2019 Coronavirus (SARS-CoV-2) hits the UK

acatweasel

Well-known Member
Thanks Mr Starfarer, that article link was very useful. I’ve had a look at the item and linked articles, and I’m sure that will be very useful work in treating the disease, vaccines production, etc. At the moment they have a lot of work to do to confirm the observations they have on immune response and a variety of symptoms. It’s going to take a while to get to the bottom of this work.

If you can stand the thoughts of Chairman Mark here, then read on. Note that I am often wrong, as my wife tells me every day, so don’t read this as gospel.

I’m having trouble believing that the virus can directly cause some of the situations being observed. It appears to me that many of the items being seen are secondary effects. Example: blood clotting. Is the virus transplanting genetic material/enzymes to cause that directly? Answer: probably not. Why/how would it? Viruses don’t carry that much genetic material, and are successful because they are very good at the reproductive job in hand.
  • Shake hands with host cell and get invited in
  • Hijack host cell to become virus factory
  • Burst cell open and spread more viruses
So try this for the story of what might be happening, sorry if it’s near the knuckle for anyone:

Scenario 1 -Virus arrives in respiratory tract. Hijacks, replicates itself and destroys host cells. Histamine released by mast and basophil cells in response to cell damage in the respiratory tract. Among other things blood vessels widen and inflammatory response starts. White Blood Cells of all types drawn to the area and they are looking for trouble. In this particular case the patient is young/strong/has previous experience dealing with a close relative to COVID-19. The WBCs chat amongst themselves, refer back to central command to refine antibodies and the killer cells, and launch the assault. Virus beaten in a matter of hours. WBCs are now circulating in the bloodstream that have this virus’s number should it appear elsewhere. Memory immune cells created.

Little damage, asymptomatic, maybe a light cough and bit of a temperature, lifelong immunity. Job done.


Scenario 2 – Same deal as above up until “In this particular case” and now the patient is old/immunocompromised/otherwise ill, or has no previous experience of dealing with COVID-19s relatives. The WBC chat consists of “What is this?” and starts trials on antibody and killer cell development. By the time the immune response is developed enough to deal with it, the virus has infected a lot of your respiratory linings and bacteria are setting up to give you pneumonia. The virus is circulating unopposed in your bloodstream.

From the evidence so far, I can’t determine if the virus can infect similar tissues, such as organ envelopes, blood vessels, etc. Maybe not, but the virus will now be detected elsewhere just because it is circulating.

By this time, you have a ventilator tube in your throat due to impaired lung function and your immune system has worked out an effective response. Unfortunately, the battle has turned into a war. Your own killer T-cells are destroying large numbers of infected cells and increasing the damage in their attempts to beat the virus, particularly in your airways and the associated blood vessels around them.

Your other systems are trying to repair the damage. Clotting agents are being produced locally, but some excess circulates in your bloodstream and produces clots in the poorly fed extremities of your body. Not only are you very sick, but to cap it all your feet hurt.

Not good, where’s that vaccine?
 
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maddy

Well-known Member
Good list of people being interviewed today:


Witness(es): Dr Ellen Brooks Pollock, Lecturer in Infectious Disease Mathematical Modelling, University of Bristol; Professor Neil Ferguson OBE, Head of the Department of Infectious Disease Epidemiology, School of Public Health, Imperial College London; Professor Matt Keeling, Professor of Mathematics and Life Sciences, University of Warwick; Dr Adam Kucharski, Associate Professor, Department of Infectious Disease Epidemiology, London School of Hygiene and Tropical Medicine
Witness(es): Dr Paul Birrell, Postdoctoral Researcher, Medical Research Council (MRC) Biostatistics Unit, University of Cambridge; Professor Mark Woolhouse OBE, Professor of Infectious Disease Epidemiology, University of Edinburgh
 

starfarer

Well-known Member
So would that fit in with this article about SARS-CoV-2 being a vasculotropic virus then?

Very interesting and the hypothesis makes sense on symptoms that they mentioned in there. Family of coronaviruses to which this Sars Cov2 belongs usually cause just upper respiratory tract diseases. From URT to blood vessel is some serious jump in their evolution process. It's a very recent publication and better to wait for more research.
 

simonblue

Distinguished Member

Ste7en

Distinguished Member
Sounds pretty similar to people with leukaemia, in some ways.

Lots of us are being told by our consultants that there is "No need to shield" and "You are no longer considered 'clinically extremely vulnerable' as you are at no greater risk of contracting COVID-19".

Totally contradicting the official government guidelines.

I've tried explaining it a bunch of times that we are at no greater risk of contracting it. But if we did get it, we'll wish we shielded"


Pretty shocking the crap people are being told :(
 

Lancia34

Distinguished Member
And more shocking news...not...

Sweden's state epidemiologist, who was behind the country's policy of not having a lockdown, has admitted it should have imposed more restrictions to control the spread of the virus.

For months Anders Tegnell defended his approach as more sustainable, while criticising other countries for their lockdowns.

But this morning, when an interviewer on Sveriges Radio said too many people had died in the country, Tegnell agreed.

He then said: "If we would encounter the same disease, with exactly what we know about it today, I think we would land midway between what Sweden did and what the rest of the world did."

Sweden has the highest per-capita death rate from coronavirus in the world. More than 4,400 people in the country have died, while neighbouring Norway, Denmark and Finland all have death tolls of fewer than 600.
 

Lancia34

Distinguished Member

richp007

Distinguished Member
I thought watching the briefing today (I only did so because Johnson was wheeled out for a cameo), both Whitty and Vallance seemed a bit frosty towards the lockdown being eased.

They just appeared a little more segregated from Johnson I felt. Like it's "them" deciding this course of action, not us.

And I got the impression Whitty wasn't overjoyed that the test and trace system wasn't upto speed.
 

Ste7en

Distinguished Member
Watching Alok Sharma in the Commons yesterday was eerily like watching Iraj Harichi back in February.

Supposedly a bout of Hay Fever, but I dunno...
 

maddy

Well-known Member
Anyone thinking of going to Spain for a holiday, given that they've reported zero deaths from COVID-19 a few times?

Have a read of this:


Their reporting methodology has changed, not for the better.
 

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