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[VMC] What is a coronavirus, and why is it no threat to you.


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What is a Coronavirus, and why is it no threat to you?

Written by Dr Danielle Shaw, Director of the Vinewood Medical Clinic

 

First of all, what do we mean when we say Coronavirus?

Coronavirus refers to a particular makeup of ribonucleic acid (RNA) in the order of around 30,000 strains long. Like all viruses, the RNA is contained within a protein-based shell with receptors on the outside acting as ‘connectors’ to various cells, in particular cells within a mammal’s respiratory system. Research thus far has shown that COVID-19 (SARS-COV-2) seems to favor a particular receptor known as ACE2 within these systems. COVID-19 is similar to the previous SARS epidemic which braced the world in the early 2000s, although SARS had a higher mortality rate (subject to change possibly with time.) There are four main types of known Coronavirus, Alpha, Beta, Gamma, and Deltacoronavirus. Alpha and Beta exclusively target mammalian species, Delta can infect both birds and mammals, whereas gamma is exclusively birds and poultry. Since the first instance of transmission for SARS-CoV-2 (COVID-19) was from a deceased bat to a human, as well as similarities to the first SARS, researches believe it is under the classification of betacoronavirus. 

 

The terms COVID-19 and SARS-CoV-2 get mixed about fairly loosely, however it's important to note the condition is COVID-19, the virus is SARS-CoV-2. Or as the media loves to just call it, Coronavirus.

 

How did it start? And where?

Like SARS before it, this particular instance of betacoronavirus started within the city of Wuhan, within the Hubei province of inner china. Researchers believe the conditions of the ‘wet’ markets within China helped facilitate its survival, and upon being consumed by its buyer, the pandemic that we know was born. Without delving into politics as that is not the aim of this news update, the conditions within China were perfect to allow an explosive transmission, infecting thousands of people within the first week. Whilst true figures are unknown, the virus likely has had an impact on at least 250,000 people so far, with the official reported figure at 118,000 individuals worldwide, with a death count of 4292 (as of writing) giving a mortality rate of 3.6% (SARS had a 12% rate). Due to the nature of how minor the virus’s symptoms are, its been able to spread easily as 80% of all cases are so minor they are hardly worse than a common cold. The only notable difference between a common cold and the common strain of SARS-CoV-2 is the fact it focuses on your respiratory system, so coughs, mucal production, and fever stand out stronger.

 

Who is at risk of the more serious side of the infection?

At the moment, with research being scarce on the condition we believe that the virus is most deadly to individuals over 60, with a logarithmic growth past age 70. If individuals in this age bracket are also immunocompromised, its almost always fatal. However, below this age bracket, you are more likely to die of alcohol poisoning, a lightning strike or being hit by a car to name a few examples. It isn’t, however, unheard of for people below this age range to develop more serious side effects, however, these effects are only fatal if you are immunocompromised or unable to access a developed world’s healthcare system. The main risk factor with individuals infected with SARS-CoV-2 will be the development of pneumonia, large sacs of pus within the lungs severely restricting the ability to breathe. 

 

How long are individuals infected with the condition once contracted?

With this factor, it’s hard to say as it depends on how robust an individual’s immune response is. However, the average factor seems to be between 5 and seven days of active symptoms, 14 days at risk of spreading the infection. The best course of advice to offer individuals infected, is to remain at home, do not have contact with other individuals and drink plenty of fluids. Even when you are feeling better, be safe and wait the full 14 days before venturing back out into the world. Whilst maintaining a clean and healthy lifestyle (regularly washing one’s hands and eating plenty of fruit and veg) can help delay infection, at this rate of progression it is inevitable that you will come in contact with it eventually. This should be no major concern to you, however, as fatality risks as mentioned above are low.

 

Will there ever be a cure for SARS-CoV-2?

Short answer, no. There is no real cure for a virus, however, work has begun on trying to isolate a vaccine to help build an immune response ready for when the real virus strikes. Unlike bacteria or fungal infections, antibiotics or antifungals do not work on viruses. A virus is capable of mutating so incredibly fast that any cure we would develop would be nullified within a week as each time the condition replicates, it has a high chance of mutating. And sadly that is the nature with almost all viruses that humanity knows of.  



 

I hope this piece is able to shine a light on COVID-19/SARS-CoV-2, and provide the public with actual information on the condition without fearmongering like media attempts to replicate.

  • Upvote 2
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 Username:  ACuriousObserver

 

Comment:  While this has some informative parts, it also contains — and I characterize it this way with all due respect to Dr. Shaw — a few inaccuracies.

