TWiV 638 Do, there is no try

This Week in Virology

Hosts: Vincent Racaniello, Dickson Despommier, Alan Dove, and Rich Condit

Guests: Viviana Simon, Daniel Griffin, and Chuck Knirsch

Aired 12 July 2020

Vincent Racaniello: This Week in Virology, the podcast about viruses, the kind that make you sick. [music] From MicrobeTV, this is TWiV, This Week in Virology, Episode 638, recorded on July 10th, 2020. I’m Vincent Racaniello and you’re listening to the podcast all about viruses. Joining me today from New York State, Daniel Griffin.

Daniel Griffin: Hello, everyone.

VR: And also from New York State, Chuck Knirsch.

Chuck Knirsch: Hi, Vincent. Hi, Daniel.

VR: Here we are, a week goes by very quickly, doesn’t it?

DG: It does actually. I feel like I started preparing for this TWiV talk a few minutes after–

VR: The last one.

DG: –we finished the last one.

VR: I meant to tell you, I really appreciate that you obviously prepare and you thought about what you’re going to say, and it shows. People like it. Thank you for that very much.

DG: Oh, certainly.

VR: We are in the first week of July. What’s going on, Daniel?

DG: I’m going to start with the quotation again. This one is sort of timely and so this is a Vincent van Gogh quotation. Thanks to the pandemic, I did not get my family trip to Amsterdam. My family are all Vincent van Gogh fans and we had this, we’ve been planning for a long time and yes, that didn’t happen. Here it is, “The fishermen know that the sea is dangerous and the storm terrible, but they have never found these dangers sufficient reason for remaining ashore.”

I say that in part because I’m going to go race sailboats after this, so that’s one good thing, but the other is that there is a pulmonologist I’ve worked with for a long time, really, really entertaining, very passionate man. Actually, the other day he was saying, “You know what, if these numbers go up the way people are predicting this winter, I may just retire. I’m not that young anymore.” I think he was overwhelmed in a lot of ways during the first period of months.

I guess this is my encouragement to all the other healthcare providers out there. Stick in there. We really need you. I know this is tough and a lot of us are anticipating it’s going to be really tough again, and in a lot of areas, it’s really tough right now. There are some areas, Florida, Texas, other areas where the ICUs are filling up. Remember, at some point, this is why you went into medicine, you went into medicine to make a difference. I know it’s tough, but this is when we can make that difference, doctors, nurses, all the people that are involved. That’s why I use that quote there.

Next, I’m going to say thank you again to everyone who’s been helping us support our fundraiser with FIMRC in Uganda. That has gone really well. Visit parasiteswithoutborders.com and keep helping us. We’re only about $7,000 away from our goal of being able to give them $40,000. Please jump there. Let me go through. What I like to do is as the week goes on, people ask me questions and then I figure like, well, if clinicians are asking me these questions, they’re being asked these questions, and I try to give a response to what might be causing this.

One of the questions that, actually, was coming up quite a bit this week was, “Why are the case numbers rising, but why aren’t the deaths rising?” I know a lot of people have been asked about this, but in the media– I heard that Anthony Fauci is going to be on TWiV next week, so I know he had some answers to this. I’m always curious, are my answers and Tony Fauci’s answers the same? If they are, that’s a good sign. I think we’re on the same page. One thing that he points out that I will echo is that we are seeing younger people infected at this point.

Early on in New York, the mean age was in the 60s. We’re now seeing that mean age drop down to the low 40s. We’ve said all along, one of the best things you could be, if you’re going to get exposed to COVID, is a young woman, but young is key as part of that. When younger people get infected, the death rate tends to be lower. The other, and I think this is true, and this is something– is that we are better at managing patients. Even if you look at people the same age that are ending up in the hospitals, there are much less likely to die. I think a lot of that is interesting.

We’re starting to get the randomized controlled trials, but a lot of things we sort of stumbled onto, we’ve arrived at initially observationally, so delaying the intubation, the proning, steroids, right time, right dose, right patient, anticoagulation, which I really think continues to make a big difference. It was just another paper out showing that the exact number is 37% of the patients I looked at had pulmonary emboli. This was huge and devastating. I think we’re also avoiding that kitchen sink of toxic cocktails. I said early on, if I can’t have a cocktail at work, I don’t want my patients to have cocktails either. I think it doesn’t help with my job performance or their outcomes.

