Monday, June 15, 2020

Asian giant hornet

Two new specimens of Asian giant hornet have turned up in the Pacific Northwest, suggesting that the invasive species made it through the winter despite efforts last year to stamp out the menace to North America’s honeybees.

A big, yellow-and-black insect found dead in a roadway near Custer, Wash., has been identified as the Asian giant hornet, or Vespa mandarinia, Sven Spichiger, an entomologist at the Washington State Department of Agriculture, announced May 29. It was “probably a queen,” he said, from a brood in a 2019 nest and now ready to found a colony of her own.

Canadian scientists have also confirmed their first giant hornet of 2020, a specimen spotted May 15 in Langley, British Columbia.

Dubbed the “murder hornet” to the annoyance of entomologists, the predator earns its nickname from its proclivity to nab a honeybee, bite off the bee’s head carried home to nourish young hornets. Raiding parties of several dozen Asian giant hornets can kill whole hives containing thousands of bees in a few hours.

Those are just some of the details that make V. mandarinia the newsiest stinging invader in years. It’s a fierce little predator, though not as apocalyptic as “murder hornet” headlines have suggested.

Amid the uproar over the “new” hornets, a few facts have been overlooked. For one, North America has previously had at least one close call — not publicized at the time — with the world’s largest hornet. Unlike the current sensational invasion, however, that early episode had a happy ending, at least for the people and native insects of North America. Not so much for the hornets. What’s more, these aren’t the only big, bad hornets that have arrived at the borders of the continent.

Here’s what we know so far, and what we don’t, about Asian giant hornets and the threats they pose.

Is this ‘invasion of the giant hornet’ really new?

Not entirely. What’s new for North America is that last year scientists confirmed Asian giant hornets in the wild.

In September 2019, beekeepers tracked down and destroyed a hornet nest about the diameter of a large grapefruit near a public footpath in Nanaimo near Vancouver, Canada. Lone flying hornets also showed up on both sides of the Canada-U.S. border, one at a hummingbird feeder near Blaine, Wash.

But that wasn’t the Asian giant hornet’s first touchdown on North American soil. California had an overlooked close call in 2016. It wasn’t just some lone hornet hiding in a cargo container, says entomologist Allan Smith-Pardo, now at the U.S. Department of Agriculture’s Animal and Plant Health Inspection Service office in Sacramento, Calif. He was the scientist charged with identifying any suspicious wasps or bees found in cargo or mail nationwide. An inspector flagged an express package coming into the San Francisco airport without any mention of insects in its labeling. Yet it held some kind of papery honeycomb-like nest.

Giant hornet nest

Is the Asian giant hornet the first hornet to try invading North America?

Far from it.

The hefty, though not record-setting, hornet V. crabro spread from Europe into New York state around the mid-19th century. Now found in scattered places east of the Rockies, the European hornets nest in hollow trees and cozy nooks within walls. Humans who blunder too close can get painful stings, says Bob Jacobson, a retired entomologist in Cincinnati with a long-standing interest in hornets and venoms. His cousin was stung by the species.

Like the Asian giant hornet, the European invader attacks honeybees, and Jacobson has seen it go after bumblebees, too, as well as yellow jackets and some other wasps. Unlike the new invader, though, a V. crabro hornet hunts alone. It picks off a bee on a flower or at a hive but doesn’t gang up in groups for mass slaughter of whole insect colonies.

Other hornets have also turned up in North America without stirring public interest. That data search of interceptions in California between 2010 and 2018 showed that inspectors stopped four other species besides the giant. In Canada, just in 2019, entomologists identified two different invasive hornet species, including V. soror, which is almost as big as the Asian giant. Whether those arrivals could make a permanent home remains to be seen.

Let’s back up. What are hornets, and why do people get so spooked by them?

True hornets are big, predatory, colony-forming wasps, in the Vespa genus. Apart from the European V. crabro, they’re native to Asia. They need meat to feed their young, unlike honeybees, which collect plant pollen as baby food. Another difference: A honeybee dies after its single-use stinger rips out of its body. Hornets, however, are among the insects that can sting and sting again.

The latest hornet identification key  lists 22 species: striped and spangled in various browns and rusts, gold and bluish-blacks. North America also has several native wasps popularly nicknamed hornets. These natives, however, belong on a nearby but different twig of the insect evolutionary tree.


More ‘murder hornets’ are turning up. Here’s what you need to know

Thursday, May 7, 2020


The coronavirus pandemic circling the globe is caused by a natural virus, not one made in a lab, a new study says.

