***NON-POLITICAL COVID-19 Discussion Thread***

[JakeF]

A couple of reminders...

Originally Posted by Bwana

Once again, don't come in this thread with some kind of political agenda, or you will be shown the door. If you want to go that route, there is a thread about this in DC.

Originally Posted by Dartgod

People, there is a lot of good information in this thread, let's try to keep the petty bickering to a minimum.

We all have varying opinions about the impact of this, the numbers, etc. We will all never agree with each other. But we can all keep it civil.

Thanks!

Click here for the original OP:

Spoiler!

Apparently the CoronaVirus can survive on a inanimate objects, such as door knobs, for 9 days.

California coronavirus case could be first spread within U.S. community, CDC says
By SOUMYA KARLAMANGLA, JACLYN COSGROVE
FEB. 26, 2020 8:04 PM

The Centers for Disease Control and Prevention is investigating what could be the first case of novel coronavirus in the United States involving a patient in California who neither recently traveled out of the country nor was in contact with someone who did.

“At this time, the patient’s exposure is unknown. It’s possible this could be an instance of community spread of COVID-19, which would be the first time this has happened in the United States,” the CDC said in a statement. “Community spread means spread of an illness for which the source of infection is unknown. It’s also possible, however, that the patient may have been exposed to a returned traveler who was infected.”

The individual is a resident of Solano County and is receiving medical care in Sacramento County, according to the state Department of Public Health.

The CDC said the “case was detected through the U.S. public health system — picked up by astute clinicians.”

Officials at UC Davis Medical Center expanded on what the federal agency might have meant by that in an email sent Wednesday, as reported by the Davis Enterprise newspaper.

The patient arrived at UC Davis Medical Center from another hospital Feb. 19 and “had already been intubated, was on a ventilator, and given droplet protection orders because of an undiagnosed and suspected viral condition,” according to an email sent by UC Davis officials that was obtained by the Davis Enterprise.

The staff at UC Davis requested COVID-19 testing by the CDC, but because the patient didn’t fit the CDC’s existing criteria for the virus, a test wasn’t immediately administered, according to the email. The CDC then ordered the test Sunday, and results were announced Wednesday. Hospital administrators reportedly said in the email that despite these issues, there has been minimal exposure at the hospital because of safety protocols they have in place.

A UC Davis Health spokesperson declined Wednesday evening to share the email with The Times.

Since Feb. 2, more than 8,400 returning travelers from China have entered California, according to the state health department. They have been advised to self-quarantine for 14 days and limit interactions with others as much as possible, officials said.

“This is a new virus, and while we are still learning about it, there is a lot we already know,” Dr. Sonia Angell, director of the California Department of Public Health, said in a statement. “We have been anticipating the potential for such a case in the U.S., and given our close familial, social and business relationships with China, it is not unexpected that the first case in the U.S. would be in California.”

It is not clear how the person became infected, but public health workers could not identify any contacts with people who had traveled to China or other areas where the virus is widespread. That raises concern that the virus is spreading in the United States, creating a challenge for public health officials, experts say.

“It’s the first signal that we could be having silent transmission in the community,” said Lawrence Gostin, director of the World Health Organization Collaborating Center on National and Global Health Law. “It probably means there are many more cases out there, and it probably means this individual has infected others, and now it’s a race to try to find out who that person has infected.”

On Tuesday, the CDC offered its most serious warning to date that the United States should expect and prepare for the coronavirus to become a more widespread health issue.

“Ultimately, we expect we will see coronavirus spread in this country,” said Nancy Messonnier, director of the CDC’s National Center for Immunization and Respiratory Diseases. “It’s not so much a question of if, but a question of when.”

According to the CDC’s latest count Wednesday morning, 59 U.S. residents have tested positive for the new strain of coronavirus — 42 of whom are repatriated citizens from a Diamond Princess cruise. That number has grown by two since Messonnier’s last count Tuesday, although the CDC was not immediately available to offer details on the additional cases.

More than 82,000 cases of coronavirus have been reported globally, and more than 2,700 people have died, with the majority in mainland China, the epicenter of the outbreak.

But public health leaders have repeatedly reminded residents that the health risk from the novel coronavirus to the general public remains low.

“While COVID-19 has a high transmission rate, it has a low mortality rate,” the state Department of Public Health said in a statement Wednesday. “From the international data we have, of those who have tested positive for COVID-19, approximately 80% do not exhibit symptoms that would require hospitalization. There have been no confirmed deaths related to COVID-19 in the United States to date.”

CDC officials have also warned that although the virus is likely to spread in U.S. communities, the flu still poses a greater risk.