The other, and I think this is big and is a bit controversial. I’m going to step into it. I think here is there’s been a lot of investigation looking at New York. Is it a witch hunt? Is it, “Let’s learn from what went wrong so we don’t make the same mistakes?” A lot of the deaths, since I think people know now in the New York area, were in the nursing homes. Let’s say about half of the deaths. How did that happen? We had a pause order that went into effect March 22nd, would have been great if it had happened sooner, but that was the whole like “What went wrong in the testing delays?”

Once we had identified community spread in New York and saw how many thousands of people were infected, that went into effect. Just a few days later, March 25th, the governor was actually, I don’t know, advised, recommended. He made an executive order and said, “Listen, our hospitals are going to get overwhelmed, so nursing homes have to take these COVID-infected, potentially contagious people back.”

In actual wording was, “No resident shall be denied readmission or admission to the nursing home solely based on a confirmed or suspected diagnosis of COVID-19,” actually prohibited requiring hospitalized residents from getting COVID-19 to affect the admission or readmission. That finally on, it was May 10th actually, was removed. That executive order was receded and we stopped doing that.

That was a disaster looking back on it. I think you look at Florida and you say, “That is a place with thousands of nursing homes, why aren’t the nursing home residents dying there?” They’ve actually not done this, they’ve been really good about testing staff and protecting vulnerable populations. I know right now there’s this big, who gave the governor that advice? The big thing is that advice we now realize didn’t allow us to protect the vulnerable population and that had a big effect.

CK: These are some of the testing in New York at the time that we do have in Florida now, so maybe a little bit of difference in time period as well on a policy, whatever, I think.

DG: I think that’s right and I think that’s what I was worried about, which hasn’t come to pass, is there was actually pressure back to the governor saying, “Even though we can test now, let’s not wait for negative PCRs before we send them back.” Sort of a pressure to just pick a random date and say, “Oh, maybe 10 days, maybe it’s 21 days.” We’re just going to say, “Oh, they’re not infectious,” and send it back.

I’m going to say, fortunately, the governor has held firm until I think we’re sure that people are not infectious. We don’t want to send them into a setting. I had a question recently in one of my roles in the sports world, if you have an athlete who’s PCR-positive, are you going to send them back to training, back to be with the team? For me, I was like, “This is an easy answer.” I know that it’s horrible for that one player who’s still PCR-positive, but if you send that person back to, we’ll use the NFL as an example, back to the Giants, and now all the Giants are sick, and you shut down the NFL. That’s a disaster. Well, I’m going to say it’s the same if you send that person to a nursing home and all the people there start getting infected.

The fourth, and I think this is true, is that it takes time to die. We will probably start seeing an uptick in deaths in the next week. I anticipate a week from now when we have our talk again– The rates, new cases, already broke 60,000 yesterday. I think the deaths will be above 1,000 just because that’s sort of part of the dynamic.

VR: Have your admissions gone up this week?

DG: Remember when I recorded last week? I had nobody in the hospital, but now, I had a couple people in this week. One of them I’m going to talk about because he’s a very interesting character. Testing, we’re having challenges again, big challenges. One is we’re having issues with getting the proper supplies. I was talking to, actually, the chief of our pediatric division at ProHEALTH, New York, Jay Berger. He’ll say, “No, no, it’s definitely a good sample because the man said they shoved that Q-tip all the way back and it was incredibly painful.” I’m like, “What kind of Q-tip did they shove back?”

We were having issues getting the proper Q-tips, the small ones where it feels like a tickle, so they were taking an oral Q-tip and shoving it back to the middle turbinate. It’s cruel and unusual. Then, we’ve had issues. I think I’ve talked about last time is resulting delays, and we don’t say this publicly, it could be an up to an eight-day turnaround in New York at some places from the time you procure the tests to the time you get a result, and that’s a disaster from identifying infectious days and stopping the spread.

CK: The commercial labs are reporting that they’ve had a doubling in their turnaround time just because of the volume, I think.

DG: Yes. That continues. Everyone can have a test, eventually, as long as they don’t mind getting the results by Christmas. This is frustrating. The other I want to talk, and this is something that keeps coming up, the concept, “Does natural infection with coronaviruses cause herd immunity? Does it protect us from reinfection?” We got an email last time from a physician down in Washington, DC. I followed up on that and I’m also going to discuss an individual that I just took care of. Well, I’m taking care of, currently.

