English 
Spanish 
This Week in Virology
Host: Vincent Racaniello
Guest: Daniel Griffin
Aired 26 June 2021
pdf of this transcript available (link)
Vincent Racaniello: This Week in Virology, the podcast about viruses, the kind that make you sick.
[music]
VR: From MicrobeTV, this is TWiV, This Week in Virology, Episode 772, recorded on June 24, 2021. I’m Vincent Racaniello and you’re listening to the podcast all about viruses. Joining me today from New York, Daniel Griffin.
Daniel Griffin: Hello everyone.
VR: This is number 68, Daniel, and over a year of updates. It seems to me that, at least here in the U.S., things are getting better.
DG: They certainly are, particularly in many parts of the U.S. We still have our regional pockets, a little shout-out to Missouri where the positivity rate is over 6%. I was on a call earlier this week where we were talking about, can we start doing nebulizers, things like that, with a little bit more flexibility. Nebulizers, if people are not familiar, is where maybe an individual comes in, they’re having trouble breathing.
We actually use a device called a nebulizer, which creates small particles that can be inhaled, that have maybe bronchodilators, medicines that will open up the airways, help them breathe better, maybe they’re having an asthma attack or a COPD exacerbation. We’ve been hesitant to use those, but we, actually, we’re saying, “Boy, if a person’s vaccinated, if you’re prevalence is– your test positivity rate is under 1%, you could start thinking about being a little bit more flexible.” We’ve always done that when it’s been really severe, in an emergency.
One of the people on the call said, “That’s pretty strict, under 1%,” and I was proud to say, “Here in New York our test positivity rate is under 1%,” and we’re doing a lot of testing. That’s not true everywhere as we sort of bring up, right?
Let’s start with our quotation, and then let’s get right into the thick of it. The quotation, “Prejudice is a burden that confuses the past, threatens the future, and renders the present inaccessible.” That’s by Maya Angelou. I like that because I feel like we all need to keep being reminded that we don’t want confirmation bias, we don’t want to go into something thinking we know what the truth is. We want to have our eyes open, so that we can actually continue to learn and move forward.
Not everything that we thought we knew a year ago has turned out to be true, and not everything we thought a year ago that was untrue [laughs] has turned out to be such. I think we still need to keep learning. We still have so much to learn and we’ll get into that as we go forward. The update really hits home with– it’s in your first question, which was how are things going. I have to say, this is a tough day, a tough week on several levels.
I don’t know if our listeners know, but one of my cows, my heifer actually died. In Uganda, there was a viral disease. The hoof-and-mouth disease was sweeping through Eastern Uganda, which periodically happens, and so my cow died, which is tragic. Tragic because you care about your animals, but also, this was a cow that was providing seven liters of milk a day to help feed people. And was even economically, this is part of the income that was helping to support Mary, my little heifer who is only about a year-old, so that’s difficult.
For those of us, we talk about how difficult the pandemic has been. We couldn’t go to that bar, we couldn’t see that movie, we were trapped in our houses. But just really to bring home, people in Uganda where the virus is surging again and there’s a vaccine shortage, this is about not having food. This is about going to bed hungry.
Here though in the U.S., today I was covering three of the hospitals and my other partner was covering the other three. There’s two of us covering these six hospitals because one of my partners, Dr. Anuja Lee, was off attending the funeral of her brother’s wife. This, I think was tragic. Anuja’s sister-in-law was in her early 50s, she did not want to get vaccinated because she had learned through social media that there were microchips in the vaccines.
She went ahead, she got infected. A little over a week later, she ended up in the hospital, intubated, died leaving behind a husband and her teenage children. It’s just tragic. I think when people make up stuff like these microchips and all these other crazy things, there’s no science there. This is not a scientific debate. It’s just untrue and that has repercussions and someone’s got to explain to these teenage children that they no longer have a mom.
As mentioned, our country is a patchwork with different ideas about– and different vaccination rates. Areas with high vaccination rates tend to be the areas with low COVID. Areas with low vaccination rates tend to be the areas where we’re seeing high COVID rates and hospitalizations, and deaths. What we’re also seeing, and I’m putting this in right before the children, we’ll get into this, is that we’re actually seeing all those common winter viruses packed into June.