Gostin said the news of potential silent transmission does not eliminate the possibility of containing the virus in the U.S. and preventing an outbreak.

“There are few enough cases that we should at least try,” he said. “Most of us are not optimistic that that will be successful, but we’re still in the position to try.”

[Marcellus]

Originally Posted by Donger

July 10 = 671
October 7 = 721

Is there a reason you posted this?

[petegz28]

Originally Posted by suzzer99

1. Texas now has more Covid deaths than California does, even though California's population is 33% bigger.

So Texas's per capita death rate from Covid is 40% higher than California's.

— James Surowiecki (@JamesSurowiecki) October 8, 2020

Another data point that masks and social distancing actually work.

Yeah but no. Can you prove every single death in Texas was because of a lack of masks and distancing? And what about the deaths in CA? What about the fact CA has more cases than TX?

I understand what you're trying to say but to just say it's all because of masks and distancing is bogus. What were the conditions of all the deaths? Ages? Underlyings? Etc.

And where do you get the data on amount of people in CA wearing masks vs. TX?

Your premise here is that CA wears masks more than TX but yet while TX does have more deaths CA has more cases. If CA was doing that much better with masks, etc. shouldn't that also be below TX if TX is doing such a bad job?

[TLO]

How are hospitalizations looking in the KC area Pete?

[petegz28]

Originally Posted by TLO

How are hospitalizations looking in the KC area Pete?

Been a bit of an uptick this last couple of weeks. Mostly from Clay County on the MO side and Wyandotte Couty on the KS side. Still no threat of being slammed though which is a good thing. Cases overall look to be on the decline though, especially on the KS side.

['Hamas' Jenkins]

Originally Posted by petegz28

Yeah but no. Can you prove every single death in Texas was because of a lack of masks and distancing? And what about the deaths in CA? What about the fact CA has more cases than TX?

I understand what you're trying to say but to just say it's all because of masks and distancing is bogus. What were the conditions of all the deaths? Ages? Underlyings? Etc.

And where do you get the data on amount of people in CA wearing masks vs. TX?

Your premise here is that CA wears masks more than TX but yet while TX does have more deaths CA has more cases. If CA was doing that much better with masks, etc. shouldn't that also be below TX if TX is doing such a bad job?

Cases per 1 million residents: California 21K, Texas 28K.

Thus, the average Texan is 33% more likely to contract COVID. That's the problem the author of the tweet is pointing out--a higher likelihood of infection.

Total Deaths per 1 million: California 415, Texas 581.

Thus, the average Texan is 40% more likely to die of COVID, not once caught, but in general. So, what is driving this? Is there a deadlier COVID strain in Texas? Are different demographics affected? Let's take a look at some raw numbers:

Once caught, the CFR of known cases is 2.05% in Texas and 1.94% in California.

The absolute difference in fatality is 0.11%, which is marginal, but the relative difference is 5.7%.

When you weigh this together, the increase in fatality rates is driven largely by the increase in caseload. Texas counties are able to apply for exemptions to the statewide mask order if they have low case levels.

I haven't look at the state by state data regarding adherence, but it's inarguable that more people are contracting COVID per capita in Texas, and you are talking about such large swaths of population (tens of millions as your pool of potential infections) that it's certainly a representative sample, especially given that there are not major demographic differences between the two states (compared to say Vermont or Iowa).

[TLO]

Originally Posted by 'Hamas' Jenkins

Cases per 1 million residents: California 21K, Texas 28K.

Thus, the average Texan is 33% more likely to contract COVID. That's the problem the author of the tweet is pointing out--a higher likelihood of infection.

Total Deaths per 1 million: California 415, Texas 581.

Thus, the average Texan is 40% more likely to die of COVID, not once caught, but in general. So, what is driving this? Is there a deadlier COVID strain in Texas? Are different demographics affected? Let's take a look at some raw numbers:

Once caught, the CFR of known cases is 2.05% in Texas and 1.94% in California.

The absolute difference in fatality is 0.11%, which is marginal, but the relative difference is 5.7%.

When you weigh this together, the increase in fatality rates is driven largely by the increase in caseload. Texas counties are able to apply for exemptions to the statewide mask order if they have low case levels.

I haven't look at the state by state data regarding adherence, but it's inarguable that more people are contracting COVID per capita in Texas, and you are talking about such large swaths of population (tens of millions as your pool of potential infections) that it's certainly a representative sample, especially given that there are not major demographic differences between the two states (compared to say Vermont or Iowa).

Hi.

Care to weigh in a bit on monoclonal antibodies while you're here?

['Hamas' Jenkins]

Originally Posted by TLO

Hi.

