has claimed millions of lives. It became available in the US in 2006, and is on the World Health Organization's list of essential medicines. The clinical trials for the rotavirus vaccine RotaTeq took four years and involved 70,000 participants – much more typical than the lightning speed of the COVID vaccine trajectory.

Here's the Q+A from December 2, lightly edited, with my explanations in parentheses. I've omitted the discussion of who gets vaccine when – that's all over the news.

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

While antibodies have been the focus of testing for past infection with COVID-19, T cells will also provide some insights -- potentially better ones, experts say.

These lymphocytes are the first responders that then coordinate the immune response while building an imprint, a memory, so that subsequent infections fade quickly, often unnoticed.

T cell tests are more complex and typically reserved for research, but some may be coming to the clinic soon, with at least one company seeking FDA emergency use authorization (EUA). Recent studies indicate that assaying T cells can even improve diagnostic accuracy and possibly predict how COVID-19 will unfold.

"Testing T cell responses can accelerate detection of an infection by as much as a week. The cells come in on day 2 and they divide very quickly, to detectable levels as early as 3 or 4 days from infection," said Dawn Jelley-Gibbs, PhD, who investigated T cells in influenza at the Trudeau Institute in Saranac Lake, New York.

"Identifying people who have been infected and become immune could have huge benefits for enabling society to safely return to normalcy. Numerous antibody tests exist, but doubts remain about their reliability and about antibody longevity post-infection," said Maria Oliver, PhD, senior scientist at Indoor Biotechnologies in Great Britain, one of several companies developing clinical T cell tests.

T Cell Basics

To continue reading, please go to MEDPAGE TODAY, where this post first appeared.