COMMENTARY

COVID Breakthrough Infections and Reinfections: Where We Stand

Anya Romanowski, MS, RD; Angela L. Rasmussen, MA, MPhil, PhD; Kartik Cherabuddi, MD; Peter M. Antevy, MD

Disclosures

January 05, 2022

This discussion was recorded on December 10, 2021. This transcript has been edited for length and clarity.

Anya Romanowski, MS, RD: Hello and welcome. I'm Anya Romanowski, editorial director of Medscape Emergency Medicine. As a follow-up to our previous interview about testing positive for COVID-19 after two doses of an mRNA vaccine, we have reassembled a panel to review important updates regarding breakthrough infections and reinfections. We will also touch on the Omicron variant circulating globally at an increased speed.

Joining us today is Dr Angela Rasmussen, a virologist of the Vaccine and Infectious Disease Organization at the University of Saskatchewan; Dr Kartik Cherabuddi, an infectious disease specialist and hospital epidemiologist at the University of Florida; and Dr Peter Antevy, an emergency physician and EMS medical director for Coral Springs-Parkland Fire Department in Florida. Welcome, everyone.

Peter M. Antevy, MD: Thank you.

Angela L. Rasmussen, MA, MPhil, PhD: Thanks, Anya.

Kartik Cherabuddi, MD: Thank you.

Romanowski: Angie, I'd like to begin with you. Can you provide us with an update regarding the nature of reinfections and breakthrough infections that we're currently seeing in the US and globally? Also, how common are the reinfections in the unvaccinated as opposed to those fully vaccinated?

Rasmussen: This is a very tricky metric to estimate for a couple of different reasons. Often, reinfections from any variant can be pretty mild and people may not seek out testing. They may not realize that they've actually had a reinfection with COVID, and many of the reinfections have been detected through asymptomatic screening, such as travel testing and things like that. People may not even realize in many cases that they have been reinfected.

The same is true for breakthrough infections. Even though we've seen an increase in the number of breakthrough infections with the Delta variant, those breakthrough infections in vaccinated people tend to be mild, especially in those who are low risk for having severe COVID-19 at all. Again, those may not be detected if people don't seek out testing. In addition to that, the CDC does not track breakthrough infections unless they result in hospitalization. The data have many holes.

One thing, though, that we do know for sure is that the Delta variant is more likely to cause breakthrough infections than other variants of concern that have circulated. It may be more likely to cause reinfections. The Omicron variant, which has now begun circulating worldwide, has an even higher likelihood of causing both breakthrough infections and reinfections.

A recent study from South Africa showed that there was about a threefold increased risk for reinfection, and a study that's just out from the UK Health Security Agency (formerly Public Health England) has determined the risk for reinfection to be threefold to eightfold higher for Omicron than it was for Delta. We are seeing variants that are more likely to cause reinfection or breakthrough infection.

The good news — and I think people really should keep this in mind — is that no matter what the risk for reinfection or breakthrough is for any variants, we can still do the same things to reduce that risk as much as possible (eg, getting a booster). It is pretty clear now that getting a third dose of vaccine (or a second dose if you've had Johnson & Johnson) will reduce your risk of getting a breakthrough infection or being reinfected. If you're fully vaccinated after prior infection, that also decreases your risk for reinfection. That's true for the Omicron variant, based on the limited data that we have so far.

Even though we are seeing, unfortunately, variants that are more likely to overcome immune defenses, whether they're acquired through infection or vaccination, we do have some tools at our disposal that can reduce our risk based on the use of vaccines. We also, of course, can continue to apply nonpharmaceutical interventions, such as wearing masks, improving ventilation, using rapid testing, and so forth, to reduce that risk further.

Romanowski: Dr Cherabuddi, after full vaccination of the two doses, are there any data reported on deaths, aside from persons with other health-related conditions that may have contributed to their deaths (ie, those who are immunocompromised or older individuals)?

