Coronavirus - Page 308 - Business, Finances and Investing Forum

Diners will get a 50% discount off their restaurant bill during August under government plans to bolster the embattled hospitality sector.

Chancellor Rishi Sunak unveiled the "eat out to help out" discount as part of a series of measures to restart the economy amid the coronavirus pandemic.

The deal means people can get up to £10 off per head if they eat out between Monday and Wednesday.

https://www.bbc.co.uk/news/business-53337170

07-08-2020 , 01:25 PM

#7677

Seedless00

journeyman

Join Date: Mar 2020 Posts: 364

Very interested to see what the death count for today will be. Does anyone have data to show what the median-age of the infected is? Would be great if a comparison could be used and compared to the first wave where we had 2k - 2.5k new deaths per day at the peak. I understand our testing may also be a bit better then it was during the first wave, so that needs to be accounted for also.

07-08-2020 , 07:44 PM

#7678

TooCuriousso1

Golden 2017

Join Date: Jul 2008 Posts: 6,711

Quote:

Originally Posted by ToothSayer

Two main reasons:

The same place where the CDC puts it - around 70% under normal conditions living a normal life. Maybe 40-50% when not living a normal life, like now?

This is the # I'm pretty interested in.
How likely is it to be accurate?
Doesn't R decrease as % infected go up?
Shouldn't we look to somewhere like Sweden? I don't understand why their graphs look the way they do if it's gonna take 50%

07-08-2020 , 08:07 PM

#7679

ToothSayer

Carpal \'Tunnel

Join Date: Jul 2015 Posts: 13,237

Quote:

Originally Posted by TooCuriousso1

Well, unless you think the magic number is 6%, the theory that antibodies are doing it just isn't viable.

Quote:

STOCKHOLM, June 18 (Reuters) - Around 6 percent of people in Sweden have developed COVID-19 antibodies, a study by the country’s Health Agency showed on Thursday.

“The spread is lower than we have thought but not a lot lower,” Chief Epidemiologist Anders Tegnell told a news conference.

It's the same everywhere in the world - antibody tests show a IFR of 1%. So if 600 per 100K have died (around the worst in the world at the country level), then they come in with a 6% rate of infection.

The data conclusively, overwhelmingly shows that it's changed behavior and not antibodies driving what we see now.

Last edited by ToothSayer; 07-08-2020 at 08:16 PM.

07-08-2020 , 08:17 PM

#7680

chezlaw

Limey Bastard

Join Date: Jan 2004 Posts: 46,888

It may be so unevenly distributed that the infected rate in areas with lots of cases and less natural separation is much higher than 6%. Maybe enough to account for a slightly slower spread than expected (if it's not already in the model)?

07-08-2020 , 08:26 PM

#7681

ToothSayer

Carpal \'Tunnel

Join Date: Jul 2015 Posts: 13,237

It's just an unimportant factor at these antibody levels by any analysis you do. Distancing and summer and still partial shutdown >>>>> antibodies except for the places where 0.3+% have died already.

And the Spanish study blows apart the node thesis, showing fairly solid uniformity that you wouldn't expect if there was a strong high spread node element to it.

It's a nice clean simple thesis (more people are immune now so it's a lot less) which is why people are getting attached to it, but the data overwhelmingly suggests that it isn't the cause of the lower transmission rates now.

07-08-2020 , 08:36 PM

#7682

JoeC2012

veteran

Join Date: May 2012 Posts: 2,717

Quote:

Originally Posted by Shuffle

I know you asked Tooth but I'm just chiming in with this:

It's chaos and dysfunction, stupid people running head first into a brick wall.

I don't think it's going to be full lockdowns everywhere at the same time, it's going to be every state and every man for himself. Some places where they are refusing to back down, being pushed in that direction from the White House it seems, are going to run head first into reality.

Think the social unrest 1-2 months ago was something? Wait until the health care sytem in some of these areas collapses and law and order breaks down. I'm predicting there will be more autonomous zones where local civil and police forces lose control of government function.

I still think unrest is going to be the biggest second-order effect of COVID that few people have sufficiently on their radar

07-08-2020 , 09:19 PM

#7683

chezlaw

Limey Bastard

Join Date: Jan 2004 Posts: 46,888

Quote:

Originally Posted by ToothSayer

Ok thanks. I haven't looked at the data so much and I'm more attached to the behavior theory anyway.

