Coronavirus: What you should know

My state (Alabama) was part of the Final Four in the March Illness bracket, but we lost to West Virginia.

Most of our cases are in the one city that actually has multiple testing sites. Imagine that. For a long time, the state was proudly saying we had no confirmed cases. At that time, they’d only tested 20 people! :stuck_out_tongue:

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Didn’t some leader claim that they didn’t have cases because the residents honor Jesus? Just shows that Jesus doesn’t honor stupidity.

I haven’t heard that in Alabama, but I also wouldn’t put it past many of our leaders. :laughing:

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Praying that our Reformed brothers and sisters in UK can all agree to kindly cease from quote mining Luther and Calvin for reasons to keep churches open. Great theologians they were; great scientists they were not. Particularly due to them having zero knowledge of infection control and viral transmission.

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I don’t know where to ask this, so if u can direct me to the proper board that would be appreciated. [What percent of known viruses cause disease?] Google and wikipedia’s refuse to answer this. By the question I’m referring to all organisms.

You already got some good science answers to it in this other thread

If you wanted more follow up on it, then best keep it in one place and not keep repeating the same question in multiple threads. Though if you want discussion to continue over on this thread, we could move it here. Just cutting down on sprawl here!

Can COVID-19’s protein coat be destroyed by water, like rain water from a storm?

OK. I was just trying the best forum to post in.

No. Coronaviruses have a lipid (fatty) envelope which can be disrupted by alcohol or detergents, which is why hand sanitizer and washing with soap and water are recommended.

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Yeah, it’s interesting that soap (I like liquid dish soap) is the preferable sanitizer compared to the corrosive and toxic effects of others.

At this point, anything that comes into my house that’s been touched by someone else is either washed off with detergent or quarantined.

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I have the advantage of being within the delivery range of our local Walmart, not that it’s particularly easy anymore to find what we need in stock or find an unfilled time slot. How long do you think it would be a good idea to quarantine grocery ‘t-shirt’ bags with unrefrigerated stuff? The delivery backs right up to the garage door and I transfer the bags right into the rear of our little SUV, and I could just leave them there. I have a sink in the garage, yay! :slightly_smiling_face:

I’m doing 1 day for mail (since cardboard and paper look good after 24 hours) and 1 week for everything else. That way I don’t have to decide whether packaging counts as paper (is it coated? does that matter?) – I just treat it all the same.

It’s a bit of an adventure ordering grocery delivery. I look for things I want that are in stock, put them in my cart, wait around for a delivery window opening, and then see what’s in my cart that’s still in stock. I keep putting in tempeh and it keeps disappearing. (But I did get one squash and three bananas last night.)

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I discovered last week when Walmart cut their times down to only two days, and the first day was full, that if I ordered right after midnight when the following day was first open. I’m not crazy about it, because it feels like “Me first!”

If I get the virus, though, and I’m in ICU and they have to triage and prioritize ventilators, I will have no problem with saying “Me last!”

More about its longevity on surfaces – we just had a grocery delivery, so I checked again:

The New England Journal of Medicine just published a study [dated last week] that tested how long the virus can remain stable on different kinds of surfaces within a controlled laboratory setting. They found that it was still detectable on copper for up to four hours, on cardboard for up to 24 hours, and on plastic and steel for up to 72 hours.

The picture for understanding of the virus is becoming more clear and why some people are more effected.

The virus binds to a receptor AcE2 that is involved in regulating blood pressure and also creating signals to stimulating your innate immune response that fight the viruses as well creating inflammation. The Ace2 receptor normally binds a protein called Angiotensin 2 that causes a raise in blood pressure and stimulating immune response and inflammation The virus somehow impairs this process and depresses the innate immune system response early in the infection allowing the virus to proliferate. This depressed innate immune response explains why people remain without symptoms so long into the infection and can pass the virus on without knowing they are infected unlike other viruses such as the flu.

