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šŸ¦˜Cacatman's Personal Coronavirus COVID-19 Update Thread

Are these all google scholar verified?? :brunette:
Where possible, I include the links so you can check yourself. Probably half are from medical journals, but some of those are yet to be peer reviewed. I made this as a quick reference for myself mainly because my FB notes was hard to do searches. With the search "this thread" key, it's really good and I can edit with ease.
 
A Quick Comparison Of Current Vaccine Candidates
(stolen from Daniel Golden - slightly formatted) Iā€™ve recently received a number of questions about Covid 19 vaccination. My social media feeds have also turned in to a lot of chatter with people in entrenched positions, with half claiming they will never receive a vaccine and the other half claiming we should make the first half vaccinate. I figured that in light of heavily polarized debate, Iā€™d give a quick primer on where we actually are with vaccines in laymen terms.

As a quick disclaimer, I am personally opposed to mandatory vaccination. I am opposed to attaching proof of vaccination to the right to engage in normal activities, and I am opposed to anyone being forced to release personal health information to anyone.

However, this doesnā€™t mean that vaccination may not ultimately make sense to do. My own personal choices will be based on the evolving science. When it crosses a threshold where I am comfortable that it is both effective and crosses a threshold where it provides a greater likelihood of benefit than risk to me, ill likely seek it out. Until then I wonā€™t.

I am incredibly non-dogmatic about vaccines. Like conversations about masks, Iā€™m not trying to force anyone to do anything. I want to present the data with my best interpretation to allow everyone to make rational decisions for themselves.

The Candidates and The Technology
As of now, there are three vaccines with a reasonable likelihood of being granted emergency use authorization in the US in the near future. One is an mRNA vaccine produced by Pfizer (hereafter called the Pfizer Vaccine), another is a different mRNA vaccines produced under ā€œOperation Warp Speedā€ by Moderna (hereafter called the Moderna Vaccine). Finally, there is the Oxford vaccine produced by the British pharmaceutical company AstraZenica.

The first two vaccine types are a technology that has not previously been approved in humans. With these vaccines, RNA that codes for the spike protein of the SARS-CoV-2 virus is injected in to muscle. The muscle cells bring that RNA in to the cell and it utilizes the internal machinery of the cell to make the spike protein from the virus without any of the other parts that make it dangerous. The body will then recognize that the spike protein isnā€™t supposed to be there and generate an immune response against it. When subsequently exposed to the actual virus, the body will recognize the spike protein and launch a rapid targeted response against it.

The Oxford Vaccine uses more established technology. It takes a neutralized adenovirus vector and inserts the code to make the spike protein in to the vector. The virus then effectively ā€œinfectsā€ the inoculated individual and effectively produces the spike protein using the same internal cell machinery to produce the spike.

The common theme with all of the vaccines is the intentional development of antibodies to the spike protein. As this is present on all effective strains of SARS-CoV-2, it will theoretically generate an immune response that will be effective against the virus. The spike protein is what makes the virus infectious.

The Pfizer Vaccine released data claiming that it was over 90% effective. What does this actually mean?
42,000 people participated in a trial. Half received the vaccine and half received a placebo. In this group, there were under 150 symptomatic infections. Over 90% of those infections were in the placebo group. In theory, this is because those that received the vaccine were comparatively protected by the immune response generated by the vaccine. Statistically, this is fairly likely to be true. This data was released 2 months after the second dose of vaccine was completed in the trial.

Earlier study in early phase trials suggested a robust T cell response as well. This is actually fairly important and we will talk about it in a bit.

This vaccine requires very cold storage, and the major logistical risks with its use are going to be cost and cold storage infrastructure.

The Moderna Vaccine
This vaccine is very similar to the Pfizer Vaccine. It released data from a similar trial with similar results claiming to be ā€œ95% effective.ā€
It differs in a couple of ways. T cell responses appeared a little more variable in earlier study. It can be stored at normal freezer temperatures and remains stable at refrigerator temperature for days. Logistically, itā€™s much easier to distribute. It also released data showing a reduction in severe infections (something I have not seen released in a statistically significant manner with Pfizer). It has also trickled put some data suggesting it reduces symptoms in the high risk group. This is obviously incredibly relevant.

The Oxford Vaccine
This vaccine has combined trials in two different continents. One showed 70% efficacy and the other showed 90% efficacy. This makes it a little harder to follow due to the data mixing.
This is the only vaccine utilizing the more established adenovirus vector technology. This of course means that there are fewer unknown risks. It also means there are more known risks. Distribution and cost are going to be much simpler with this vaccine. Oxford also did periodic asymptomatic testing on its groups, and there is some data not yet released as a peer reviewed study suggesting it may help reduce secondary transmission. This data doesnā€™t exist for the other two vaccines.

What Do We Actually Know?
As of now, these trials were built in all cases to look for a reduction in symptomatic infections. By definition, these trials were also short. Phase III vaccine trials usually last years. These were completed in months. When someone says that these vaccines went through all the usual safety steps, they are right. When someone says that steps were rushed and that we donā€™t have as much information as we usually do when a vaccine is widely distributed, they are also right.

As of now, it seems likely these vaccines will reduce symptomatic Covid in the short term. We can say that it is highly likely that a person vaccinated will be much less likely to develop a symptomatic Covid infection for the first couple of months after inoculation. That we can say pretty strongly. This is very good news.

