On this week's COVID-19 update, Dr. Bishop did a deep dive into how the Merck and Pfizer COVID pills function, touched on immunity from Regeneron, and provided an update on the vaccination process for children 5 to 11. Watch the video below or read on for our full recap.
I've got an article here for you guys from the New York Times talking about first the Pfizer COVID pill. And then I've got a second article I'm going to link to from the New York Magazine Intelligence series to what to know about the new COVID-19 anti-viral pills.
These pills are both interesting for different reasons, and I think they're both going to have their place and have a certain group of people that are going to be useful for.
I think we're probably going to wind up using the Pfizer pill more frequently, and it's going to have a faster uptake than the Merck pill, just because of some current concerns about long-term side effects for the Merck pill that are theoretical at this point but are giving people a little bit of pause.
Let's start with —what's the point of the antiviral pills?
Both of the antiviral pills are trying to mess up the virus's ability to replicate itself in the body. Both the Pfizer pill and the Merck pill interfere with the virus's ability to replicate and produce more copies of itself.
Going way back to high school biology or college biology, a virus works primarily by hijacking human cells and using the human and machinery in the cell to create copies of itself. A virus is really just a parasite. It can't really live on its own. It requires humans or animals, whatever type of virus it is, or even plant viruses, to do the same thing.
It requires a host to use that host's cellular machinery to replicate and recreate itself and propagate. That is the entire purpose of the virus. That is what they do. So a lot of antiviral drugs that we've created, both for humans and animals, the way that they function is by interfering with that replication process.
They actually stop the virus's genes or DNA or RNA or whatever it is from being able to effectively replicate itself. Or they cause problems in the replication cycle, such that the replicated copies are ineffective and meaning they can't go out and attack other cells.
Again, getting a little bit back to biology, most of the symptoms that we have from viral infections are actually from the body's own attempts to contain that replication process and keep the infection from spreading. It's the inflammation that the body causes trying to stop the virus from spreading further.
Most of the symptoms you have from a viral infection are from your body's own attempt to clear the virus, kill it, get rid of it, rather than from the virus itself. What these drugs attempt to do is come in and say, "okay, we're going to stop your ability to replicate or inhibit your ability to replicate in an appropriate way so that you can't spread as fast from cell to cell within the body and to reduce the risk that you transmit the virus to other people."
For example, most of our HIV drugs, this is a way they work. They prevent HIV from replicating in the body. It doesn't necessarily get rid of the virus entirely from the body, but it prevents the virus from replicating at a sufficient level to cause further damage or to spread to other people.
Most of the treatments we have now for HIV not only halt the progress of the virus in the body but actually prevent you from spreading it to other people. It's excellent in that way.
A lot of the other drugs we have for some other viruses basically function the same way. Valtrex for cold sores or Tamiflu for the flu, same kind of thing. They all work roughly in a similar way.
These drugs are no different. And in fact, the Pfizer drug is actually two drugs. It's some unnamed compound, that's got a serial number designation, which doesn't mean anything except to the scientists who know about it.
And then it's got a drug called Ritonavir, which is actually a drug that was originally used to treat HIV, that is now being used as a combo pill with this other drug that Pfizer has created to create what they're going to call PAXLOVID. That's going to be the name brand, PAXLOVID, of the Pfizer drug.
What it actually does is go in and severely inhibit the enzyme that allows the virus to replicate itself. Again, the theory is that it halts the virus from continuing to make more copies, so it gives the body time to marshal its immune defenses to get rid of the copies that are already there and shut down the entire replication process. It provides this relief mechanism.
It doesn't totally clear the body of the virus. The immune system still has to come in and do that for it, but it halts the virus from continuing to replicate. It gives the body some time to do that process.
The trials that they have done — they're small trials — but you can read in the second article I linked there, the reduced risk of hospitalization or death was 89% in patients given the drug within three days of developing symptoms and 85% when given within five days of developing symptoms.
So it's like Tamiflu or Valtrex for cold sores. You want to give the drug as soon as you start having symptoms. Because again, the idea is you want to stop the replication as quickly as possible so the immune system can come in and mop up and get rid of the virus before it spreads out of control.
The later you give the treatment, the less effective it's going to be. Just like if you have already had the flu for four or five days, giving Tamiflu probably isn't going to help you very much versus if you take it after you've only had symptoms for a few hours or a day or so. That's the idea with both of these drugs.
Again, the Pfizer one seems to work quite well. The Merck one, which is called Molnupiravir, doesn't have a great name yet. It looks like it's going to work quite well. Initial trial data showed about a 50% reduction in hospitalization or death when given within the first five days.
These drugs do seem to work well. We haven't seen the full data sets yet. They both are asking for approval from the FDA to get those under a EUA so those can be out there publicly available, but they haven't been approved just yet.
When they do have those meetings, we will see the full data sets come out and then hopefully get a better idea of both the effectiveness and the side effects.
One of the reasons that people are a little bit concerned about the Merck drug, Molnupiravir, is that the way that it works is a little bit different. It doesn't just inhibit the replication of the virus. It actually interferes with the appropriate replication of the virus.