Cherabuddi: The deaths we are seeing, to a very large extent, are in those who are unvaccinated. This is true for Delta that we've seen across our own hospitals across the globe. Early data from South Africa also show the same. Although there are certain hospitalizations and some episodes of severe disease, deaths have uniformly been in unvaccinated or incompletely vaccinated individuals.

Romanowski: Let's talk a little bit more about the Omicron variant. Can you describe the evidence of the immune escape or evasion in those who are fully vaccinated with two doses of Pfizer?

Rasmussen: For the neutralization assays that have been largely used to quantify this, I really want to stress that these are laboratory tests. Basically, you take sera from people who have been vaccinated, not vaccinated, or infected and then vaccinated. You dilute that sera and then you incubate it with either the live virus or with a pseudovirus (another virus that's expressing the spike protein from SARS-CoV-2 or the variant of concern that you're looking at), and you see at what dilution those antibodies in the serum samples can still neutralize that virus.

What we've seen with the data so far from Omicron — and now there are multiple studies coming out of South Africa, the United Kingdom, Germany, and Austria that have looked at this both with live virus and with pseudoviruses — they've all seen pretty much the same thing. The Omicron variant, which has a lot of mutations in the spike protein and particularly within the receptor binding domain of the spike protein that's thought to be important for neutralization, has 20- to 40-fold reductions in antibody neutralization compared with other variants.

Now that's bad, and it certainly that does indicate that antibodies induced by vaccination will be less capable of protecting against infection from this variant. There is some good news, too, and that suggests that vaccination on top of a prior infection or a third booster shot really boosts the levels of those neutralizing antibodies, up to the point that they will still be somewhat protective against infection from Omicron.

I also really want to clearly make the distinction that reduction in neutralizing antibody titers does not reflect the ability of the entire immune system to protect against disease. Although we can look at these neutralizing data and say it's likely and this would be predicted based just on Omicron sequencing that this too is going to result in more breakthrough infections or reinfections, that doesn't necessarily mean that the vaccines or prior infection won't induce immunity that's protective against severe disease.

Antevy: We've been doing many antibody studies and in particular in nursing homes here in South Florida. We've noticed that, number one, the elderly population was not generating such a high number of neutralizing antibodies, and that stair-step started at around 60 years of age. More important, after 6 months, we saw that across the board, the antibody levels for those participants reduced greatly. All of those folks who are sitting out there with only two doses — and I do agree with Angie that we have to get those people that third dose because when that wave comes and hits here in South Florida, where we have a large elderly population — they will be at much higher risk.

Cherabuddi: Just one more thing to add. I think it's natural to see antibody levels fall — but the lower titers, again, it's in a test tube, like Dr Rasmussen said. Additionally, I think Alessandro Sette's Lab showed that the CD4+ and CD8+ T cells do have retained function similar to prior variants, so there's more to the immune system than just neutralizing antibodies.

I completely agree that the best way to protect yourself against Omicron or even against Delta infection, if you're in a high-risk group for severe disease or otherwise, is going to be getting your third dose. Get vaccinated: two doses on top of your natural infection, or all three doses to complete your series.

Romanowski: In your opinion, are the booster shots for the general public warranted at 6 months or even sooner at 3 months, based on the data that you're currently seeing? That has been the biggest question so far: When should you get the booster shot?

Antevy: The data that we have show that 6 months is appropriate. However, I will say that in children, that probably doesn't hold true. I think that kids have a much more robust immune response, and just the minimal data that we have on kids are showing kids who are about 7 months old with neutralizing antibody numbers on the machine that we use still in the high 90s, as opposed to the adults who are probably in the 30%-40% range with the Pfizer shot.

Romanowski: Angie, any thoughts on that? Anything you would like to add?

Rasmussen: I would agree with that. I actually haven't seen the data on the neutralizing antibody responses in kids, but that doesn't surprise me. Kids are certainly known to mount more robust neutralizing antibody responses. I think with regard to 3 vs 6 months, we need to be very careful with that. Last year, people were talking about how long the vaccination clinical trial process normally takes. One of the things that happens during that process is they optimize dosing regimens and dosing schedules. With these vaccines, obviously, it was a huge public health emergency, and so it was really, I think, very appropriate and urgent to expedite those trials and get people vaccinated as soon as possible.