07-10-2020 , 01:18 AM

#7684

Kelhus100

banned

Join Date: Mar 2020 Posts: 2,504

Quote:

Originally Posted by Shuffle

Lots of studies now showing that antibodies only last for a few weeks or few months, at most.

https://news.yahoo.com/research-coal...194200542.html

Well, that is the norm for cold viruses (which include human coronaviruses). There are a lot of cold viruses, but there aren't that many. If immunity lasted a long time, we would stop getting colds at some point.

Of course even if plasma cells stop actively pumping out antibodies, you still have dormant memory B cells (the precursor for antibody producing plasma cells) and memory T cells that might react to the virus faster and more effectively the second time around, so infection won't be as severe.

Of course there are also reports that some subset of people may have permanently weakened immune systems from Covid, so they might be more vulnerable to a second round of Covid (and a lot of other diseases).

07-10-2020 , 04:51 AM

#7685

chytry

Pooh-Bah

Join Date: Feb 2010 Posts: 4,334

^^ Cold viruses mutate much much faster than coronaviruses.

07-10-2020 , 05:56 AM

#7686

Kelhus100

banned

Join Date: Mar 2020 Posts: 2,504

Quote:

Originally Posted by chytry

^^ Cold viruses mutate much much faster than coronaviruses.

Coronaviruses are a subset of cold viruses, that constitute about 1/3 of common colds. So you really can't treat them as 2 non-overlapping entities.

Also, I don't know if COVID-19 actually mutates slower than other coronaviruses because of some unique physiological limitation that can't be overcome, or we just aren't seeing a lot of new mutations take over right now. Maybe you have information it actually mutates slower?

Mutation is random, but generally viruses (and all other life forms) evolve in response to need and opportunity. COVID-19 has little need to evolve right now, as it is spreading just fine as is. If/when we develop better therapeutics and vaccines, there will be selective pressure on COVID-19 to evolve as a countermeasure, and we may find it has the capacity to mutate just fine.

07-10-2020 , 09:32 AM

#7687

chytry

Pooh-Bah

Join Date: Feb 2010 Posts: 4,334

Quote:

Originally Posted by Kelhus100

https://www.livescience.com/coronavi...tion-rate.html
https://medicalxpress.com/news/2020-...owly-good.html

07-10-2020 , 11:34 AM

#7688

Kelhus100

banned

Join Date: Mar 2020 Posts: 2,504

Quote:

Originally Posted by chytry

https://www.livescience.com/coronavi...tion-rate.html
https://medicalxpress.com/news/2020-...owly-good.html

The first article is comparing it to flu virus, so that is completely irrelevant.
That is basically arguing one species of elephant evolves faster than other species because dolphins evolve faster.

The second article is addressing how the virus is evolving in the moment, not whether it has the capacity to evolve.

Neither of those articles addresses my point at all.

If/When there is a vaccine or effective therapeutic that inhibits the virus's ability to replicate, that will create a selective pressure, and we don't know how COVID will respond to the pressure. We are hoping it won't be able to respond at all, and we will defeat it, but I am not sure the totality of evidence suggests that is the likely scenario.

07-10-2020 , 02:18 PM

#7689

bucktotal

old hand

Join Date: May 2006 Posts: 1,667

Corona viruses typically have relatively low mutation rates, much lower than the flu, more like measles, making it a good candidate for vaccines. But, they also tend to induce short antibody responses, like months, making them typically a bad candidate for vaccines.

For the common cold viruses, including coronaviruses, the effects are not severe enough to warrant getting repeated vaccinations. But for Covid-19, if its worth it, i'm sure some people like health care workers, would take a vaccine every few months.

07-10-2020 , 02:36 PM

#7690

chezlaw

Limey Bastard

Join Date: Jan 2004 Posts: 46,888

fwiw the oxford vaccine is expected, if it works, to produce a strong T-cell response as well as an antibody one.

And they seem to think that taking the vaccine every year or 2 would be likely to be enough.

07-10-2020 , 04:06 PM

#7691

WollyMammoth

newbie

Join Date: Jun 2020 Posts: 19

Shut down the world... over the "cold virus"

More like economic coup attempt and War on the Middle Class.

07-10-2020 , 06:03 PM

#7692

Cuepee

Carpal \'Tunnel

Join Date: Feb 2010 Posts: 17,339

Miami Dade mayor issues stay at home order as things spike even more out of control.

Florida Governor immediately issues statement that the Mayor's order is more a request than an order since he does not have the authority to enforce it.

sigh.

07-10-2020 , 10:48 PM

#7693

5 south

Carpal \'Tunnel

Join Date: Aug 2008 Posts: 6,678

Quote:

Originally Posted by Cuepee

Nothing like having your legs chopped out from under you.
Resident YouTube Dr Campbell reported that 33% of Miami CV deaths are under 60.