Now that everyone’s taking off their masks, everyone’s celebrating, everyone’s getting all the kids together and such, the CDC actually had to issue an alert regarding a rapid rise in RSV, respiratory syncytial virus, particularly in the South. But we’re also seeing spikes in parainfluenza, common coronaviruses, particularly OC43. I actually had recently a question from, actually a clinician, which sort of shocked me, they were asking whether or not I thought the COVID vaccines were causing these people to develop upper respiratory infections.
There is, I have to say, “No way that a COVID vaccination will give parainfluenza virus or RSV,” so no. This is behavioral and I think a lot of times we like to try to blame something else, but no, these viruses are now spreading, we’re seeing a lot of this. In New York, we’re not seeing much COVID-19, but we are seeing a lot of these URIs, so it’s important for people to realize that.
Children and COVID. Children are at low-risk, but they’re not at no risk. Never miss an opportunity to test. I’m going to jump right forward here. I don’t think this will shock anyone, but it’s going to tie right into the kids again. This was the article, “Assessing the Association Between Social Gatherings and COVID-19 Risk Using Birthdays,” and this was published in JAMA Internal Medicine.
This was a cross-sectional study using administrative healthcare data on 2.9 million households from the first 45 weeks of 2020. They found that among households in the top decile of the country, as far as COVID-19 prevalence, those with birthdays had more diagnoses of COVID-19 compared with households that have not had a birthday in the two weeks after that birthday was held.
Now, what I will say here is, this really was significant in areas where there was a high incidence of COVID. If there’s a high incidence of COVID and you have a birthday party, that’s what’s going to spread. If COVID incidence is low, they did not see this. Here, I think this is a perfect example here in New York, when people are having birthdays and other celebrations, it’s the common coronaviruses, it’s RSV, it’s the rhino-enteroviruses. It’s the other common colds that are spreading.
I think that this is critical. As people are making decisions, it’s really– prevalence issue is important as you’re making decisions about what to do. The other thing that is coming up here, I’m going to– a subtlety, a nuance here, so we’re back in the times of low prevalence and poor positive predictive value in many parts of our country.
People may remember that word, orthogonal or orthogonal testing, so if an individual comes in maybe it’s a screening, they’re asymptomatic, they need a negative test for some reason, it comes back positive. I]If your prevalence is less than 1%, that’s probably a false positive. From a medical, scientific point of view, you can repeat that to clarify the picture. But most jurisdictions, the Department of Health is still operating under the, and I hate these words, abundance of caution. You still need to treat that positive as a positive. If that individual was going to be heading off to camp, they’ve got to wait those 10 days of isolation. We’ll see where that goes going forward.
Active vaccination, never miss an opportunity to vaccinate and, as I still believe, vaccines are how this pandemic ends. This comes up all the time, so I will touch on it. Maybe this is, I guess, more of interest to physicians, more of interest to people with immune suppression, but I think it’s of interest to everyone. Another article was published, “Safety and Immunogenicity of a Third Dose of SARS-CoV-2 Vaccine in Solid Organ Transplant Recipients: A Case Series,” published in the Annals of Internal Medicine. A little background with which our regular listeners are probably familiar, the antibody response after two doses of an mRNA vaccine against SARS-CoV-2 is excellent in the general population, but can be markedly attenuated or even undetectable in transplant recipients.
Here, the authors reported on 30 patients that received a third dose of vaccine. In 22 patients, maintenance immunosuppression included tacrolimus or cyclosporine plus mycophenolate. In addition, corticosteroids were used for 24 patients, sirolimus for one, and belatacept for one. The median time between transplantation and initial vaccination was 4.5 years. What did they find? Before they received their third dose of vaccine, 24 of the 30 patients had negative antibody titers and six had low-positive antibody titers. Remember, this is a case series that we’re looking at.