Essentially, it induces, for lack of a better word, mutations in the virus. And the mutations that it induces are designed to actually cause such havoc that the virus stops replicating and can no longer function.
And that's fine. Some of the drugs we use again for HIV and other things are similar. There's nothing wrong with that in theory, but it does raise some concerns though about how targeted the drug is and whether it can cause problems either reproductively or for cancer risk and things like that. We just don't know yet about that and that concern is detailed a little bit further in the New York Times article.
I think people are a little bit wary about that drug because of that potential. It's a theoretical potential concern at this point, just based on how the drug works by causing mutations versus halting replication altogether.
Time will tell on that, but I think because of that concern, you're going to see much easier pickup and uptake of the Pfizer version, their PAXLOVID medication, versus the other one by Merck. We'll see what the data sets show when they come out and when the FDA takes those up.
I have not seen a date yet for when FDA is going to take those up in committee to review the requests. So we'll have to wait and see on that.
But two interesting things coming out. I think it's good to keep watching the therapeutic space. In addition to the monoclonal antibody treatments, having a pill available is going to be a good thing to treat people who have not been vaccinated or can't be vaccinated, but also vaccinated people who have breakthrough infections. These types of treatments will be good to have on hand.
"I'm hoping to follow up on the Regeneron news from last week. At what point do you have high confidence in the immunity/prevention from Regeneron lasting as long as 8 months? For those that still don't want to vaccinate, what treatment would you suggest once their Regeneron immunity period has passed?"
There's no new follow-up from that. I think what the study shows is that the immunity, that protection from infection and hospitalization, in particular, does last about eight months after getting a dose of Regeneron.
I think the question is going to become I think once that immunity — passive immunity is really what we're talking about — once it wears off, it's worn off. I think at that point, that person's going to need to make a decision. Is it time to reconsider getting vaccinated at this point because maybe more time has passed and I feel a little bit better about it? Or are they waiting until they have another indication to get another dose of Regeneron? Say they get exposed to someone and they have post-exposure prophylaxis treatment with another dose of Regeneron at that point.
I think they're going to have to continually make those choices every time their immunity wears out, probably every six to eight months or so.
And part of the trouble there, too — and I think, again, this gets to the way a lot of the messaging has been handled or not handled well by the public health officials related to the vaccines — the vaccines, while yes, we're having discussions about boosters and recommending people get boosters, especially people in certain age groups, in certain risk categories, I have not seen any data yet indicating that the protection from hospitalization and death for people after the first two falls off for most people.
Now it's different for people in that like 65 and 75 and up crowd. Yes, the protection does wane after six to eight months, but for the bulk of people, there's really not a significant amount of data showing that the protection from hospitalization and death falls off after vaccination after six to eight months.
But that is going to be true for the Regeneron. That protection is going to fall off pretty dramatically after the antibodies wear off and wear out, whereas you will not have that probably issue, certainly not as quickly, with vaccination. They will last longer and that protection from hospitalization and death will last longer.
We did see that big detriment in protection from transmission but that's a different question.
"I had of Moderna booster shot on August 15th. Do I need another one?"
I would ask your doctor about it to be sure, because if you're talking about a third dose of Moderna, then no. There have been no recommendations for anything beyond the third dose of Moderna. There are no recommendations for anything beyond a third dose for Moderna at this point.
"What is your recommendation for boosters? I got the J&J vaccine back in April, trying to decide on which booster to get."
What I've been telling my patients is to stick with the horse you rode in on unless you have a specific reason that you need to change for a very specific reason, like I had a bad reaction to the first one or I'm worried about a particular side effect, etc, from one vaccine or the other.
But stick with the one you started with. So if you started with J&J, I would recommend you get boosted with J&J. Same thing with Moderna or Pfizer.
The FDA and CDC have said it's okay to mix and match. And that is certainly fine if that's what you want to do. I don't think it's particularly dangerous to do that, but I know for myself and what I've been recommending for my patients, I think it's best just to stick with what you've already been known to tolerate well and what has protected you so far.
I don't think we have extensive data on mixing and matching vaccines. So in good conscience, I can't recommend that as a routine matter. Of course, if you want to mix and match, it is okay.
There's no specific data showing it's dangerous. I just am a little bit more conservative in the way I interpret data and so I would want to see some specific trials or a much larger dataset showing that mixing and matching is safe in order to recommend that to people at scale.
But I think for most people, I would say stick with the one you with.
I saw a headline today that about 10 to 15% of five to 11-year-olds across the country have been vaccinated at this point, which is good news. That does seem to be rolling out fairly quickly.
We'll keep watching the VAERS system and the news media for any issues that come about with that, but I have not heard of any problems today. I know lots of friends and colleagues who have gotten their kids vaccinated at this point and haven't had any issues with it other than the mild common side effects. And even that has actually been fairly uncommon.
I haven't heard significant issues with those side effects — fever, chills, body aches, that sort of stuff — from the vaccine in five to 11-year-olds. That seems to be going well so far. We'll see as more data continues to roll in on that. So that is good news as well.
Because of the Thanksgiving holiday, we will take next week off. The next update will be on Wednesday, December 1 at 1:00 pm on our Facebook page. For those without Facebook, we will post our written recap on Thursday morning.