However, that good news really needs to be tempered with the limitations of the data.
We have no idea how long this protection lasts. For all we know, the immunity disappears at 4 months. Iā€™m not saying it does. Iā€™m simply saying we donā€™t know. Itā€™s a fairly relevant question however in terms of ending the pandemic.

We currently have limited information about forward transmission. In other words we know that the vaccinated group sees at least a short term reduction in symptomatic infections, but we donā€™t know if it simply makes those infections asymptomatic. We also donā€™t know if it reduces the ability of the vaccinated group to infect others. The Oxford Vaccine has some early data which suggests it might, but this is far from established with any of the 3 vaccines.
None of these trials were built to effectively show whether the vaccine reduces deaths. Thatā€™s also deeply relevant. Remember, most people donā€™t die when infected with Covid. There was a single placebo group death in the Oxford trial and no other deaths in any of the trials. Thus, we donā€™t know if we are only reducing symptoms in people who werenā€™t going to actually die from those symptoms. Thatā€™s not a bad thing, but it isnā€™t enough to solve the problem. Iā€™m not saying it doesnā€™t prevent deaths. Iā€™m saying we havenā€™t yet proven it prevents deaths.
Further questions are related to the high risk nursing home population. This group isnā€™t well represented in trials, so we donā€™t know if the immunity is actually conferred to the group that makes up 40+% of deaths. This seems deeply relevant.

What Are The Risks?
No vaccine is risk free. Large trials now suggest that serious short term side effects are fairly rare. Side effects from the vaccine itself are largely mild to moderate, mimicking cold or flu like symptoms. There have been no deaths from the vaccines. There was one patient who possibly had a serious autoimmune reaction in the trial. We donā€™t know if frequent autoimmune reactions will turn up later. As more time goes by, this becomes less likely
Hereā€™s the issue. We donā€™t know what long term side effects might be. We donā€™t know if this will set people up for autoimmune disease in the future. We donā€™t have years of trial data like we normally do.

MRNA vaccines are new. Will we see a not yet predicted side effect from these vaccines? Maybe. Maybe not. Itā€™s too early to really know that.

Adenovirus vector was previously associated with increased susceptibility to HIV when they attempted to develop a vaccine to that virus with it. Is there some risk of increased susceptibility to other viruses? Itā€™s not clear there is itā€™s too early to say for sure.
There also a risk of something called antibody dependent enhancement (ADE). This is where the antibodies actually make the infection worse. Early trials are encouraging that this doesnā€™t happen, but it may manifest as antibodies start to fade, so we donā€™t know if it will set people up for ADE. We donā€™t actually really know whether T cells or antibodies are the primary mechanism by which our immune system neutralizes the virus. This is important, because we donā€™t know if a robust antibody response is important. A dysregulated response between these two cell types would enhance the likelihood of ADE. Going back to Pfizer versus Moderna, the potential difference in T cell responses may be relevant here.

As a final question, it is highly likely there have been 50-100 million true infections in the US already. We donā€™t know if the vaccine will impact these people differently. One trial did include those with antibodies, so thatā€™s encouraging. However, this was a small percentage of people. This question just hasnā€™t been answered. Could it set them up for ADE in the future? Could we see aggressive immune responses to the vaccine itself? We donā€™t truly know yet.

What Does This All Mean?
At the end of the day, all of these decisions are comparing risks and benefits. When vaccines are available, I would certainly feel differently as a high risk person than a low risk person. If I were obese, over the age of 65, or suffered from significant underlying medical comorbidities, Iā€™d be more eager to be vaccinated than if I wasnā€™t those things. Healthcare workers who have not previously been infected but are constantly exposed to virus may be another group who would rationally pursue the vaccine.

There are also clearly people who will use the short term reduction as a tool to stop isolating. It may make sense for these individuals as well. In truth, who would benefit the most is a moving target as new data comes in.

I would be very cautious right up front if youā€™ve already been infected or if you are a child. Children are not represented well in these trials. We donā€™t know the risks in children, and we know the virus is usually fairly benign (with occasional exceptions) in this specific group.
In summary, the early data is encouraging, but it still hasnā€™t answered some of the most important questions. I discussed the differences between the vaccine types. I discussed the potential benefits and the unanswered questions. Finally, I discussed the potential risks of vaccination and the risk/benefit decisions people will likely need to make when being vaccinated.

Stay safe and Happy Thanksgiving.
 
The case for a 7 day quarantine from start of symptoms vs 10 days.
Peak of live viral shedding occurs within the first 5 days.

This finding is supported by the observation in contact-tracing studies that the highest risk of transmission occurs very early in the disease course (a few days before and within the first 5 days after symptom onset).


Shedding occurs when we talk, cough, sneeze or exhale. It can be shed in a person's stool (Error - Cookies Turned Off)

Virus can shed from 8 days (Virological assessment of hospitalized patients with COVID-2019) after symptom onset to up to 70 days after diagnosis in an immunocompromised person (https://www.cell.com/cell/fulltext/S0092-8674(20)31456-2)

It peaks at 4-6 days after infection

Typical shedding lasts around 17 days

But can persist for more than 80 days in the upper respiratory tract and over 120 days in the stool

We donā€™t fully understand the factors that make a person a ā€œlong shedderā€, but research into this is ongoing. Certain groups have been associated with prolonged SARS-CoV-2 shedding, including males, children, older adults, and people with compromised immune systems.

Thereā€™s also speculation factors such as the amount of SARS-CoV-2 which caused the infection (the viral dose), and possibly the viral strain, may play a role.
 
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