The only other thing, given the dosing schedules weren't optimized, that we've seen from other countries — specifically Canada and the UK, where they have extended dosing intervals between the first and second dose for all the vaccines that were used there (primarily Pfizer, Moderna, and AstraZeneca) — is that people who had a longer dosing interval between those first two doses seemed to mount better and more durable immune responses.

That makes me wonder if waiting 6 months for a booster — which I think is very much warranted, especially now with the data that we have about Omicron and its impact on vaccine effectiveness — is something we shouldn't stick to. The first two doses for those 6 months do result in fairly high neutralizing antibody titers, and we have observed that those titers really do start to wane at about the 6-month mark, at least for people who got the doses on the 3- to 4-week schedule that's common for Pfizer and Moderna. I'm not sure that it's essential, and I don't really know what the effect would be if you moved up the third booster dose to 3 months after your second dose rather than 6 months. It may not have any impact at all, or it may result in a similar effect as what you would see at 6 months. Without data, it's hard to make that call.

Given that I think it is really urgent to make sure that we are using these boosters to provide them first with priority to the people whom Peter and Kartik were talking about — the people who are the most vulnerable, particularly in those in long-care facilities, people with existing comorbidities that we know put them at much higher risk for severe disease — those people really should be prioritized for booster doses rather than sort of making it a free-for-all for anyone who had their second dose 3 months ago or less.

Cherabuddi: I completely agree with Dr Rasmussen. I want to talk about two things. For children aged 5-16 years, stay with the two doses — no booster at this time. For immunosuppressed patients, especially severely immunosuppressed patients, I would stress that the recommendation is to get shots at 0, 1, and 2 months; three doses constitute that series, and then get the booster 6 months later. I think that's something that's been lost. Many severely immunocompromised patients who I deal with haven't received their third dose, or even the third dose followed by a booster. So, we really have some catching up to do there.

Antevy: Kartik, we saw that in our initial antibody trials of the immunocompromised. Because we are testing folks with the bedside antibody tests quite frequently, we are finding that those people did need a booster shot much earlier, so that's a very important point.

Romanowski: Let's talk a little bit about the vaccine effectiveness. All reports that we see so far out of South Africa, the US, and throughout Europe seem to indicate that the Omicron strain causes mild symptoms in both vaccinated and unvaccinated individuals, with no reported increase in severe disease or hospitalization.

Cherabuddi: I think we have to be careful about the mild cases vs severe cases. I think all countries are very different, especially while predicting this. The kind of vaccine schedules are different, when the first doses were received are different (we were much more an early population compared with South Africa). Many folks who did not get infected through the Delta surge, maybe due to prior infections or vaccinations that they took many months ago. There are many differences.

We have to reserve judgment on saying that Omicron causes more mild cases. Certainly, compared with their prior wave, it seems to be fewer cases in South Africa. Again, just the overwhelming switch to Omicron and that we're seeing even more cases and the exponential growth in cases will mean more hospitalizations, more severe disease, and the hospital system getting overwhelmed, and then that immediately leads to increased mortality. We've seen this with every single wave of infection we've had. We need to be very cautious about labeling Omicron as just mild.

Rasmussen: I couldn't agree more. I think that even if you have a smaller relative percentage of cases that develop severe disease, if you have enough people getting infected, that still is overall an absolutely large number, and it's often much more than what different health systems can accommodate.

Here in Saskatchewan, we just have finished a pretty significant Delta wave that was severe even though many people had been vaccinated when it started (our province was at about 70% vaccination). So, we're behind much of the rest of Canada, but many people were still fully vaccinated. Of course, the majority of people in the hospital and in the ICU were unvaccinated people, but it overwhelmed our healthcare system to the point that we were exporting patients to Ontario because we did not have the ICU capacity to manage those patients.