People with high blood pressure often take what is called Ace enzyme inhibitors. These Ace enzyme inhibitors like Captopril inhibit the formation of the Angiotensin 2 and t reduce blood pressure. An interesting side effect of the Ace inhibitors is the lost of taste. Loss of taste is one of the symptoms of Covid 19 infection indicating that the virus is interfering with this Angiotensin 2 pathway likely by effecting the Ace2 receptor as well as explaining the depression of the Innate immune system allowing the virus to proliferate. This is why people with already weakened immune systems are more susceptible to getting the virus.

In the more severely effected patients the virus later in its progression causes an over response of the immune system resulting in extreme inflammation in the lungs (pneumonia and acute respiratory distress ARDS needing ventilators) and other organs and tissues. There is likely a genetic component related to this. There are two forms of the Ace enzyme D and I. The D form of the enzyme is more active forming the Angiotensin 2 which we know increases blood pressure and inflammation. People that have the D form of the enzyme usually have higher blood pressure as you would expect (this is not the only cause of high bp) and importantly they are more likely to get and succumb to the respiratory distress ARDS. These people are very likely most susceptible to Covid 19. It seems that many people maybe 90% of the infected never even know they are infected or have just mild symptoms. It seems that the virus initially inhibits the immune response with no symptoms and then the virus runs its course without generating an over responsive immune system. However in the more severely effected the virus initially inhibits the innate immune response but then the immune response goes into hyperdrive causing extreme inflammation and the ARDS needing ventilation. This would suggest that this hyper response is in part mediated along this Angiotensin 2 pathway.

This viral immunosuppression suggests that the this RAS pathway becomes hyper sensitized in certain individuals resulting in the severe ARDS. This hyper immune response seems to happen very quickly where a stable patient requires intubation ventilator very quickly. This is not normally seen in other types of viruses and is specific to Covid 19. This hyper immune response should be able to be prevented quite possibly with the drugs being investigated in the US and around the world. It is clear that we must intervene with a preventative drug regimen before this occurs especially based on high risk individuals. It’s a losing game to fight this disease with ventilators as patients require up to 25 days of hospilization.

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Interesting stuff. I had been taking an ACE inhibitor, but stopped as it seems folks taking them do worse (?increased receptors?).
I was reading an anecdotal report that 70% or so that go on vents go on to die, which is not surprising though the popular press tends to give the impression that if we just have enough vents all would be well. It does make one consider that DNR directives are important, as CPR places lots of people at risk and is exceedingly unlikely to have positive effect in someone with end stage respiratory failure and probable cardiomyopathy.

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Thank you Phil. I think it best to discuss any medication changes with your doctor. The jury is out on this and being actively debated. It does seem theoretically that the Ace inhibitors and maybe the ARBs May aid in the virus infection and asymptiomatic proliferation. However, it is quite possible that these same agents could be used after symptoms appear to mitigate the hyper immune response leading to ARDs and ventilation. Have a look at this very good video from Dr Sehault about this. Also there is a report out of Iran from Dr. Reza Nejat using Losartan and Chloroquine showing effective treatment of the ARDS. It may be beneficial due to the blood pressure variations in these patients to directly nebulize the Losartan into the lung to increase efficacy directly and bypass general blood pressure effects.

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Further study shows hydroxychloroquine and azithromax may not have any effect after all.No evidence of rapid antiviral clearance or clinical benefit with the combination of hydroxychloroquine and azithromycin in patients with severe COVID-19 infection - ScienceDirect

I suspect this is not the final word, but appears to be a more reliable study than Gautret’s, and vindicates Fauci’s reserved response on the subject.

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Francis last night mentioned how it’s not been researched for its effectiveness against COVID and is not considered any type of good treatment at this time. and that everyone should just listen to Dr. Fauci all the time. Hopefully that will quell some people.

Although news broke today that the president may be pushing the drug so much because he has a financial stake in the company that produces the brand name version…so there’s that.

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