Care to weigh in a bit on monoclonal antibodies while you're here?

In what regard? Their pharmacology, likelihood of approval, efficacy, all of the above?

[TLO]

Originally Posted by 'Hamas' Jenkins

In what regard? Their pharmacology, likelihood of approval, efficacy, all of the above?

All of the above - if you have the time.

['Hamas' Jenkins]

Originally Posted by TLO

All of the above - if you have the time.

Pharmacology 101:

It helps to think of drugs as working like a key and lock mechanism.

The receptor is the lock and the drug is the key. In some cases, they work via simple chemical interactions.
For example, lisinopril is the most prescribed ACE inhibitor—that is, it inhibits the function of angiotensin converting enzyme, which is a protein that converts angiotensin I to angiotensin II. Angiotensin II leads to constriction of blood vessels (among other effects). Lisinopril inhibits ACE rather simply—one of the side chains of the drugs has a positive charge. This interacts with the protein structure of ACE and prevents it from functioning correctly. No ACE, no angiotensin II; no angiotensin II, less vasoconstriction = lower blood pressure.

Well, how do viruses enter cells? They work very similar to the above lock and key mechanism. In the case of HIV, there are receptors on the surface of immune cells called CCR-5 and CXCR4. HIV binds to these receptors as the initial process of viral entry. In this case there are mutations more common in northern Europeans (CCR5 delta 32) where the CCR5 receptor can be absent. These people are far less likely to contract HIV, and if they do, they are much more likely to survive for decades without a need for antiretroviral therapy.

In the case of SARS-CoV2, a spike protein binds to a receptor on ACE-2 as part of its initial entry into the cell. So, if you block the ACE-2 receptor, you block entry into the cell? Well, it’s not quite that simple. Viruses can mutate and the mutation in the spike protein could render a single antibody less effective (or completely worthless). This is why monotherapy with traditional drugs for HIV is ineffective. One solution is to target multiple pathways to limit the possibility of mutation. This is the principle behind HAART in anti-HIV therapy, and it’s what Regeneron is attempting to do—they’ve created two different monoclonal antibodies in one package that target different areas (epitopes) of the spike protein so that a single mutation will not render the drug ineffective.

What is a monoclonal antibody?

Human B-cells are a type of immune cell that secrete antibodies. In this case, drug developers have come up with a several methods to allow these cells to secrete very specific antibodies for the treatment of a variety of conditions—from rheumatoid arthritis to lung cancer. Once developers have the antibody they want, they are purified and amplified so that you end up with the antibodies you want and in great quantity. The methods for doing so are numerous and beyond the scope of my expertise.

The downsides of monoclonal antibodies are that production at scale is more difficult than what we call small molecule drugs, which can be produced on an industrial scale using organic chemistry, and that administration is more specialized. Because they are proteins, they are sensitive to heat and pH. Example: eggs solidify when you cook them because albumin, a protein, coagulates when exposed to heat. Changes in pH (your stomach has a pool of hydrochloric acid in it) can cause conformational changes in the protein structure, which alters folding of the protein, and ultimately, its function. Thus, most are given via injection—this can be IV or subcutaneously.

How likely is this to be approved?

EUA’s are being handed out like candy in the current climate, both for tests and therapeutics. It is not the finest hour for our drug development processes in that regard. I would be extremely surprised if it wasn’t granted an EUA.

What is the efficacy?

Without data from Phase II/III trials, it’s impossible to discern. Far too much science is being interpreted through press releases instead of medical journals, and it clouds the evidence. See my earlier post about the Lilly drug as another example. Without an analysis of the biostatistics, we cannot make sound clinical decisions regarding efficacy and safety.


Hope all is well. Did you ever get your clonazepam levels figured out?

[O.city]

Well...had to take my aunt back to the hospital, not doing well. Said they may have to intubate tonight or tomorrow.

Not ideal

[petegz28]

Originally Posted by O.city

Well...had to take my aunt back to the hospital, not doing well. Said they may have to intubate tonight or tomorrow.

Not ideal

Damn, dude......

[Pasta Little Brioni]

Originally Posted by Donger

Cases are rising and their pandemic is over.

Makes sense...

Caaes mean jack shit

[Donger]

56,600 new cases yesterday.

[TLO]

Originally Posted by 'Hamas' Jenkins

Pharmacology 101:

It helps to think of drugs as working like a key and lock mechanism.