If we have a situation with Omicron where a lot of people are getting breakthrough infections, even if they're getting mild disease (those people that Peter and Kartik were talking about earlier who are more vulnerable and more likely to develop severe disease), they may still end up having severe disease even if a larger proportion of people who contract it don't. That's still devastating for them, for their families, and for our healthcare system as a whole. I couldn't agree more that we really need to be very careful with making declarations that Omicron is less severe than other variants that have circulated, as if that's a good thing or that allows us to dismiss the level of concern and urgency we should have.

Antevy: Anya, I would just like to put a cherry on top of Angie's point there. Many people have tried to make predictions about this virus and look where that's led us. I do think that it's very early. We should not be thinking that this virus is suddenly going to be like the common cold, which you see happening on social media. I do think that when the numbers go up that high, we still have tens of millions of people in this country who are still unvaccinated and many people who have just gotten the disease itself, the first form of the disease (the OG), and they think they're perfectly fine. I think that there is wood left to burn here, especially in the United States. I would offer a word of caution to everybody listening.

Cherabuddi: A 15% increase in cases can overwhelm our emergency rooms and hospitals. I don't think people realize that a 10%-15% increase — especially going into the winter, where we tend to see other respiratory illnesses, including the flu — is potentially going to be a problem because we've seen fewer flu vaccinations as well.

Romanowski: Some question whether an increase in cases in South Africa contributes to the whole concept of natural immunity. They're saying, "Well, it's low vaccination rates, and we don't yet know the death rates with the new COVID-19 strain." What advice do you give to those people?

Antevy: If you look at what happened in India — and remember when the rest of the world was struggling — you saw that line in India, where there were very few cases and everyone was saying it was natural immunity, and then India blew up, if you will. Since then, a number of reports that have come out to show that the vaccinated are much more secure and safe than the unvaccinated or even those who have been naturally infected.

Rasmussen: With the situation in India, I think tremendous harm was done by clinicians, including many in the US, who made very declarative statements at the beginning that herd immunity had been reached in India, and therefore that allowed the Indian government to justify policies that permitted very large gatherings to happen. Those were then later thought to be super-spreader events that really helped kick off that absolutely devastating surge that India experienced. That's also where we got the Delta variant from.

People really do need to understand that all immunity is actually natural, whether it's infection acquired or vaccine acquired. Infection-acquired immunity is very variable. In some people, it's as robust and protective as vaccine-induced immunity, but in many others it's not. You won't know if you're one of those people who has the equivalent of vaccine-induced immune protection or somebody who doesn't. The only way that you will find that out is if you get infected or not, which is really not a very good way to make that determination.

We should not ignore the importance of infection-acquired immunity. In fact, the data for Omicron from South Africa indicate that vaccination on top of infection-acquired immunity really produces substantial protective immunity. We should not be ignoring infection-acquired immunity, but we also shouldn't be relying on it. Also, we shouldn't be telling people that they have nothing to worry about if they've had COVID-19 before because I think all the evidence, time and time again, has shown that that's not true.

There was a statement called the Great Barrington Declaration that came out in 2020 that basically encouraged people who were supposedly not vulnerable (which was poorly defined) to go out and live their lives and get COVID-19, and you're going to be contributing to the solution because then we're all going to reach the herd immunity threshold.

That same crowd — which has sort of morphed into saying some stuff that's not always explicitly anti-vaccine but is very anti-vax adjacent — has now latched on to this idea that Omicron is mild and therefore we don't have to worry about it, and you can just get Omicron and it's going to be no big deal. It's going to be like having a cold.

Well, I did my PhD on rhinovirus, which actually causes colds. I've certainly worked on seasonal flu as well as emerging influenza viruses. Just because a virus doesn't kill you, it doesn't mean that it doesn't have lasting effects. I think that people really need to understand that just because COVID-19 might not kill you, it doesn't mean that you aren't going to be set back healthwise and potentially economically, financially, and mentally as well.

