COVID-19 is caused by a coronavirus called SARS-CoV-2. Coronaviruses belong to a group of viruses that infect animals, from peacocks to whales. They’re named for the bulb-tipped spikes that project from the virus’s surface and give the appearance of a corona surrounding it.

A coronavirus infection usually plays out one of two ways: as an infection in the lungs that includes some cases of what people would call the common cold, or as an infection in the gut that causes diarrhea. COVID-19 starts out in the lungs like the common cold coronaviruses, but then causes havoc with the immune system that can lead to long-term lung damage or death.

SARS-CoV-2 is genetically very similar to other human respiratory coronaviruses, including SARS-CoV and MERS-CoV. However, the subtle genetic differences translate to significant differences in how readily a coronavirus infects people and how it makes them sick.

SARS-CoV-2 has all the same genetic equipment as the original SARS-CoV, which caused a global outbreak in 2003, but with around 6,000 mutations sprinkled around in the usual places where coronaviruses change. Think whole milk versus skim milk.

Compared to other human coronaviruses like MERS-CoV, which emerged in the Middle East in 2012, the new virus has customized versions of the same general equipment for invading cells and copying itself. However, SARS-CoV-2 has a totally different set of genes called accessories, which give this new virus a little advantage in specific situations. For example, MERS has a particular protein that shuts down a cell’s ability to sound the alarm about a viral intruder. SARS-CoV-2 has an unrelated gene with an as-yet unknown function in that position in its genome. Think cow milk versus almond milk.

How the virus infects

Every coronavirus infection starts with a virus particle, a spherical shell that protects a single long string of genetic material and inserts it into a human cell. The genetic material instructs the cell to make around 30 different parts of the virus, allowing the virus to reproduce. The cells that SARS-CoV-2 prefers to infect have a protein called ACE2 on the outside that is important for regulating blood pressure.

The infection begins when the long spike proteins that protrude from the virus particle latch on to the cell’s ACE2 protein. From that point, the spike transforms, unfolding and refolding itself using coiled spring-like parts that start out buried at the core of the spike. The reconfigured spike hooks into the cell and crashes the virus particle and cell together. This forms a channel where the string of viral genetic material can snake its way into the unsuspecting cell.

An illustration of the SARS-CoV-2 spike protein shown from the side (left) and top. The protein latches onto human lung cells. 5-HT2AR/Wikimedia

SARS-CoV-2 spreads from person to person by close contact. The Shincheonji Church outbreak in South Korea in February provides a good demonstration of how and how quickly SARS-CoV-2 spreads. It seems one or two people with the virus sat face to face very close to uninfected people for several minutes at a time in a crowded room. Within two weeks, several thousand people in the country were infected, and more than half of the infections at that point were attributable to the church. The outbreak got to a fast start because public health authorities were unaware of the potential outbreak and were not testing widely at that stage. Since then, authorities have worked hard and the number of new cases in South Korea has been falling steadily.

How the virus makes people sick

SARS-CoV-2 grows in type II lung cells, which secrete a soap-like substance that helps air slip deep into the lungs, and in cells lining the throat. As with SARS, most of the damage in COVID-19, the illness caused by the new coronavirus, is caused by the immune system carrying out a scorched earth defense to stop the virus from spreading. Millions of cells from the immune system invade the infected lung tissue and cause massive amounts of damage in the process of cleaning out the virus and any infected cells.

Each COVID-19 lesion ranges from the size of a grape to the size of a grapefruit. The challenge for health care workers treating patients is to support the body and keep the blood oxygenated while the lung is repairing itself.

How SARS-CoV-2 infects, sickens and kills people

SARS-CoV-2 has a sliding scale of severity. Patients under age 10 seem to clear the virus easily, most people under 40 seem to bounce back quickly, but older people suffer from increasingly severe COVID-19. The ACE2 protein that SARS-CoV-2 uses as a door to enter cells is also important for regulating blood pressure, and it does not do its job when the virus gets there first. This is one reason COVID-19 is more severe in people with high blood pressure.