07-10-2020 , 11:15 PM

#7694

PuttingInTheGrind

banned

Join Date: Jan 2020 Posts: 172

Quote:

Originally Posted by chezlaw

Britain can achieve anything if we put or mind to it. Didn't have the greatest ever empire in history for no reason.

The remainer losers are moaning at the fact that the UK opted out of the EU Covid-19 vaccine scheme. However the European Commission suggested London would be unable to take part in the plan’s governance or negotiating team. Therefore we would not have had any say in which vaccines to procure, at what price or in what quantity and to what delivery schedule.

The UK is also leaps and bounds ahead of the pathetic EU when it comes to getting a vaccine.

07-11-2020 , 01:35 AM

#7695

nutella virus

banned

Join Date: Mar 2016 Posts: 3,628

All hail britain

07-11-2020 , 03:40 AM

#7696

O.A.F.K.1.1

Ted Patrick

Join Date: Dec 2007 Posts: 27,952

Yep all hail leaves on the track Britain.

07-11-2020 , 05:42 AM

#7697

despacito

old hand

Join Date: Nov 2018 Posts: 1,369

Neurological complications of Covid-19 can include delirium, brain inflammation, stroke and nerve damage, finds a new UCL and UCLH-led study.

https://www.ucl.ac.uk/news/2020/jul/...inked-covid-19

Quote:

Published in the journal Brain, the research team identified one rare and sometimes fatal inflammatory condition, known as ADEM, which appears to be increasing in prevalence due to the pandemic.

Some patients in the study did not experience severe respiratory symptoms, and the neurological disorder was the first and main presentation of Covid-19.

Joint senior author Dr Michael Zandi (UCL Queen Square Institute of Neurology and University College London Hospitals NHS Foundation Trust) said: “We identified a higher than expected number of people with neurological conditions such as brain inflammation, which did not always correlate with the severity of respiratory symptoms.

“We should be vigilant and look out for these complications in people who have had Covid-19. Whether we will see an epidemic on a large scale of brain damage linked to the pandemic – perhaps similar to the encephalitis lethargica outbreak in the 1920s and 1930s after the 1918 influenza pandemic – remains to be seen.”

The study provides a detailed account of neurological symptoms of 43 people (aged 16-85) treated at the National Hospital for Neurology and Neurosurgery, UCLH, who had either confirmed or suspected Covid-19.

The researchers identified 10 cases of transient encephalopathies (temporary brain dysfunction) with delirium, which corresponds with other studies finding evidence of delirium with agitation. There were also 12 cases of brain inflammation, eight cases of strokes, and eight others with nerve damage, mainly Guillain-Barré syndrome (which usually occurs after a respiratory or gastrointestinal infection).

Most (nine out of 12 cases) of those with brain inflammation conditions were diagnosed with acute disseminated encephalomyelitis (ADEM). ADEM is rare and typically seen in children and can be triggered by viral infections: the team in London normally sees about one adult patient with ADEM per month, but that increased to at least one per week during the study period, which the researchers say is a concerning increase.

The virus causing Covid-19, SARS-CoV-2, was not detected in the cerebrospinal brain fluid of any of the patients tested, suggesting the virus did not directly attack the brain to cause the neurological illness. Further research is needed to identify why patients were developing these complications.

In some patients, the researchers found evidence that the brain inflammation was likely caused by an immune response to the disease, suggesting that some neurological complications of Covid-19 might come from the immune response rather than the virus itself.

The findings add clinical descriptions and detail to another recent study, which also involved Dr Zandi and co-author Dr Hadi Manji (UCL Queen Square Institute of Neurology and UCLH) identifying 153 people with neurological complications from Covid-19.* This paper also confirms the previously reported findings of a higher than expected number of patients with stroke which results from the excessive stickiness of the blood in COVID-19 patients.**

Joint first author Dr Ross Paterson (UCL Queen Square Institute of Neurology) said: “Given that the disease has only been around for a matter of months, we might not yet know what long-term damage Covid-19 can cause.

“Doctors needs to be aware of possible neurological effects, as early diagnosis can improve patient outcomes. People recovering from the virus should seek professional health advice if they experience neurological symptoms,” he added.

Joint first author Dr Rachel Brown (UCL Queen Square Institute of Neurology and UCL Infection & Immunity) said: "Our study advances understanding of the different ways in which Covid-19 can affect the brain, which will be paramount in the collective effort to support and manage patients in their treatment and recovery.”

Joint senior author Dr Hadi Manji said: “Our study amalgamates, for the first time, the clinical presentations of patients with Covid-19 neurological disease with MRI and laboratory features including, in one case, a brain biopsy.

