COVID-19 starts out in the lungs like the common cold coronaviruses, but then causes havoc with the immune system that lead to LONG TERM LUNG DAMAGE

[SBFNews]

Electron Micrograph of SARS-CoV-2. (National Institute of Allergy and Infectious Diseases/NIH/Flickr/Public Domain)
HEALTH

Virologist Explains What The Coronavirus Does to Your Body That Makes It So Deadly

BENJAMIN NEUMAN, THE CONVERSATION
6 APRIL 2020

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.

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.

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.

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.

 

[Leongsam]

Flu which is far more dangerous because it causes a large number of deaths every single year and it also kills the young in far greater numbers.

H1N1 killed up to 500,000 people in one year during the swine flu epidemic. The claim that covid-19 is ten times more lethal than flu has already been debunked.


sciencedaily.com

How Flu Damages Lung Tissue


4-5 minutes


A protein in influenza virus that helps it multiply also damages lung epithelial cells, causing fluid buildup in the lungs, according to new research from the University of Alabama at Birmingham (UAB) and Southern Research Institute. Publishing online the week of July 13 in the journal of the Federation of American Societies for Experimental Biology, the researchers say the findings give new insight into how flu attacks the lungs and provides targets for new treatments.

In severe cases of flu, fluid accumulates in the lungs, making it difficult to breathe and preventing oxygen from reaching the blood stream. The researchers report that M2, a protein in the flu virus, damages a protein responsible for clearing fluid from the lungs by increasing the amount of oxidants, or free radicals, within the cells. Oxidants are necessary for proper cell function, but can become toxic if uncontrolled.

"Under normal conditions, oxidants play an important role, as they destroy pathogens in cells. But our findings suggest that lowering the number of oxidants, or preventing their increase, would prevent damage to the lungs resulting from the M2 protein," said Sadis Matalon, Ph.D., vice chairman for research and professor of anesthesiology at UAB and principal investigator of the study.

The researchers say the recent outbreak of H1N1 influenza and the rapid spread of this strain across the world highlight both the need to better understand how the virus damages the lungs and the urgency to find new treatments. Influenza is a contagious disease leading to about 36,000 human deaths and 200,000 hospitalizations every year in the United States alone.

Matalon, along with co-investigators Ahmed Lazrak, Ph.D., and Karen E. Iles, Ph.D., from the Department of Anesthesiology at UAB, and James W. Noah, Ph.D., and Diana L. Noah, Ph.D., of Southern Research, injected frog eggs with M2 protein and the lung protein involved with fluid removal. Using molecular biology techniques, they removed part of the flu protein until they could isolate the segment responsible for the lung injury.

"We found that when the flu protein was shortened in length, it did not damage the lung protein responsible for removing fluid from the lungs," said Diana Noah. "This is important information as it will enable us to design drugs that will hopefully prevent this M2 flu protein from functioning properly, making it possible for those infected with the flu to recover faster."

Another set of experiments involved injecting intact flu proteins and their target lung proteins into frog eggs along with agents that remove oxidants. The findings of the study show that following this procedure the lung proteins were no longer damaged by the flu viruses.

The team then repeated the experiments in cells from human lungs and found the same results. "We were able to understand the basic mechanisms by which the flu damages key components of the lungs in a simple system, such as the frog eggs, and then confirm these findings in human lung cells," said Matalon.
The researchers are hesitant to say that these results indicate a simple antioxidant, such as vitamin C, can prevent or minimize flu. "The issue is too complex and we simply can't answer that yet," said James Noah. "Vaccination is our leading defense against flu and we have anti-viral drugs that are effective in some cases, but flu viruses show a remarkable ability to mutate, rendering vaccines and drugs less effective. Having a new target for potential interventions opens up an entirely new approach to combating influenza."

Funding came from the National Heart, Blood and Lung Institute and the National Institute of Environmental Health Sciences, parts of the National Institutes of Health, and the UAB Department of Anesthesiology.

 

[SeeFartLoong]

Ah Nehs will sneak and Toilet Break out to rape John Tan's Daughters & Wife at night. When KKJ got stiff and Tak Boleh Tahan.

 

[nightsafari]

Electron Micrograph of SARS-CoV-2. (National Institute of Allergy and Infectious Diseases/NIH/Flickr/Public Domain)
HEALTH

Virologist Explains What The Coronavirus Does to Your Body That Makes It So Deadly

BENJAMIN NEUMAN, THE CONVERSATION
6 APRIL 2020

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.

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.

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.

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.

excellent detail! I also note the part about how it's more severe than the flu because of duration.