The virus’s genetic makeup reveals that SARS-CoV-2 isn’t a mishmash of known viruses, as might be expected if it were human-made. And it has unusual features that have only recently been identified in scaly anteaters called pangolins, evidence that the virus came from nature, Kristian Andersen and his colleagues report March 17 in Nature Medicine.

When Andersen, an infectious disease researcher at the Scripps Research Institute in La Jolla, Calif., first heard about the coronavirus causing an outbreak in China, he wondered where the virus came from. Initially, researchers thought the virus was being spread by repeated infections jumping from animals in a seafood market in Wuhan, China, into humans and then being passed person to person. Analysis from other researchers has since suggested that the virus probably jumped only once from an animal into a person and has been spread human to human since about mid-November (SN: 3/4/20).

But shortly after the virus’s genetic makeup was revealed in early January, rumors began bubbling up that maybe the virus was engineered in a lab and either intentionally or accidentally released.

An unfortunate coincidence fueled conspiracy theorists, says Robert Garry, a virologist at Tulane University in New Orleans. The Wuhan Institute of Virology is “in very close proximity to” the seafood market, and has conducted research on viruses, including coronaviruses, found in bats that have potential to cause disease in people. “That led people to think that, oh, it escaped and went down the sewers, or somebody walked out of their lab and went over to the market or something,” Garry says.

Accidental releases of viruses, including SARS, have happened from other labs in the past. So “this is not something you can just dismiss out of hand,” Andersen says. “That would be foolish.”

Looking for clues

Andersen assembled a team of evolutionary biologists and virologists, including Garry, from several countries to analyze the virus for clues that it could have been human-made, or grown in and accidentally released from a lab.

“We said, ‘Let’s take this theory — of which there are multiple different versions — that the virus has a non-natural origin … as a serious potential hypothesis,’ ” Andersen says.

Meeting via Slack and other virtual portals, the researchers analyzed the virus’s genetic makeup, or RNA sequence, for clues about its origin.

It was clear “almost overnight” that the virus wasn’t human-made, Andersen says. Anyone hoping to create a virus would need to work with already known viruses and engineer them to have desired properties.

But the SARS-CoV-2 virus has components that differ from those of previously known viruses, so they had to come from an unknown virus or viruses in nature. “Genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone,” Andersen and colleagues write in the study.

“This is not a virus somebody would have conceived of and cobbled together. It has too many distinct features, some of which are counterintuitive,” Garry says. “You wouldn’t do this if you were trying to make a more deadly virus.”

No, the coronavirus wasn’t made in a lab. A genetic analysis shows it’s from nature

Thursday, April 23, 2020


UNITED KINGDOM LIVE CORONA VIRUS TRACKER




UNITED STATES OF AMERICA - USA Live Corona Tracker

Sars-CoV-2 virus illustration (stock image). | Credit: (c) dottedyeti / stock.adobe.com
Researchers at MIT; the Ragon Institute of MGH, MIT, and Harvard; and the Broad Institute of MIT and Harvard; along with colleagues from around the world have identified specific types of cells that appear to be targets of the coronavirus that is causing the Covid-19 pandemic.


Using existing data on the RNA found in different types of cells, the researchers were able to search for cells that express the two proteins that help the SARS-CoV-2 virus enter human cells. They found subsets of cells in the lung, the nasal passages, and the intestine that express RNA for both of these proteins much more than other cells.

