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.

Imagine trying to cope with a pandemic like COVID-19 in a world where microscopic life was unknown. Prior to the 17th century, people were limited by what they could see with their own two eyes. But then a Dutch cloth merchant changed everything.

His name was Antonie van Leeuwenhoek, and he lived from 1632 to 1723. Although untrained in science, Leeuwenhoek became the greatest lens-maker of his day, discovered microscopic life forms and is known today as the “father of microbiology.”

Visualizing ‘animalcules’ with a ‘small see-er’

Leeuwenhoek opened the door to a vast, previously unseen world. J. Verolje/Wellcome Collection, CC BY

Leeuwenhoek didn’t set out to identify microbes. Instead, he was trying to assess the quality of thread. He developed a method for making lenses by heating thin filaments of glass to make tiny spheres. His lenses were of such high quality he saw things no one else could.

This enabled him to train his microscope – literally, “small see-er” – on a new and largely unexpected realm: objects, including organisms, far too small to be seen by the naked eye. He was the first to visualize red blood cells, blood flow in capillaries and sperm.

Drawings from a Leeuwenhoek letter in 1683 illustrating human mouth bacteria. Huydang2910, CC BY-SA

Leeuwenhoek was also the first human being to see a bacterium – and the importance of this discovery for microbiology and medicine can hardly be overstated. Yet he was reluctant to publish his findings, due to his lack of formal education. Eventually, friends prevailed upon him to do so.

He wrote, “Whenever I found out anything remarkable, I thought it my duty to put down my discovery on paper, so that all ingenious people might be informed thereof.” He was guided by his curiosity and joy in discovery, asserting “I’ve taken no notice of those who have said why take so much trouble and what good is it?”

When he reported visualizing “animalcules” (tiny animals) swimming in a drop of pond water, members of the scientific community questioned his reliability. After his findings were corroborated by reliable religious and scientific authorities, they were published, and in 1680 he was invited to join the Royal Society in London, then the world’s premier scientific body.

Leeuwenhoek was not the world’s only microscopist. In England, his contemporary Robert Hooke coined the term “cell” to describe the basic unit of life and published his “Micrographia,” featuring incredibly detailed images of insects and the like, which became the first scientific best-seller. Hooke, however, did not identify bacteria.

Despite Leuwenhoek’s prowess as a lens-maker, even he could not see viruses. They are about 1/100th the size of bacteria, much too small to be visualized by light microscopes, which because of the physics of light can magnify only thousands of times. Viruses weren’t visualized until 1931 with the invention of electron microscopes, which could magnify by the millions.

An image of the hepatitis virus courtesy of the electron microscope. E.H. Cook, Jr./CDC via Associated Press

A vast, previously unseen world

Leeuwenhoek and his successors opened up, by far, the largest realm of life. For example, all the bacteria on Earth outweigh humans by more than 1,100 times and outnumber us by an unimaginable margin. There is fossil evidence that bacteria were among the first life forms on Earth, dating back over 3 billion years, and today it is thought the planet houses about 5 nonillion (1 followed by 30 zeroes) bacteria.

Some species of bacteria cause diseases, such as cholera, syphilis and strep throat; while others, known as extremophiles, can survive at temperatures beyond the boiling and freezing points of water, from the upper reaches of the atmosphere to the deepest points of the oceans. Also, the number of harmless bacterial cells on and in our bodies likely outnumber the human ones.

Viruses, which include the coronavirus SARS-CoV-2 that causes COVID-19, outnumber bacteria by a factor of 100, meaning there are more of them on Earth than stars in the universe. They, too, are found everywhere, from the upper atmosphere to the ocean depths.

A visualization of the human rhinovirus 14, one of many viruses that cause the common cold. Protein spikes are colored white for clarity. Thomas Splettstoesser, CC BY-SA

Strangely, viruses probably do not qualify as living organisms. They can replicate only by infecting other organisms’ cells, where they hijack cellular systems to make copies of themselves, sometimes causing the death of the infected cell.

It is important to remember that microbes such as bacteria and viruses do far more than cause disease, and many are vital to life. For example, bacteria synthesize vitamin B12, without which most living organisms would not be able to make DNA.

Likewise, viruses cause diseases such as the common cold, influenza and COVID-19, but they also play a vital role in transferring genes between species, which helps to increase genetic diversity and propel evolution. Today researchers use viruses to treat diseases such as cancer.

Scientists’ understanding of microbes has progressed a long way since Leeuwenhoek, including the development of antibiotics against bacteria and vaccines against viruses including SARS-CoV-2.

But it was Leeuwenhoek who first opened people’s eyes to life’s vast microscopic realm, a discovery that continues to transform the world.

By Richard Gunderman, Chancellor's Professor of Medicine, Liberal Arts, and Philanthropy, Indiana 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