The patients received the third dose of vaccine a median of 67 days after the second dose of that initial vaccine series. 15 patients received the J&J (Johnson & Johnson/Janssen), nine received Moderna, six received Pfizer-BioNTech. What did they find? Repeated antibody testing a median of 14 days after the third dose of a vaccine revealed that of the six patients with low-positive antibody titers before the third dose, all had high-positive antibody titers after the third dose.
In contrast, the 24 patients with negative antibody titers before the third dose, 25% went on to have high-positive titers, 8% had low-positive titers and the remainder, so 67%, just remained negative. This is interesting and I agree with the author’s comments. There were certain limitations here, limitations of the study obvious right off, this was a small and heterogeneous convenience sample and there were no assays for neutralizing antibody, no specific B cell memory, or T cell response assays.
This is interesting, we still need additional trials to determine whether booster doses to prevent COVID-19 in transplant patients is warranted. Of course, in my mind, the biggest thing here is we do not have a correlate of immunity in the antibody test, right? We keep asking this question, “What does it mean if you are vaccinated and your antibody test is negative?” We still, across the board, say in general, don’t rush out and get your serology test after vaccination. These vaccinations are incredibly effective.
Conversation I was having with one of the oncologists today is we’re not seeing all these transplant patients, all these people with hematological malignancies, who’ve been vaccinated ending up in the hospital. We’re actually getting an experience that supports the efficacy of these vaccines.
Another article, and I think this goes into the same area on natural infection and protection against re-infection. I have a few comments on this, but the article is, “Re-infection with SARS‐CoV‐2 in Patients Undergoing Serial Laboratory Testing.” This was published in CID. Here, the authors analyzed 9,119 patient with SARS‐CoV‐2 infection, who received serial tests in total of 62 healthcare facilities in the United States between December 1st, 2019 to November 13, 2020. They identified re-infection in 0.7% during an average mean of 116 days or about four months, and there were two deaths associated with re-infection.
The re-infections were associated with a 3.2% mortality. A great discussion here where they compare their data to the 1.8% re-infection rate seen in the UK SIREN study. That had been published in “SARS‐CoV‐2 infection rates of antibody-positive compared with antibody-negative healthcare workers in England: a large, multicentre, prospective cohort study (SIREN)” that had been published in The Lancet back in April.
I did find it interesting that the infection fatality rate was higher than most of us think, right? Most of us are thinking, “Well, if you get re-infected, it’ll be more mild.” But an infection fatality rate of over 3%, in this case, a couple people died in this small cohort. We would not only expect with improved therapeutics and close monitoring– These people are being closely monitored and picked up early. I would not have expected to see deaths in people who’ve been previously infected and vaccines are available.
I know the authors use the word, ‘only,’ but my interpretation is that in about four to five months after infection, we’re already seeing re-infections, we’re already seeing deaths. I think the data has continued to support that vaccines are a little bit better than just natural infection.
The period of detectable viral replication, the viral symptom phase. What I like to say, “The time for monitoring and monoclonals.” And I like to add, “Where you get your test is where you should get your monoclonals.” I have a couple of things here before we hit monoclonal. The first is, what about antibiotics? We all know a significant amount of antibacterial therapeutics have been given for this viral disease. The article, “Efficacy and safety of azithromycin in COVID-19 patients: A systematic review and meta-analysis of randomized clinical trials,” was published in Reviews of Medical Virology.
Now, the author’s analysis included seven studies with 8,822 patients. The use of azithromycin, that is an antibacterial antibiotic, the Z-Pak, which is quite popular here in the U.S., was not associated with an impact on mortality in COVID-19 patients. The use of azithromycin was not associated with an impact on need for invasive mechanical ventilation or length of stay.
The results in this rather large study showed that azithromycin as routine therapy in COVID-19 patients is not justified due to a lack of efficacy and potential risk of bacterial resistance. I thought it was interesting because I looked through the comments and one of the comments was someone said, “We already know this and this doesn’t add much to the literature.” Unfortunately, as I’ve pointed out, 88% of people with COVID have ended up getting antibiotics. Unfortunately, no, people seem not to know this.