The receptor is the lock and the drug is the key. In some cases, they work via simple chemical interactions.
For example, lisinopril is the most prescribed ACE inhibitor—that is, it inhibits the function of angiotensin converting enzyme, which is a protein that converts angiotensin I to angiotensin II. Angiotensin II leads to constriction of blood vessels (among other effects). Lisinopril inhibits ACE rather simply—one of the side chains of the drugs has a positive charge. This interacts with the protein structure of ACE and prevents it from functioning correctly. No ACE, no angiotensin II; no angiotensin II, less vasoconstriction = lower blood pressure.

Well, how do viruses enter cells? They work very similar to the above lock and key mechanism. In the case of HIV, there are receptors on the surface of immune cells called CCR-5 and CXCR4. HIV binds to these receptors as the initial process of viral entry. In this case there are mutations more common in northern Europeans (CCR5 delta 32) where the CCR5 receptor can be absent. These people are far less likely to contract HIV, and if they do, they are much more likely to survive for decades without a need for antiretroviral therapy.

In the case of SARS-CoV2, a spike protein binds to a receptor on ACE-2 as part of its initial entry into the cell. So, if you block the ACE-2 receptor, you block entry into the cell? Well, it’s not quite that simple. Viruses can mutate and the mutation in the spike protein could render a single antibody less effective (or completely worthless). This is why monotherapy with traditional drugs for HIV is ineffective. One solution is to target multiple pathways to limit the possibility of mutation. This is the principle behind HAART in anti-HIV therapy, and it’s what Regeneron is attempting to do—they’ve created two different monoclonal antibodies in one package that target different areas (epitopes) of the spike protein so that a single mutation will not render the drug ineffective.

What is a monoclonal antibody?

Human B-cells are a type of immune cell that secrete antibodies. In this case, drug developers have come up with a several methods to allow these cells to secrete very specific antibodies for the treatment of a variety of conditions—from rheumatoid arthritis to lung cancer. Once developers have the antibody they want, they are purified and amplified so that you end up with the antibodies you want and in great quantity. The methods for doing so are numerous and beyond the scope of my expertise.

The downsides of monoclonal antibodies are that production at scale is more difficult than what we call small molecule drugs, which can be produced on an industrial scale using organic chemistry, and that administration is more specialized. Because they are proteins, they are sensitive to heat and pH. Example: eggs solidify when you cook them because albumin, a protein, coagulates when exposed to heat. Changes in pH (your stomach has a pool of hydrochloric acid in it) can cause conformational changes in the protein structure, which alters folding of the protein, and ultimately, its function. Thus, most are given via injection—this can be IV or subcutaneously.

How likely is this to be approved?

EUA’s are being handed out like candy in the current climate, both for tests and therapeutics. It is not the finest hour for our drug development processes in that regard. I would be extremely surprised if it wasn’t granted an EUA.

What is the efficacy?

Without data from Phase II/III trials, it’s impossible to discern. Far too much science is being interpreted through press releases instead of medical journals, and it clouds the evidence. See my earlier post about the Lilly drug as another example. Without an analysis of the biostatistics, we cannot make sound clinical decisions regarding efficacy and safety.


Hope all is well. Did you ever get your clonazepam levels figured out?

Awesome explanation. Thank you.

Still working with my doctor trying to figure out why the clonazepam isn't showing up. I went back to give a 3rd sample yesterday. The nurse said if this comes back negative they aren't going to worry about doing another test. They said they had been in contact with the lab and were going to try "something different" this time. I didn't inquire about what they were trying different, but hopefully it works.

[Chitownchiefsfan]

Originally Posted by 'Hamas' Jenkins

Cases per 1 million residents: California 21K, Texas 28K.

Thus, the average Texan is 33% more likely to contract COVID. That's the problem the author of the tweet is pointing out--a higher likelihood of infection.

Total Deaths per 1 million: California 415, Texas 581.

Thus, the average Texan is 40% more likely to die of COVID, not once caught, but in general. So, what is driving this? Is there a deadlier COVID strain in Texas? Are different demographics affected? Let's take a look at some raw numbers:

Once caught, the CFR of known cases is 2.05% in Texas and 1.94% in California.

The absolute difference in fatality is 0.11%, which is marginal, but the relative difference is 5.7%.

When you weigh this together, the increase in fatality rates is driven largely by the increase in caseload. Texas counties are able to apply for exemptions to the statewide mask order if they have low case levels.

I haven't look at the state by state data regarding adherence, but it's inarguable that more people are contracting COVID per capita in Texas, and you are talking about such large swaths of population (tens of millions as your pool of potential infections) that it's certainly a representative sample, especially given that there are not major demographic differences between the two states (compared to say Vermont or Iowa).

Do you know what the numbers like this look like for in Illinois? I know Chicago and suburbs are really big on social distancing and masks. I live in the burbs now and its been ages since I've seen someone in store wo a mask.