“This now sets up a template for other researchers around the world, facilitating coordinated research to optimise the diagnosis and treatments of these complications, which to date, has proved difficult. In addition, patients are going to require long term follow up.”

The researchers were supported by the National Institute for Health Research UCLH Biomedical Research Centre, Medical Research Council, Alzheimer's Association, and the UK Dementia Research Institute.

Full study manuscript in Brain journal:
https://academic.oup.com/brain/artic...waa240/5868408

Quote:

Originally Posted by Study Abstract

Preliminary clinical data indicate that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with neurological and neuropsychiatric illness. Responding to this, a weekly virtual coronavirus disease 19 (COVID-19) neurology multi-disciplinary meeting was established at the National Hospital, Queen Square, in early March 2020 in order to discuss and begin to understand neurological presentations in patients with suspected COVID-19-related neurological disorders. Detailed clinical and paraclinical data were collected from cases where the diagnosis of COVID-19 was confirmed through RNA PCR, or where the diagnosis was probable/possible according to World Health Organization criteria. Of 43 patients, 29 were SARS-CoV-2 PCR positive and definite, eight probable and six possible. Five major categories emerged: (i) encephalopathies (n = 10) with delirium/psychosis and no distinct MRI or CSF abnormalities, and with 9/10 making a full or partial recovery with supportive care only; (ii) inflammatory CNS syndromes (n = 12) including encephalitis (n = 2, para- or post-infectious), acute disseminated encephalomyelitis (n = 9), with haemorrhage in five, necrosis in one, and myelitis in two, and isolated myelitis (n = 1). Of these, 10 were treated with corticosteroids, and three of these patients also received intravenous immunoglobulin; one made a full recovery, 10 of 12 made a partial recovery, and one patient died; (iii) ischaemic strokes (n = 8) associated with a pro-thrombotic state (four with pulmonary thromboembolism), one of whom died; (iv) peripheral neurological disorders (n = 8), seven with Guillain-Barré syndrome, one with brachial plexopathy, six of eight making a partial and ongoing recovery; and (v) five patients with miscellaneous central disorders who did not fit these categories. SARS-CoV-2 infection is associated with a wide spectrum of neurological syndromes affecting the whole neuraxis, including the cerebral vasculature and, in some cases, responding to immunotherapies. The high incidence of acute disseminated encephalomyelitis, particularly with haemorrhagic change, is striking. This complication was not related to the severity of the respiratory COVID-19 disease. Early recognition, investigation and management of COVID-19-related neurological disease is challenging. Further clinical, neuroradiological, biomarker and neuropathological studies are essential to determine the underlying pathobiological mechanisms, which will guide treatment. Longitudinal follow-up studies will be necessary to ascertain the long-term neurological and neuropsychological consequences of this pandemic.

Last edited by despacito; 07-11-2020 at 05:49 AM.

07-11-2020 , 05:51 AM

#7698

despacito

old hand

Join Date: Nov 2018 Posts: 1,369

High frequency of cerebrospinal fluid autoantibodies in COVID-19 patients with neurological symptoms (PRE-PRINT, not peer reviewed, German study):

Quote:

COVID-19 intensive care patients occasionally develop neurological symptoms. The absence of SARS-CoV-2 in most cerebrospinal fluid (CSF) samples suggests the involvement of further mechanisms including autoimmunity. We therefore determined whether anti-neuronal or anti-glial autoantibodies are present in eleven consecutive severely ill COVID-19 patients presenting with unexplained neurological symptoms. These included myoclonus, cranial nerve involvement, oculomotor disturbance, delirium, dystonia and epileptic seizures. Most patients showed signs of CSF inflammation and increased levels of neurofilament light chain. All patients had anti-neuronal autoantibodies in serum or CSF when assessing a large panel of autoantibodies against intracellular and surface antigens relevant for central nervous system diseases using cell-based assays and indirect immunofluorescence on murine brain sections. Antigens included proteins well-established in clinical routine, such as Yo or NMDA receptor, but also a variety of specific undetermined epitopes on brain sections. These included vessel endothelium, astrocytic proteins and neuropil of basal ganglia, hippocampus or olfactory bulb. The high frequency of autoantibodies targeting the brain in the absence of other explanations suggests a causal relationship to clinical symptoms, in particular to hyperexcitability (myoclonus, seizures). While several underlying autoantigens still await identification in future studies, presence of autoantibodies may explain some aspects of multi-organ disease in COVID-19 and can guide immunotherapy in selected cases.