The individual that I just readmitted this weekend is a gentleman who I took care of in the end of March. He’s actually a friend of mine, a fellow clinician. He contacted me at the end of March. He was sick, his family was sick. We arranged for everyone to get tested. That was a Herculean task at the time, but they were all confirmed PCR-positive. I took care of him in the outpatient setting. He was sick for a couple of weeks, and finally, was better, returned to work, and he looked like he’d been through quite a bit at that point, but then he was better.

He’s out doing his job, seeing patients. Last Saturday, fevers, chills, wasn’t feeling well, we ended up readmitting him. We did a COVID PCR, it’s four months later, and that COVID PCR was positive. This gentleman, interesting, allowed us and he had such high antibodies back in April that he was actually a plasma donor for Mount Sinai. Repeat serology testing and his antibodies are barely detectable. He had his neutrophil-lymphocyte ratio was in the 30s. His D-dimer was 1,300. His interleukin-6 was up in the 30s. He actually also has bacteremia he’s got, looks like an infected finger.

How much of this is the bacteremia, but I’m not sure bacteremia gives you a positive COVID PCR four months out. I called up and I spoke to the person who emailed me just because one anecdote is an anecdote, two anecdotes are two anecdotes, not data, but I spoke to the gentleman about the Washington, D.C. case and it was very similar. It was a gentleman early April, got sick, PCR-positive. Middle June, his son was sick and he thought, as I think a lot of people, “Oh, I’ve already had this. I should have protection.” A week later, felt sick. Two weeks later, sick enough to go to the ER, COVID PCR-positive after having a couple of negatives to go back to work, and sicker the second time than the first, just like my individual, first time outpatient, not a problem, now in the hospital.

Starting to worry about the idea that this, like every other coronavirus, may not give long-lasting immunity, so herd immunity from natural infection maybe something beyond us. As I talked to my colleagues, I talked to a different pulmonologist today and he was saying, “Yes, I’ve seen a bunch of people and they seem sicker and I would have thought it was the COVID, but you really can’t get that twice, so I haven’t been testing them.” I’ve noticed that a lot of doctors instead of saying “I don’t know” have been reassuring people who have positive serology saying, “Well, it looks like you’ve got some protection here.”

I think we have to be honest and say we don’t know, and all strategies where we’re saying, “Oh, well, if people get infected, they go to parties, if it spreads, the next time around or well at least a portion of the population will be immune.” From the studies with antibodies dropping, from a couple of these experiences that we’re starting to have, I’m starting to get a little bit worried, so I’ll put it there. Vincent, get that hand up.

VR: Yes. These are two cases, but maybe for these two, they’re 200 where people recovered and are not getting very sick, so you’re going to see that always in infectious disease where a lot of people are infected. So maybe it’s not as bad as you’re thinking?

DG: I hope not. The tough thing is that if you look at the common coronaviruses, they don’t give us a long-lasting immunity and they, traditionally, you could be reinfected multiple times in the same year. There’s a preprint initially coming back out because you have to publish something– after ten years it becomes invalid, but we’ve known this for the other coronaviruses that if you get -OC43 or -229E or any of the other, you don’t get life-long immunity. You can get sick again, and it’s not clear that that second infection is milder than the first. Just my word of caution to be careful about when we hear that 5% or 10% of the population is seropositive, I don’t know what that means yet.

CK: What about recrudescence though, and I guess we need the virus before the first virus and the second virus because it is not unheard of to have viral recrudescence as well?

DG: Yes, that’s interesting, right, when I looked at the literature again, I was like how do we even know what the old– when we saw the same like we do these rapid viral panels when we say, “Oh, you know you had this two months ago, it’s coming up positive again.” How do we know that that isn’t just that coronaviruses have this recrudescence. Yes, I don’t know.

CK: Sorry, Vincent, go ahead.

VR: If you had virus isolates, you could sequence them because that would tell you they should be distinct, right?

DG: Yes and I would love that, a call out to our listeners, someone please let us know. Because this is– really has a big effect on how we approach this. I was asked a month or so back, we were signing large treatment trials, vaccine trials, and trying to pick where to do it. You want to predict a place where there’s got to be a large amount of infections and I actually was suggesting Chicago because in my head I was thinking because I don’t know, it may be that New York, that there is some of this herd immunity and we don’t get it as bad the next time, but again, I don’t know. This will be something we find out.