The researchers hope that their findings will help guide scientists who are working on developing new drug treatments or testing existing drugs that could be repurposed for treating Covid-19.
"Our goal is to get information out to the community and to share data as soon as is humanly possible, so that we can help accelerate ongoing efforts in the scientific and medical communities," says Alex K. Shalek, the Pfizer-Laubach Career Development Associate Professor of Chemistry, a core member of MIT's Institute for Medical Engineering and Science (IMES), an extramural member of the Koch Institute for Integrative Cancer Research, an associate member of the Ragon Institute, and an institute member at the Broad Institute.
Shalek and Jose Ordovas-Montanes, a former MIT postdoc who now runs his own lab at Boston Children's Hospital, are the senior authors of the study, which appears today in Cell. The paper's lead authors are MIT graduate students Carly Ziegler, Samuel Allon, and Sarah Nyquist; and Ian Mbano, a researcher at the Africa Health Research Institute in Durban, South Africa.
Digging into data
Not long after the SARS-CoV-2 outbreak began, scientists discovered that the viral "spike" protein binds to a receptor on human cells known as angiotensin-converting enzyme 2 (ACE2). Another human protein, an enzyme called TMPRSS2, helps to activate the coronavirus spike protein, to allow for cell entry. The combined binding and activation allows the virus to get into host cells.
"As soon as we realized that the role of these proteins had been biochemically confirmed, we started looking to see where those genes were in our existing datasets," Ordovas-Montanes says. "We were really in a good position to start to investigate which are the cells that this virus might actually target."
Shalek's lab, and many other labs around the world, have performed large-scale studies of tens of thousands of human, nonhuman primate, and mouse cells, in which they use single-cell RNA sequencing technology to determine which genes are turned on in a given cell type. Since last year, Nyquist has been building a database with partners at the Broad Institute to store a huge collection of these datasets in one place, allowing researchers to study potential roles for particular cells in a variety of infectious diseases.
Much of the data came from labs that belong to the Human Cell Atlas project, whose goal is to catalog the distinctive patterns of gene activity for every cell type in the human body. The datasets that the MIT team used for this study included hundreds of cell types from the lungs, nasal passages, and intestine. The researchers chose those organs for the Covid-19 study because previous evidence had indicated that the virus can infect each of them. They then compared their results to cell types from unaffected organs.
"Because we have this incredible repository of information, we were able to begin to look at what would be likely target cells for infection," Shalek says. "Even though these datasets weren't designed specifically to study Covid, it's hopefully given us a jump start on identifying some of the things that might be relevant there."
In the nasal passages, the researchers found that goblet secretory cells, which produce mucus, express RNAs for both of the proteins that SARS-CoV-2 uses to infect cells. In the lungs, they found the RNAs for these proteins mainly in cells called type II pneumocytes. These cells line the alveoli (air sacs) of the lungs and are responsible for keeping them open.

In the intestine, they found that cells called absorptive enterocytes, which are responsible for the absorption of some nutrients, express the RNAs for these two proteins more than any other intestinal cell type.
"This may not be the full story, but it definitely paints a much more precise picture than where the field stood before," Ordovas-Montanes says. "Now we can say with some level of confidence that these receptors are expressed on these specific cells in these tissues."
Fighting infection
In their data, the researchers also saw a surprising phenomenon -- expression of the ACE2 gene appeared to be correlated with activation of genes that are known to be turned on by interferon, a protein that the body produces in response to viral infection. To explore this further, the researchers performed new experiments in which they treated cells that line the airway with interferon, and they discovered that the treatment did indeed turn on the ACE2 gene.
Interferon helps to fight off infection by interfering with viral replication and helping to activate immune cells. It also turns on a distinctive set of genes that help cells fight off infection. Previous studies have suggested that ACE2 plays a role in helping lung cells to tolerate damage, but this is the first time that ACE2 has been connected with the interferon response.
The finding suggests that coronaviruses may have evolved to take advantage of host cells' natural defenses, hijacking some proteins for their own use.
"This isn't the only example of that," Ordovas-Montanes says. "There are other examples of coronaviruses and other viruses that actually target interferon-stimulated genes as ways of getting into cells. In a way, it's the most reliable response of the host."
Because interferon has so many beneficial effects against viral infection, it is sometimes used to treat infections such as hepatitis B and hepatitis C. The findings of the MIT team suggest that interferon's potential role in fighting Covid-19 may be complex. On one hand, it can stimulate genes that fight off infection or help cells survive damage, but on the other hand, it may provide extra targets that help the virus infect more cells.
"It's hard to make any broad conclusions about the role of interferon against this virus. The only way we'll begin to understand that is through carefully controlled clinical trials," Shalek says. "What we are trying to do is put information out there, because there are so many rapid clinical responses that people are making. We're trying to make them aware of things that might be relevant."
Shalek now hopes to work with collaborators to profile tissue models that incorporate the cells identified in this study. Such models could be used to test existing antiviral drugs and predict how they might affect SARS-CoV-2 infection.
The MIT team and their collaborators have made all the data they used in this study available to other labs who want to use it. Much of the data used in this study was generated in collaboration with researchers around the world, who were very willing to share it, Shalek says.
"There's been an incredible outpouring of information from the scientific community with a number of different parties interested in contributing to the battle against Covid in any way possible," he says. "It's been incredible to see a large number of labs from around the world come together to try and collaboratively tackle this."

The research was funded by the Searle Scholars Program, the Beckman Young Investigator Program, the Pew-Stewart Scholars Program for Cancer Research, a Sloan Fellowship in Chemistry, the National Institutes of Health, the Aeras Foundation, the Bill and Melinda Gates Foundation, the Richard and Susan Smith Family Foundation, the National Institute of General Medical Sciences, the UMass Center for Clinical and Translational Science Project Pilot Program, and the Office of the Assistant Secretary of Defense for Health Affairs.