Certainly, besides long COVID, there are serious consequences sometimes to being in the hospital for a long time, to being in the ICU, and to being on a ventilator, which my physician colleagues here can talk about with much more experience than I can. Having a so-called mild infection is not something that you should just dismiss. It's still a major public health problem, just like seasonal influenza is a major public health problem every year.

Our healthcare system isn't really equipped to deal with large numbers of people, even when a small fraction of them ends up with severe disease. It's not equipped to deal with a mild disease that infects everybody, all at the same time.

Antevy: I think that's the hidden pandemic, Angie. I have the privilege of working with over 2000 paramedics, and the list of those paramedics who have long-hauler COVID-19 is just tremendously long. We've had these young, burly guys who are having MIs, DVTs, strokes — you name it. They can't walk from one room to the other without getting short of breath.

You won't hear about any of those stories in the media, but those numbers of patients are just piling up. It's going to create an entire new specialty of medicine because of what's happened to these folks who never got immunized and just got the disease. They didn't die of it, so they're not a statistic, but they're a statistic in their own right with their long-hauler symptoms.

Cherabuddi: Economically as well, it's going to set us back quite a bit, right? Every family that's gone through this go to multiple clinics to recover from COVID after being hospitalized.. A study done at the University of Florida (UF) has shown that your risk of dying is so much higher up to 12 months later.

This long, drawn-out, painful death just burdens you economically and socially as well. You cannot work. You are not prepared for taking months off work. We don't not have that kind of social support. The families are devastated by this, and it's going to have this long-term impact, both from mild cases and having long-term symptoms, like Peter said. Even the severe hospitalizations where we do everything we can in the ICUs and on the floors, we get a successful discharge and we all clap about it. But if we follow these patients 6 months later, they're still not back to where they were — not even close.

Romanowski: Kartik, do you see COVID-19 soon becoming an endemic?

Cherabuddi: I study reemerging viruses and emerging viruses, and the thought is that all viruses eventually become endemic. That's probably true, but the timeline of it varies significantly. This can happen over decades, or it can happen over years. The important thing with SARS-CoV-2 is that it doesn't really have to become mild to be more efficient at spreading. It spreads extremely well in the presymptomatic and asymptomatic phases, so there's not a strong selective pressure to become milder. I think that's the other thing that many people have cleared up. "Oh, it's already come to the endemic stage, and Omicron is actually good news." No, it's not. We're getting way ahead of ourselves. Sure, it might become endemic decades from now or years from now. We have not reached that point yet.

Rasmussen: I couldn't agree with you more, Kartik. I will just say that another one of my pet peeves is the very assured statement that viruses always evolve to be less virulent. That is absolutely not true, and there's no selection pressure whatsoever on SARS-CoV-2 to become less virulent. The only reason a virus would potentially do that is if it's killing its host before it can transmit to another host. In SARS-CoV-2, the majority of the transmission (and this is why this pandemic has been so difficult to control) occurs before most patients are even symptomatic. This is spreading before people even start to get sick, much less die of it. There's no evolutionary pressure whatsoever on this virus to become less virulent.

If you look at 1918, for example, 1918 didn't go away. It just basically became more of a seasonal flu. That required the majority of the world's population to get infected since at the time, we didn't have a vaccine for it.

There are really two ways that we can look at this pandemic. Everybody is going to be exposed to it at some point, and we can either choose to be exposed in a way that is safe and doesn't result in massive deaths (ie, vaccination), or we can do it the hard way that we've done throughout history and have a pandemic that has an even more sizable death toll than what's already happened.

I think people really should understand that. This virus isn't going to be magically eliminated. The attitude that we if we just stay at home indefinitely and be very careful, and maybe get vaccinated or maybe not, we can eliminate it somehow. That's not going to happen with this virus. We will be exposed to this virus, and we really have a choice as to what type of risk we're going to assume. At least those of us in the US and Canada and countries that have easy access to vaccines, we have that choice to decide if we're going to be exposed in a way that that is not dangerous or a way that is potentially lethal.