 

1.  At the bottom of the article, the process which this article calls a mutation is called antigenic drift.  And it’s most common in influenza viruses — not almost all viruses known to science.  While antigenic drift does occur during viral replication inside an infected host, I would be careful calling it a mutation when the intended audience is the public.  The public’s conception of “mutation” typically evokes associations with science fiction — they tend to envisage a virus rapidly acquiring devestating characteristics (as seen in the 1994 bestseller The Hot Zone — and its corresponding 2019 miniseries by the same name, as well as the 1995 film Outbreak — where an Ebola-like virus in Chimpanzees rapidly became airborne); the term “mutation” evokes images of Marvel figures acquiring supernatural abilities from dramatized mutations.  The reality is markedly different.  For many folks, I think a gentle reminder that changes to virus genetics in the virus’ population is quite undramatic and boring might be in order.  While a virus can become more virulent (cause more serious disease / poorer prognosis) or more infectious (transmit easily between hosts), or jump between host species (e.g. pangolins to humans), these changes can be self-limiting and are always affected by the niceties of nature selection, which Hollywood depictions of outbreaks tend to gloss over.

 

Antigenic drift is even a less dramatic than what’s depicted by Hollywood cinema.  All it involves is changing the antigen markers on the surface (or ”viral protein envelope,” for microbiology lingo) of the virus.  What this ultimately does is disguise the virus from the host’s immune system — it can be likened to a robber putting on a disguise to become unrecognizable when they enter the same bank to rob it again.  In the first instance of the virus’ exposure to a host’s immune system, during the immune response, markers known as antibodies are developed to match the antigens on the surface of the virus.  That way, next time the the virus invades a host, its immune system immediately recognizes it as a foreign pathogen and B Cells (a type of lymphocyte, and part of the immune response) can release antibodies to attack the antigens on the virus.  
 

But when a virus such as one of the influenza viruses undergoes antigenic drift (changes its antigens), the host’s antibodies no longer match the new antigens — it can be said that the influenza has disguised itself.  Influenza viruses often disguise themselves through antigenic drift, which explains why new vaccines have to be developed every year.  But it is wrong to say that SARS-CoV-2 or novel Coronavirus 2019 is capable of antigenic drift and, as a consequence, avoid any vaccine developed for it — it’s quite possible that a vaccine will, eventually, eradicate it.  It’s too soon to say that novel Coronavirus 2019 is as elusive as influenza viruses.  
 

SARS did not have a vaccine because the 2003 epidemic ended before the vaccines being developed at the time could reach clinical trials; it is not because SARS virus “overcame” any vaccine with antigenic drift and that this change spread in the SARS population.  It simply became obsolete and so the vaccines were never brought to clinical trials.

 

2.  The advice in the fourth answer is a bit worrisome.  Fourteen days used to be regarded as the average incubation period (a study at John Hopkins University estimates an incubation period average of as low as 5.1 days; but it can be as low as two days).  This is the period during which one is generally contagious and is asymptomatic (not displaying any symptoms).  It is unclear if every asymptomatic person can transmit the virus, but they generally can.  And even after developing symptoms at 14 days, one can still be contagious and release aerosol droplets when they cough.  The takeaway is 14 days is the minimum — one should self-isolate, and otherwise show basic courtesy (eg. coughing into a tissue and disposing it properly) to avoid spreading it.
 

Good hygienic practice is always helpful, but one study out of Singapore suggested that regular cleaning of surfaces, especially surfaces which which people frequently come into contact, is also necessary.  That study found those who were carriers would shedded it everywhere — on surfaces too, not just through aerosol droplets. P
 

3.  I am skeptical of the first para. where it says “the first instance of transmission [...] was from a deceased bat to a human.”  I am curious to see the source here.  While two Chinese studies (here and heresuggested a bat origin, there is a theory that, for 2019-nCoV, there is an intermediate host, and that pangolins are that host. In other words, the jump was from pangolins to humans, at least that’s how the theory goes. 
 

A lot of the recent studies — if not all — are inconclusive.  (Some are published without being peer-reviewed because of the overwhelming number of submissions journals receive).  It should be recalled that both SARS and MERS (another virus in the same family) had non-bat intermediate hosts; for SARS, recent evidence pointed to civets (a cat-like mammal) and for MERS, camels.  Like SARS and MERS, I don’t think COVID-19 came directly from bats; the pangolin theory might turn out to be correct. 
 

For those who are concerned, basic hygienic practice is all that’s necessary on your part (especially if you live with someone whose medication or condition suppresses their immune system, or if they have other underlying conditions).  Don’t be indifferent or complacent, but there’s also no reason to be panicking — the virus will not undergo a Hulk-like transformation. 
 

 


 


 


 


 

 


 

Edited by Midsummer Night's Dream
  • Upvote 1
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On 3/12/2020 at 4:47 AM, Midsummer Night's Dream said:

 Username:  ACuriousObserver

 

Comment:  While this has some informative parts, it also contains — and I characterize it this way with all due respect to Dr. Shaw — a few inaccuracies.