I recently had a conversation with someone taking care of a patient in India and the comment was, “We really had nothing to give them except for antibiotics,” and I said, “What do you mean except for antibiotics?” They’re like, “We didn’t have oxygen. We didn’t have steroids. All we had on-hand was antibiotics and we wanted to give them something.” Don’t give them antibiotics, that is not giving them something, that’s not helpful. By giving them HCQ, Hydroxychloroquine, you’re going to do harm. You are not being helpful. This concept that only a minority of patients admitted with COVID have a secondary bacterial infection.
We had another article, “Characterization of Bacterial and Fungal Infections in Hospitalized Patients With Coronavirus Disease 2019 and Factors Associated with Health Care-Associated Infections.” This was published in Open Forum Infectious Diseases. Whenever I read a good article, I always remember Steve Goff giving me a hard time asking me if that was a real journal. I want to point out, if Steve is listening, that this was published by the Columbia Infectious Disease Physicians. They’re at this prestigious university, Columbia University, there in New York City. Magda Sobieszczyk, the head of our department, was among the authors.
I was actually presenting to the group this morning, if anyone’s listening, I’m reading and highlighting your article. My colleagues evaluated adult patients diagnosed with COVID-19 between the 2nd of March and the 31st of May, 2020 that had been hospitalized for greater than 24 hours. They included a total of over 3,000 patients. Community-associated co-infections, when they were admitted, were identified in only 6% of patients. This is an important point. This is during that acute inflammatory phase. This is when they’re ending up in the hospital. 94% did not have an acute bacterial infection that would benefit from antibacterial therapy.
Later on, and we’ve talked about this before, if you continue in the hospital, you can go on to develop a healthcare-associated infection. This is usually in week two or three of your hospital stay. They did see that in 12% of these patients, and most of those infections were gram-negative bacteria, but also about 20% were due to fungi. Then as time went on, they were actually seeing more drug-resistant organisms causing these.
Monoclonals, can’t leave monoclonals out, there’s always a little more data. The article, “Effect of monoclonal antibody treatment on clinical outcomes in ambulatory patients with COVID-19,” also published in Open Forum Infectious Diseases. The authors reported when they compared rates of emergency department visits or hospitalizations among ambulatory COVID-19 patients treated with monoclonal antibody, that was an n=305 versus untreated, that was 6,354, that treatment was associated with decreasing counters within 30 days, so odds ratio of 0.23, so about a 77 reduction.
Just, we keep hitting on this, the most effective thing we can do if we have missed that opportunity to get someone vaccinated is treatment with monoclonals. As we mentioned last time, if they show up at the hospital and they’re still serology negative, meaning they do not yet have detectable antibodies, there may still be some benefit– Not this dramatic benefit we’re seeing in that first week, but still a little bit in some patients.
Early inflammatory phase. We did get a press release from Gilead, and this was Gilead’s remdesivir. I’ve actually replaced their brand name with remdesivir all throughout this, but “Associated With a Reduction in Mortality Rate in Hospitalized Patients With COVID-19 Across Three Analyses of Large Retrospective Real-World Data Sets—Real-World Evidence from Nearly 100,000 Hospitalized Patients Provides Clinical Insights on the Use of REMDESIVIR for the Treatment of COVID-19.” Now, this data was presented at the World Microbe Forum. Vincent, I don’t know if you attended World Microbe Forum. I see a shaking head, no. [laughs]
At that forum, they presented three real-world data analysis that included 98,654 patients hospitalized with COVID-19. Let’s run through the three trials. One was the double-blind, placebo-controlled Adaptive COVID-19 Treatment Trial, so that’s ACTT-1. This was looking at hospitalized patients with COVID-19. There was a trend toward reduced mortality, 11% versus 15%, and the remdesivir-treated patients, that was an n=541 compared with the placebo n=521. Now, in the overall study population, a trend means this was not statistically significant looking at over a thousand treated patients.
Then they went and did a post-hoc analysis. In this post-hoc analysis, remember this data mining as I like to say, patients requiring low-flow oxygen baseline achieved a 70% reduction in mortality, that they did claim was statistically significant. The difference in mortality in the other subgroups was not statistically significant. I think these play into our practice, we are not recommending remdesivir for people who come in without the requirement of low-flow oxygen. We already have some data– we were concerned about once they progress, once they end up in the ICU or a ventilator, that maybe they do worse.