Cherabuddi: Pandemics are not brief. There are major reasons why pandemics arise at a certain time. We forget, and we think of these as very short events. All previous pandemics, whether it's cholera or plague and so on, were long, drawn-out events that killed 20%-40% of populations in many countries.

Romanowski: One of the last topics I want to address and discuss is treatment. What are the current recommendations on reducing the progression of COVID-19, particularly the Omicron strain? Is the monoclonal antibody strategy still effective with the Omicron variant? What are some of the new suggestions for treatments moving forward?

Antevy: I can tell you what I've been doing here in my jurisdiction. I'll start with testing before we get to what I'm doing with monoclonal antibodies. I've implemented RT-LAMP across two cities now, which is a molecular test (based on colorimetric detection of SARS-CoV-2) that I can do on mass scale. I'm not testing every firefighter every shift, or every city employee twice a week. I'm doing that all in-house, under surveillance testing.

I picked up an asymptomatic individual who was sitting in an office full of people, and we effectively took him out of circulation, if you will. That person then comes into our headquarters and that person gets Regeneron, which is what we currently are using, because that did show some good efficacy against Delta. The new data suggest that it may not. The state of Florida is moving now to sotrovimab, so I'm able to have that medication on premises for these city employees.

What I'm really most excited about are these oral medications that I'd love to hear my colleagues talk about. Merck's came out (to very little fanfare and some resignations from the FDA), and it seems like a more worrisome type of medication. The Pfizer medication, which is still in the FDA approval phase, seems very promising. I believe it's an 89% reduction in severe disease and death.

If you have testing in place and you have access to the monoclonals, which may reduce by 70% the severity of the disease and death (and they may be replaced by new oral medications), I think we'll finally be able to live in an environment where we can feel safe kind of getting back to normal again. I'd love to hear what my colleagues say on this as well.

Cherabuddi: I agree completely with Peter. Testing has to be the way to treatment. Test and treat has to be linked the way we talked about test and trace. This phase, if it is to be successful, it's going to be test and treat.

For the Pfizer product, Paxlovid, I really want to see the data on it. All we have right now is a press release. There's a 3-day window from symptom onset to treatment. The Pfizer folks claim that the data have similar efficacy with 5 days. I really want to go through that and look at the numbers more closely. If what they state is true, then it's more promising.

A couple of advantages with these oral meds is that they tend to not be affected as much with variations in the spike protein. Sure, there can be other things down the line that can do that. We see it with HIV medications, and I've seen it in the people whom I treat. These are protease inhibitors, and you could potentially see a change down the line, but overall, they're more resistant to mutations and variants affecting them. That's good. The bad part is how to roll this out. We've not been so good at rolling out anything so far. That makes me more trepidatious in looking at how this treatment is going to work.

Additionally, with the monoclonal antibodies, it seems like it should do a better job if you're looking at the sort of virus testing they did with S gene mutations. Again, rolling that out is going to be tough. We saw that there were clear differences in access to monoclonal antibodies. Richer folks with better access get them earlier. It's hard to get them to our poor folks and rural folks. It's extremely challenging. We even go out with the van to try to get them. The good thing with this product is it's intramuscular (IM). It makes it easier than subcutaneous or IV infusions. That is more promising for me with the monoclonal antibody from GSK, remdesivir; they've looked at the Omicron variant as well, and it seems to function, based on the data that have been released. Again, the efficacy is somewhat questionable overall when you look at it globally. The variants do not change that for it.

Finally, with treatments, I was going to talk about the issues with even detecting Omicron right now. The TaqMan assay, which sort of gives you a soft clue, is not used as much in the United States. We have four different tests and all of them will detect the S gene target failure, if you will. Our genotyping is much better than it was, but it's still not up there. We send a few isolates to the health department and then we sequence our inpatients, but there's a huge lag. Maybe Angie and Peter can speak about this a little bit more.