I know I’ve had a lot of people say that it would be great in addition to the serology to have a T cell assay. We would love to have that by the way, researchers who are listening, the clinicians would love to be involved in studies looking into that as well. I’m going to close on this last one. I get a lot of questions about the school reopenings, and this is a tough one. Vincent and I were chatting just briefly before we started here. It’s hard. I think there’s a lot of us, even the American Academy of Pediatrics, that are saying the goal should be to open the schools.

I don’t think any of us are saying the goal is to open the schools in a way that is unsafe, and I was using the analogy, they’re saying, “Oh, it’s safe to drive, but we’ve taken away your brakes and your seatbelt.” It’s not safe to drive without brakes and seatbelts. If we’re going to get kids back to school, it’s got to be done safely. It’s going to require testing and we have a number of papers out looking at what that frequency is going to be.

The reason I say it’s going to require testing is we’re learning, and sometimes it takes us a while to learn, but even people who become symptomatic, probably half of the spreading events occur before the symptom onset, certainly before they know and get a positive test, and then people who are asymptomatic and spread are spreading while asymptomatic. So without testing, without surveillance, yes this is not going to go well.

VR: You mentioned the average age going down to the 40s, right?

DG: Yes.

VR: Is that the average age of infection or serious disease?

DG: It’s the average age of people who are diagnosed. I think we’ve seen pretty consistently that if you look at people who end up getting admitted to the hospital, it’s older people. I think we talked the last time, you look at people who end up in the outpatient setting, well, they’re younger, it’s the reverse of that. Yes, we’re seeing consistency as far as the people who end up admitted tend to be the older individuals.

VR: Okay. All right, I wonder if I could have both of your opinions on this Brain paper that came out this week describing a range of neurological findings like encephalomyelitis and neurological disorders, Guillain-Barré. What do you guys think? Are you seeing this, Daniel?

DG: I think I tried to share a bit of this early on and we certainly, in a number of patients, saw the Guillain-Barré. I think I may have asked Dickson to help me pronounce that early on. But we would see, and it made sense as far as the timing would go. This would be about week three when we would expect a robust antibody response. We think of this disorder as being antibody-mediated, but we saw delusion. There was a nurse actually, she was an ICU nurse who ended up in the hospital and when I first saw her, anytime you would touch her, she basically starts screaming, “I’m falling, I’m falling.”

It was really quite frightening and then the next day she was like, “Oh my gosh, I feel so bad about how I acted.” I was like, “No, it’s fine.” We saw this throughout, we saw it in ICU patients who would end up extubated and there was this fog that would last for a while. Then even patients that I think I described in the long-haulers, people describing it or saying, “I have this brain fog. It’s just not as sharp as it used to be. It takes me a little time.” Strokes, we certainly saw, that was one of the red flags that even outpatients are susceptible to thromboembolic phenomenon.

I think that they described the delirium, the psychosis, which we certainly saw. What we thought was an inflammatory process, I think we saw that Guillain-Barré– I think everything they’re describing here was consistent with our early experience.

VR: This is just a quantification in their area of the patients. I think you mentioned earlier none of this is related to virus being in the brain. It’s probably secondary to immune responses, right?

DG: I think so. If you think Guillain-Barré, we’ve always thought of that as an immune response, that they respond quite well to intravenous immunoglobulin, so IVIG, steroids. Strokes, again, we think it’s a thromboembolic. I think these are immune thromboembolic, other complications, not at the virus. At least, that’s my impression to date.

VR: Story in The Times today, 68% of patients in a storefront medical office in Queens were seropositive. Now based on your discussion just now, I’m not sure what that means, but that’s pretty high. You think that it just happens to be that these are people on the front line that are working and they’re getting infected?

DG: It was interesting because it was actually an ER doc who wanted to talk to me about this just today. He’s an ER doc who got sick in early March but never seroconverted, stayed antibody negative. He brought this up with the idea, “Look at these people in these communities, they’re protected, they’re going to be fine. They won’t have to worry about the next wave.” I was like, “Yes, I don’t know about that.” That’s interesting because people take that– In certain communities, I think there was a large percentage of people that ended up getting exposed. The big issue for us is what does that mean this coming winter?

CK: I hope they’re protected because the borough of Queens was just devastated. Elmhurst Hospital and that area was just overwhelmed. I’m hoping they have some community protection for this winter.