Researchers identify cells likely targeted by COVID-19 virus

Doctor administering supplemental oxygen

As part of the COVID-19 response team at O’Connor Hospital in San Jose, Calif., Nivedita Lakhera wasn’t prepared to see her intensive care unit filled with so many young patients. Many of those patients had no medical condition other than obesity.
“They are young and coming to the ER and just dropping dead,” she says.
Age, particularly those over 65, as well as having a compromised immune system are still major risk factors for being hospitalized with, and dying from, COVID-19. But some doctors say that some of their sickest patients are those under 60 who are obese.
The Centers for Disease Control and Prevention’s list of high-risk individuals includes the severely obese, defined as people with a body mass index, or BMI, over 40. While studies on coronavirus often focus on demographic breakdowns such as age, sex and race (SN: 4/10/20), some now are starting to track COVID-19 patient BMIs.  
For instance, of 180 patients hospitalized from March 1 to March 30, the most prevalent underlying condition for adults ages 18 to 49 was obesity. Of 39 patients in that age range, 23, or 59 percent, were obese, researchers report in the April 17 Morbidity and Mortality Weekly Report.
“BMI is the Achilles’ heel for American patients,” says Jennifer Lighter, an epidemiologist at New York University’s Langone School of Medicine. That could be a crucial factor in the death toll, particularly for those under 60, she says. “In China it was smoking and pollution, and Italy had a larger older population, and many grandparents lived with extended families. Here, it’s BMI that’s the issue.” 
In the United States, 42 percent of adults have a BMI over 30, the threshold for obesity, and more than 9 percent are classified as severely obese with a BMI over 40, according to the CDC. People with obesity can have other high-risk health conditions, such as hypertension or diabetes (SN: 3/20/20). But some doctors suggest a high BMI should be a risk factor in itself.
Lighter and her colleagues found that patients under 60 with a BMI over 35 were at least twice as likely to be admitted to the ICU for coronavirus than patients with healthy BMIs, the researchers report April 9 in Clinical Infectious Diseases. Those same patients were three times more likely to die from the infection than those with a lower BMI, she says.
The team tracked 3,615 people who tested positive for SARS-CoV-2, the virus that causes COVID-19, at a New York City hospital from March 4 to April 4. Of those, 1,370, or 38 percent, were obese. In patients over 60, weight did not appear to be a factor in hospital admission or the need for intensive care, she says.
A hospital in Lille, France, also found that the higher the BMI, the more likely a patient needed to be ventilated. Of 124 patients admitted to intensive care for COVID-19, almost half were obese or severely obese, researchers report April 10 in Obesity. Of the 85 patients who were intubated, nearly 90 percent had a BMI over 35, the data show. 
“The need for invasive mechanical ventilation was associated with severe obesity and [was] independent of age, sex, diabetes and hypertension,” the study says.
Sanjum Sethi, a cardiologist at Columbia University Medical Center, says his hospital is seeing a surprising number of younger patients with obesity, but no other conditions such as diabetes or high blood pressure. On April 12, he tweeted that, for obese patients, “the prognosis is extremely grim. They are NOT dying from comorbidities. They are dying from COVID-19.”
People with a high BMI already tend to have problems breathing; they carry more weight on their chest, which compresses the lungs. Because COVID-19 is mainly a respiratory disease, that may put heavier patients at a disadvantage, doctors say.
Obese people “already have lower oxygen levels, they are predisposed to pulmonary dysfunction, and they have decreased chest function because of the weight on their chest. And many have sleep apnea. So they’re at pulmonary risk already,” says Samuel Klein, a gastroenterologist and the director of the Center for Human Nutrition at Washington University School of Medicine in St. Louis.
Public health officials say people with obesity shouldn’t feel stigmatized or avoid seeking medical care; it’s important to be aware of threat COVID-19 poses. People with high BMIs might want to practice extra caution, wear a mask outside and have groceries delivered instead of going out into public, Sethi says.
“I worry this is going to have even more impact where obesity is more endemic, like in the South,” he says.   
The data should be a wake-up call for people with obesity, agrees Donna Ryan, president of the London-based World Obesity Federation. “If they do develop fever or shortness of breath, they should not hesitate, call their doctor and get tested.”
Doctors might take specific measures when treating obese patients for COVID-19, says Rekha Kumar, an obesity specialist at Weill Cornell Medical College in New York City. That might include giving them oxygen early or keeping them in the hospital longer.

COVID-19 is hitting some patients with obesity particularly hard