Then we have the real-world retrospective comparative analysis from the Premier Healthcare Database. This looked at mortality in hospitalized patients who were treated with remdesivir. Bigger numbers here n=28,855 versus matched patients who are not treated. Those were the n=16,687, and this looked between August and November of 2020. The analysis included adult hospitalized patients treated within the first two days. Patients were matched on baseline level of oxygenation, and they all stayed in the hospital for a minimum of three days. The primary endpoint was time to death.
In this large analysis, they report that they saw a significantly lower risk of mortality in patients that got remdesivir versus those did not, across all severity levels. People coming in with low amounts of oxygen, higher amounts of oxygen, etc. Finally, they referred in this press release to the SIMPLE-Severe study, which is a randomized, open-label, multicenter, Phase 3 study in hospitalized adult patients with severe COVID-19 (oxygen saturation less than 94% on room air, or receiving supplemental oxygen and radiological evidence of pneumonia).
As the primary objective of the study, five-day and 10-day dosing durations of remdesivir, they did not include a standard of care comparator arm when they initially set this up. Then, ahead, the retrospective real-world analysis that was presented at the WMF, compared mortality outcomes of hospitalized patients who received remdesivir in the open-label extension phase. They continued this study into an open-label extension phase, here we had in that an n=197,524, and then they created a propensity score weighted comparator arm, patients not treated with remdesivir was an n=1,426.
The primary endpoint was time to all-cause death, and the analysis found that in the overall population treatment with remdesivir was associated with this statistically significant mortality risk, at 28 days versus those not treated. Again, regardless of the baseline oxygen requirements. I’m starting to feel a little bit better about all the money and resources we’re putting on remdesivir, but these are huge numbers needed to show a significant impact. I just want to give that as a caveat. [crosstalk]
VR: Daniel, do you use remdesivir on your patients?
DG: We still do. There’s really a window in a sense of when we consider it. This is not giving it to every patient who walks in the door, only patients who have an oxygen requirement, or are oxygen saturation less than 94% in room air, and then not giving it to people with advanced disease who require mechanical ventilation. In that little window, we are doing five days of treatment. I guess I’ll throw in the caveat, Vincent. If that person is getting better, we’re not keeping them in the hospital for that extra day four, day five. If they’re getting better, we let them go, again not feeling like that extra day in the hospital is worth getting an extra one or two days of remdesivir.
VR: At the same time, you’re probably giving them monoclonals?
DG: That’s the challenge. Again, it’s all back to our timing. If they show up within the first 7 to 10 days, we’re giving monoclonals and a 70%, 80% reduction in them even coming to the hospital. If they do come to the hospital, the data would now say if they show up and they’re still serology negative and have yet to mount an antibody response, monoclonals are still potentially of some benefit. That’s the group that we’re looking at remdesivir. After the first week we’re getting into the second week, they’re starting to get some degree of hypoxemia, that’s when we’re giving the remdesivir.
VR: Got it.
DG: It is interesting because you would think we’d want to give it during that first week. It’s an antiviral [laughs]. Let’s give it when they have– Interesting enough, we have not been able to show, and I think it’s because we don’t know in that group– 97% of people are going to survive, probably 80% are not even going to progress to need the hospital, so you end up treating so many people who probably don’t need exposure to remdesivir.
Now, I’m going to jump to the long phase, long COVID. I’m going to try to keep these down to 30 minutes. People have been letting me know we’ve been getting a little long, and then maybe that’s okay, here we got long COVID. A couple things I want to say at the end– This is really important if you’re a clinician, pause it here, get yourself a pen and some paper, be ready to go back to this.
It’s really critical for us as far as long COVID to know who has it, and this as silly as it seems, we need to have this coded so that people can look through and see, “Hey we’re starting to see a lot of people with long COVID.” What have we heard? I talked a little bit about this last time is we got some guidance from the CDC. We have a code on the horizon, this is U09.9 post-COVID-19 condition code, not yet available in the U.S., but we expect it to be available in October 2021.