VR: I just don’t know any virus that infects you and then your immunity is gone in three months and you get reinfected with serious disease. Do you know of any such virus?

DG: I was thinking about several different pathogens, I’ll say. Well, through a start, viruses. You don’t get herd immunity to dengue. Every year, there are 500 million. If anything, if your antibody’s dropped to the wrong level, people don’t do well. Malaria is a classic. You get exposed, if you stay exposed, you do okay, but then boom. HIV is probably perfect. You don’t get exposed to HIV and become immune. I think there’s a number of pathogens that are like this. I think as a viral strategy, this is a very consistent genetic code.

Influenza, which transmits in a similar pattern, a lot of pre-symptomatic tread, it can change its genetic code so it doesn’t really care that you get antibodies to that strain than the next strain. This one, for these coronaviruses to circulate, they need to basically somehow succeed in not creating a long-lasting immunity or they die out to become a low prevalent infection. Chuck, I don’t know if you had any–

CK: We need to study it. I don’t know. I’m hoping that this one is more like SARS-1 where we do seem to have more persistence of antibody. We didn’t have the infection dynamics to know whether reinfection was possible as opposed to the coronaviruses that the children get. I’m hoping it’s more like SARS-1, but if you’re sick, you develop all the T and B cell response that will be protective in the future.

VR: There’s a Queens’ community, which is Corona.

DG: Yes, yes.

CK: It is Corona.

VR: How about that? It would be interesting to see if they get reinfections in the next months.

DG: The nice thing about the serology testing, a lot of people pooh-poohed it, “Why are we doing this? What do we get to do with this?” I say, “You know what, we don’t know what we’re going to do with it now. It’s almost like the smartphone when it first came out. We don’t just use it for phone calls. But we are going to be able to get a sense of people who were infected who had positive serologies titers at whatever.

We’ll know a year from now very much what reinfection rates are, or what happens. Because right now, we’re saying, “Oh, to really know in such a short window, you need sequence, you need that original virus, you need the second virus.” But when numbers go up again in New York, we’re going to see readmitting the same person we readmitted last year.

VR: Let’s hope that this doesn’t happen with vaccine immunity.

DG: My hope is it doesn’t. People take what I say and they say, “Oh my gosh, this means the vaccines won’t work.” I’m not saying that, actually. I think that this is about the virus’ ability to subvert a proper durable immune response. If you use Moderna, if you use one of these synthetic vaccines, it makes me worry a bit about attenuated viral vaccines because maybe you just leave in there the parts that prevent long-lasting immunity.

VR: Inactivated vaccine should be okay also.

DG: Yes. It should. It shouldn’t be producing whatever proteins are triggering this.

VR: I’d like to know what that protein is. I’m sure you would too.

DG: Yes. [laughs]

VR: Two emails today, your two, three-ish. Thomas writes, “I’m an adult cardiologist in Philadelphia with a four-year-old son. February this year, he tested positive for influenza, and three days later after persistent fevers, started on cephalosporin for bilateral otitis media, completed a 10-day course. Then about four days later around the last week of February, developed a terrifying constellation of symptoms I’d never seen in him before, not being a pediatrician. His hands feet, knees, wrists, elbows became swollen red and painful, he could not walk, fit into shoes, complained of a headache and stomach ache, broke out in a rash, spiked a fever. These persisted a week.

COVID was supposedly not yet in Pennsylvania, and the pediatric ED diagnosed him with serum sickness from the cephalosporin, but I wonder if he actually had COVID and that was multi-system inflammatory syndrome. Now that we know that this coronavirus was present in the population much earlier than previously thought. So what it was the likelihood was present in Pennsylvania early in February is the way to determine whether strange cases like this actually represent MIS-C. Is the antibody test of any use, and what are the recommendations for following children who have had MIS-C? Do they need to see a pediatric cardiologist, pulmonologist, rheumatologist? Kids survive, but for some of them, this is just the beginning. Thank you for sharing your knowledge and brilliance with the world. We need so much more of it.” He means you, Daniel.

DG: [laughs] I’m sure he’s referring to everyone, but thank you. In cases like this, and if you actually look at the original UK analysis, thinking things like serology because by the time you have symptoms that might be the multi-inflammatory syndrome of children, it might be hard to detect the virus. Maybe in a case like this because we do think it’s antibody-mediated, it’s being treated with IVIG and steroids, so serology is potentially an avenue to pursue to try to see if that might be what happened here. Again, in people that have that, maybe I would suspect that those antibodies are going to persist longer.