SARS-CoV-2 is more severe than seasonal influenza in part because it has many more ways to stop cells from calling out to the immune system for help. For example, one way that cells try to respond to infection is by making interferon, the alarm signaling protein. SARS-CoV-2 blocks this by a combination of camouflage, snipping off protein markers from the cell that serve as distress beacons and finally shredding any anti-viral instructions that the cell makes before they can be used. As a result, COVID-19 can fester for a month, causing a little damage each day, while most people get over a case of the flu in less than a week.

At present, the transmission rate of SARS-CoV-2 is a little higher than that of the pandemic 2009 H1N1 influenza virus, but SARS-CoV-2 is at least 10 times as deadly. From the data that is available now, COVID-19 seems a lot like severe acute respiratory syndrome (SARS), though it’s less likely than SARS to be severe.

What isn’t known

There are still many mysteries about this virus and coronaviruses in general – the nuances of how they cause disease, the way they interact with proteins inside the cell, the structure of the proteins that form new viruses and how some of the basic virus-copying machinery works.

Another unknown is how COVID-19 will respond to changes in the seasons. The flu tends to follow cold weather, both in the northern and southern hemispheres. Some other human coronaviruses spread at a low level year-round, but then seem to peak in the spring. But nobody really knows for sure why these viruses vary with the seasons.

What is amazing so far in this outbreak is all the good science that has come out so quickly. The research community learned about structures of the virus spike protein and the ACE2 protein with part of the spike protein attached just a little over a month after the genetic sequence became available. I spent my first 20 or so years working on coronaviruses without the benefit of either. This bodes well for better understanding, preventing and treating COVID-19.

By Benjamin Neuman, Professor of Biology, Texas A&M University-Texarkana. This article is republished from The Conversation under a Creative Commons license. Read the original article.

With people confined to their homes, there is more interest in home-baked bread than ever before. And that means a lot of people are making friends with yeast for the first time. I am a professor of hospitality management and a former chef, and I teach in my university’s fermentation science program.

As friends and colleagues struggle for success in using yeast in their baking – and occasionally brewing – I’m getting bombarded with questions about this interesting little microorganism.

A little cell with a lot of power

Yeasts are single-celled organisms in the fungus family. There are more than 1,500 species of them on Earth. While each individual yeast is only one cell, they are surprisingly complex and contain a nucleus, DNA and many other cellular parts found in more complicated organisms.

Yeasts break down complex molecules into simpler molecules to produce the energy they live on. They can be found on most plants, floating around in the air and in soils across the globe. There are 250 or so of these yeast species that can convert sugar into carbon dioxide and alcohol – valuable skills that humans have used for millennia. Twenty-four of these make foods that actually taste good.

Among these 24 species is one called Saccharomyces cerevisiae, which means “sugar-eating fungus.” This is bread yeast, the yeast we humans know and love most dearly for the food and drinks it helps us make.

An invisible organism with worldwide influence. KATERYNA KON/SCIENCE PHOTO LIBRARY via Getty Images via The Conversation

The process starts out the same whether you are making bread or beer. Enzymes in the yeast convert sugar into alcohol and carbon dioxide. With bread, a baker wants to capture the carbon dioxide to leaven the bread and make it rise. With beer, a brewer wants to capture the alcohol.

Bread has been “the staff of life” for thousands of years. The first loaf of bread was probably a happy accident that occurred when some yeast living on grains began to ferment while some dough for flatbreads – think matzo or crackers – was being made. The first purposely made leavened bread was likely made by Egyptians about 3,000 years ago. Leavened bread is now a staple in almost every culture on Earth. Bread is inexpensive, nutritious, delicious, portable and easy to share. Anywhere wheat, rye or barley could be grown in sufficient quantities, bread became the basic food in most people’s diet.

Yeast makes bread fluffy and flavorful. Poh Kim Yeoh/EyeEm via Getty Images via The Conversation

No yeast, no bread

When you mix yeast with a bit of water and flour, the yeast begins to eat the long chains of carbohydrates found in the flour called starches. This does two important things for baking: It changes the chemical structure of the carbohydrates, and it makes bread rise.

When yeast breaks down starch, it produces carbon dioxide gas and ethyl alcohol. This CO2 is trapped in the dough by stringy protein strands called gluten and causes the dough to rise. After baking, those little air pockets are locked into place and result in airy, fluffy bread.

But soft bread is not the only result. When yeast break down the starches in flour, it turns them into flavorful sugars. The longer you let the dough rise, the stronger these good flavors will be, and some of the most popular bread recipes use this to their advantage.