Even getting that soft signal of how much Omicron we're seeing is going to be tough unless we sequence more. The treatment and testing are linked. Getting enough rapid tests and PCR tests to folks before holidays is going to continue to be a huge challenge in order to treat them with any of these products.

Rasmussen: I agree completely with that, and I agree with both of you that that all of the drugs have promise, but how effective they're going to be at scale depends on how they're used and the type of access that people can have to them. Even the monoclonal antibodies — at this point, there are many different monoclonal antibodies, including other therapies that are in the pipeline. We can tell pretty easily whether a monoclonal antibody is going to work against a given variant, given that we know which epitopes those monoclonal antibodies are specific to. They've done quite a bit of work, including with Omicron, to look at some of the monoclonal antibodies and how they're affected by different variants.

The oral medications will potentially make a big difference, but as Peter said, the Merck drug is a mutagen that drives the virus to error catastrophe. It seems that they may have overstated the effectiveness of that drug in the press release compared with the documents that they submitted to the FDA, and it really barely just squeaked by getting authorization with the FDA. The Pfizer drug, which is a protease inhibitor, has less of a risk of potentially inducing new mutations, but there is a risk that it could select for resistant variants if it's not used in combination with some other drugs.

For all of the antiviral drugs — I don't care if it's a monoclonal antibody, I don't care if it's an oral medication that works by these different mechanisms — the key is to make sure that you're treating people early. COVID-19 disease is actually caused by an aberrant immune and inflammatory response to the infection. If you already have a severe enough infection that that response has begun and that immunopathology is occurring, then treating with an antiviral and getting rid of the virus at that point isn't going to be particularly helpful.

I would defer to both Peter and Kartik as clinicians, but as far as I understand it, that's the point when you start treating with dexamethasone or the IL-6 inhibitors to reduce the inflammation — where you're really treating the pathology of the disease, you're treating the host, and you're not focusing on the virus anymore. I think that these drugs have the potential to make this something that's very manageable, particularly combination therapies of oral medications, but it will mean that people have to have their infections diagnosed very early, it will mean that people will have to have access to those medications, and it will mean that they have to be affordable for people.

Monoclonal antibodies are great, but I think, as Kartik said, it can be really challenging to deliver those because they're not just medications that you can go to the pharmacy, get a prescription for, and take them home. I think treatments are really important. I'm glad that we have many of them in the pipeline.

With SARS-CoV-2, making this into a manageable, treatable condition that is going to be effective worldwide and not select for new variants that might be resistant to these drugs is a tremendous logistical challenge.

I'm excited about the future in the sense of all the promise that this has, but at the same time, I'm not optimistic because we've been talking for almost an hour now about how we keep making the same mistakes over and over again in terms of how we deal with pandemics, how we treat patients, and how we roll out vaccine and drug therapy campaigns.

I hope that we can really do right by people, but I'm also somewhat cynical, unfortunately, about our ability to actually do it.

Romanowski: I want to thank all of you for taking the time to join us today in this quite informative and lively discussion. I also want to thank our viewers for joining as well.

Anya Romanowski, MS, RD, is an editorial director at Medscape who primarily covers emergency medicine, critical care and hospital medicine. She is based in New York City, and you can follow her on Twitter.

Angela L. Rasmussen, MA, MPhil, PhD, has studied a variety of viruses, including Ebola, using systems biology and genomics to examine the virus and host responses. In the current pandemic, she's used Twitter to counter misinformation and misinterpretation of data.

Kartik Cherabuddi, MD serves as a specialist for antibiotic resistant pathogen infections and is the director of the antimicrobial stewardship program at UF Health. He has advised and volunteered with education efforts around the world, including in Asia (India, Nepal) and Africa (Democratic Republic of Congo), in regard to COVID-19 control and management.

Peter M. Antevy, MD, is an EMS physician and medical director for Coral Springs-Parkland Fire Department in Florida. He is a member of the EMS World editorial advisory board.

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