 

1.  At the bottom of the article, the process which this article calls a mutation is called antigenic drift.  And it’s most common in influenza viruses — not almost all viruses known to science.  While antigenic drift does occur during viral replication inside an infected host, I would be careful calling it a mutation when the intended audience is the public.  The public’s conception of “mutation” typically evokes associations with science fiction — they tend to envisage a virus rapidly acquiring devestating characteristics (as seen in the 1994 bestseller The Hot Zone — and its corresponding 2019 miniseries by the same name, as well as the 1995 film Outbreak — where an Ebola-like virus in Chimpanzees rapidly became airborne); the term “mutation” evokes images of Marvel figures acquiring supernatural abilities from dramatized mutations.  The reality is markedly different.  For many folks, I think a gentle reminder that changes to virus genetics in the virus’ population is quite undramatic and boring might be in order.  While a virus can become more virulent (cause more serious disease / poorer prognosis) or more infectious (transmit easily between hosts), or jump between host species (e.g. pangolins to humans), these changes can be self-limiting and are always affected by the niceties of nature selection, which Hollywood depictions of outbreaks tend to gloss over.

 

Antigenic drift is even a less dramatic than what’s depicted by Hollywood cinema.  All it involves is changing the antigen markers on the surface (or ”viral protein envelope,” for microbiology lingo) of the virus.  What this ultimately does is disguise the virus from the host’s immune system — it can be likened to a robber putting on a disguise to become unrecognizable when they enter the same bank to rob it again.  In the first instance of the virus’ exposure to a host’s immune system, during the immune response, markers known as antibodies are developed to match the antigens on the surface of the virus.  That way, next time the the virus invades a host, its immune system immediately recognizes it as a foreign pathogen and B Cells (a type of lymphocyte, and part of the immune response) can release antibodies to attack the antigens on the virus.  
 

But when a virus such as one of the influenza viruses undergoes antigenic drift (changes its antigens), the host’s antibodies no longer match the new antigens — it can be said that the influenza has disguised itself.  Influenza viruses often disguise themselves through antigenic drift, which explains why new vaccines have to be developed every year.  But it is wrong to say that SARS-CoV-2 or novel Coronavirus 2019 is capable of antigenic drift and, as a consequence, avoid any vaccine developed for it — it’s quite possible that a vaccine will, eventually, eradicate it.  It’s too soon to say that novel Coronavirus 2019 is as elusive as influenza viruses.  
 

SARS did not have a vaccine because the 2003 epidemic ended before the vaccines being developed at the time could reach clinical trials; it is not because SARS virus “overcame” any vaccine with antigenic drift and that this change spread in the SARS population.  It simply became obsolete and so the vaccines were never brought to clinical trials.

 

2.  The advice in the fourth answer is a bit worrisome.  Fourteen days used to be regarded as the average incubation period (a study at John Hopkins University estimates an incubation period average of as low as 5.1 days; but it can be as low as two days).  This is the period during which one is generally contagious and is asymptomatic (not displaying any symptoms).  It is unclear if every asymptomatic person can transmit the virus, but they generally can.  And even after developing symptoms at 14 days, one can still be contagious and release aerosol droplets when they cough.  The takeaway is 14 days is the minimum — one should self-isolate, and otherwise show basic courtesy (eg. coughing into a tissue and disposing it properly) to avoid spreading it.
 

Good hygienic practice is always helpful, but one study out of Singapore suggested that regular cleaning of surfaces, especially surfaces which which people frequently come into contact, is also necessary.  That study found those who were carriers would shedded it everywhere — on surfaces too, not just through aerosol droplets. P
 

3.  I am skeptical of the first para. where it says “the first instance of transmission [...] was from a deceased bat to a human.”  I am curious to see the source here.  While two Chinese studies (here and heresuggested a bat origin, there is a theory that, for 2019-nCoV, there is an intermediate host, and that pangolins are that host. In other words, the jump was from pangolins to humans, at least that’s how the theory goes. 
 

A lot of the recent studies — if not all — are inconclusive.  (Some are published without being peer-reviewed because of the overwhelming number of submissions journals receive).  It should be recalled that both SARS and MERS (another virus in the same family) had non-bat intermediate hosts; for SARS, recent evidence pointed to civets (a cat-like mammal) and for MERS, camels.  Like SARS and MERS, I don’t think COVID-19 came directly from bats; the pangolin theory might turn out to be correct. 
 

For those who are concerned, basic hygienic practice is all that’s necessary on your part (especially if you live with someone whose medication or condition suppresses their immune system, or if they have other underlying conditions).  Don’t be indifferent or complacent, but there’s also no reason to be panicking — the virus will not undergo a Hulk-like transformation. 
 

 


 


 


 


 

 


 

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Comment: nerd

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