The supermarket’s out of yeast; now what?

Baking bread at home is fun and easy, but what if your store doesn’t have any yeast? Then it’s sourdough to the rescue!

Yeast is everywhere, and it’s really easy to collect yeast at home that you can use for baking. These wild yeast collections tend to gather yeasts as well as bacteria – usually Lactobacillus brevis that is used in cheese and yogurt production – that add the complex sour flavors of sourdough. Sourdough starters have been made from fruits, vegetables or even dead wasps. Pliny the Elder, the Roman naturalist and philosopher, was the first to suggest the dead wasp recipe, and it works because wasps get coated in yeasts as they eat fruit. But please don’t do this at home! You don’t need a wasp or a murder hornet to make bread. All you really need to make sourdough starter is wheat or rye flour and water; the yeast and bacteria floating around your home will do the rest.

To make your own sourdough starter, mix a half-cup of distilled water with a half-cup of whole wheat flour or rye flour. Cover the top of your jar or bowl loosely with a cloth, and let it sit somewhere warm for 24 hours. After 24 hours, stir in another quarter-cup of distilled water and a half-cup of all-purpose flour. Let it sit another 24 hours. Throw out about half of your doughy mass and stir in another quarter-cup of water and another half-cup of all-purpose flour.

Keep doing this every day until your mixture begins to bubble and smells like rising bread dough. Once you have your starter going, you can use it to make bread, pancakes, even pizza crust, and you will never have to buy yeast again.

Yeast is used in laboratories and factories as well as kitchens. borzywoj/iStock/Getty Images Plus via Getty Images via The Conversation

More than just bread and booze

Because of their similarity to complicated organisms, large size and ease of use, yeasts have been central to scientific progress for hundreds of years. Study of yeasts played a huge role in kick-starting the field of microbiology in the early 1800s. More than 150 years later, one species of yeast was the first organism with a nucleus to have its entire genome sequenced. Today, scientists use yeast in drug discovery and as tools to study cell growth in mammals and are exploring ways to use yeast to make biofuel from waste products like cornstalks.

Yeast is a remarkable little creature. It has provided delicious food and beverages for millennia, and to this day is a huge part of human life around the world. So the next time you have a glass of beer, toast our little friends that make these foods part of our enjoyment of life.

By Jeffrey Miller, Associate Professor, Hospitality Management, Colorado State University. This article is republished from The Conversation under a Creative Commons license. Read the original article.

Sudden oak death, caused by the pathogen Phythophthora ramorum, is one of the most ecologically devastating forest diseases in North America, responsible for the deaths of millions of oaks and tanoaks along the coast.

Science to the rescue? After the success of genetically modified organisms in things like insulin and food, a recent trend is Genetically Rescued Organisms. These GROs would use science to create natural resistance, like a vaccine for plants, and reduce the impact of altered species composition, released carbon pools, and greater fire risk the deaths bring.

Before that can happen, scientists need to better understand the basic biology of Phythophthora ramorum, including how well it sporulates on common plants.

Image by RegalShave from Pixabay

Scientists at the University of California, Davis, set out to investigate the sporulation potential of this pathogen on common California plant species. They collected leaves from 13 common plant hosts in the Big Sur-region and inoculated them with the causal pathogen. They found that most of the species produced spores, though there was a ride range, with bay laurel and tanoak producing significantly more sporangia than the other species. They also observed an inconsistent relationship between sporulation and lesion size, indicating that visual symptoms are not a reliable metric of sporulation potential.

 “Our study is the first to investigate the sporulation capacity on a wide range of common coastal California native plant species and with a large enough sample size to statistically distinguish between species," explained first author Dr. Lisa Rosenthal. "It largely confirms what was previously reported in observational field studies – that tanoak and bay laurel are the main drivers of sudden oak death infections—but also indicates that many other hosts are capable of producing spores.”

Citation: Lisa M. Rosenthal, Sebastian N. Fajardo, and David M. Rizzo, Sporulation Potential of Phytophthora ramorum Differs Among Common California Plant Species in the Big Sur Region, Plant Disease 17 Aug 2021 https://doi.org/10.1094/PDIS-03-20-0485-RE