We do know now that this virus has been circulating in the Tri-State area for longer than we realized. Cases definitely in mid-February, and serologies were already positive in mid-February, which means people were getting infected in January in the Tri-State area, so the timing doesn’t throw me on this. As far as follow-up, a lot of us are extrapolating from Kawasaki disease, so yes, these kids should get regular follow-up. We’re extrapolating, so hopefully, that will be sorted out. We have hundreds of confirmed cases in the New York area, so it might make sense for a child like this to try to go to one of those centers where they have enough individuals that they’re going to have an experience.

VR: Iwa writes, “I’m a pharmacist and medical journalist from Sweden. I regularly listen to your podcast and usually write a summary of Daniel Griffin’s part for the physicians that are too busy to listen for themselves. I was a bit intrigued by some data from yesterday.” I believe that was last week, I guess. “If I understood correctly, Daniel said that serology starts trending down and at about six minutes in, if you look at people months out, everybody’s antibody levels are trending downward, and if you look at people with more milder disease, maybe 40% are now serology positive. People who were sick enough to have high antibody titers, you start to see them turn serology negative.”

Then she gives a link to a Nature paper which says, “40% of symptomatic individuals became seronegative, and 12.9% of the symptomatic group became negative for IgG in the early convalescent phase.” She writes, “I just want to make sure that I understood and pass it on correctly. Could you help me find out if Daniel has another source or if he meant to say serology negative? I also want to send my warmest thanks for a great pod and that we really appreciate Daniel’s updates. You were all great.”

DG: Yes, it was serology. She got it correct. I misspoke. 40% of the asymptomatic become seronegative.

VR: Got it.

DG: It’s a good paper. It’s just a paper in Nature Medicine. A lot of what bothered me, a lot of the basis of my concerns, were figure 3 of that paper, where they look at the proportion that are IgG negative during the convalescence phase. Those are the numbers; 60% are IgG positive, these are the asymptomatic, we’ll call them mild. 40% are IgG negative. Then, it’s a lower percent are losing their antibodies. If you look at the slope of everyone, asymptomatic and symptomatic, the slope is going down for both groups.

VR: Okay. Finally, from Richard. “Dear TWiVers, ivermectin was addressed in an earlier TWiV. It’s apparently being used extensively in South America and Asia. Please comment and ask Dr. Griffin if he has any take on use of this medicine for C-19.”

DG: I’m expanding which hospitals I go to. Chuck, I don’t work enough, right? I wanted to add another hospital that I could visit and add to my day. I was over at St. Joseph’s, it’s one of the Catholic Health System hospitals here in the New York area, and as I’m coming new on staff, you meet with the credentialing committee. Actually, one of the people in that committee was like, “So, let me ask you about ivermectin,” and the story was he knew someone who was in South America who got ivermectin and they got better, so obviously, it was the ivermectin.

Vincent, I discussed your wife and Campbell and the fact that if you took 50,000 pills to get to the therapeutic level of ivermectin that was shown in the cell culture. That paper, I hate the title of that paper, the FDA-approved medicine ivermectin is effective for SARS-CoV-2 because it makes it sound like it’s FDA-approved for COVID-19 treatment. Because people all the time say, “Look, it’s FDA-approved.” I’m like, “Yes, not for that.”

It is interesting if you look at some of the physician experiences down in South America. They’ve been using it quite a bit, but again, it’s outside of randomized control trials. “Hey, the people we gave it to who could take oral ivermectin did better than the people who we decided not to give it to.” I’m not sure there’s a lot of, in my mind, science that explains to me why it should work, but it looks like there are going to be some trials so we will probably get some data on ivermectin.

VR: Okay. By the way, St. Joseph’s, is that in Patterson, New Jersey?

DG: You know, there’s a bunch of St. Joseph’s all over the place, but this is St. Joseph’s on Long Island.

VR: Long Island. Okay, because my dad worked at a St. Joseph’s in Patterson, that’s why. It would be funny if you were there.

DG: [chuckles] Yes.

VR: All right. Daniel, thank you again. Have a great weekend.

DG: My pleasure as always.

VR: Chuck, thank you for joining us.

CK: Good to see you both. Be well, Daniel.

[00:33:15] [END OF AUDIO]

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