In the meantime, when you see someone more than four weeks after acute COVID, they’re still continuing to suffer, the CDC is recommending we use the code B94.8 sequelae of other specified infectious and parasitic diseases. We really need to start tracking who are these people, where are they, what resources do they need?
This is really a huge issue. It’s a huge issue for the millions of people that are still suffering. It’s a huge issue for the employers, it’s a huge issue for us as a society, so it’s really important that we’re able to identify who these people are, so that we can connect them with the resources they need. One of the resources they need is research.
I do want to offer a bit of hope to all these individuals suffering with long COVID. It’s unfortunate that this is impacting so many people, but the other side of that is– It is impacting so many people, this cannot and will not be ignored. There’s a tremendous amount of research and medical attention being put on this topic, so I’m really optimistic in the coming months.
We’ll be shifting some of our discussion away from vaccinations and monoclonals to, “What are the therapeutics for these individuals who got COVID before we could prevent it?” Or even, “Who got COVID after we could prevent it, and are still suffering from long COVID?” Before we hit emails, I will say please take a moment through the months of May, June, and July, we are continuing to help support Foundation for International, Medical Relief of Children. They operate throughout the world, South America, the Pacific, India, Africa– these places are really having a tough time.
When you’re planning that big celebration, maybe take a moment and send a few dollars to Parasites Without Borders so we can continue to help FIMRC.
VR: Daniel, what happened to the observation in the long COVID patients that vaccination seemed to help some of them?
DG: We are still seeing that in about 40% of patients. I should mention that they are doing a study up at Yale, [email protected]. I’m waiting for a little bit more science, but we just keep seeing this, clinically, we’re seeing not quite half, but a little less than half of patients who have the brain fog, the loss of smell, the fatigue. If you have pulmonary scarring, if you’ve had heart damage, if you had a stroke, the vaccine isn’t going to undo the permanent damage but it continues to be encouraging seeing patients that have had this.
I guess the next question I think about the renal transplant, the people that 25% got better with the first dose, we get up to 40% with the second dose. Do we give them a third dose? I’m looking forward to studies on that. Also, this will be an interesting population to look at. Do antivirals work in these people? Is this being driven by viral persistence or is it a pure immunological issue? I’m looking forward to some more insights into this.
VR: Time for some email questions. If you’d like to send one to Daniel it’s [email protected]. Jenny writes, “I got J&J vaccine back in March. Recently, I heard on the news that J&J vaccine is less effective against Delta variant than any two-dose vaccines. I’m wondering if I should consider getting a second dose Pfizer, Moderna to increase my protection against delta variant from 60% to 80%?”
DG: I have to say that’s a great question and a lot of people are asking it. The party line, I’m going to give the party line, first, but then we’ll go into the weeds. The party line is all of these vaccines are incredibly effective. Even should you get COVID after vaccination, it goes from being a severe life-threatening disease to maybe the sniffles, something mild in most cases.
The subtleties would be if you said, “Oh, but I’m 80-years-old and I have multiple comorbidities and I’m homebound and I don’t have a good care network.” Then you start thinking about– In general, the vaccines are all incredibly effective. We’re not recommending that someone who is vaccinated with J&J go ahead and get an mRNA vaccine.
VR: David writes, “I’m especially vulnerable to COVID as the result of age and a number of underlying conditions. I was vaccinated in February, was beginning to feel freer in what I could do until I read a newspaper article reporting on a study finding that even low doses of prednisone could dramatically reduce antibody production from the vaccine. I was taking five mgs of prednisone at the time. I was vaccinated for an autoimmune lung disease. I took the antibody test, the result was that there were no detectable antibodies.
My doctor informs me that I probably still have some protection through other mechanisms, but there’s no way of knowing if this is the case or how significant the other protections are. Doctor prescribing prednisone has told me I could stop it temporarily to get re-vaccinated. If I do this and then resume the prednisone, are the antibodies likely to be suppressed? Is there any way of measuring what degree of protection I have absent measurable antibodies? Any advice for me?”
DG: We keep hitting on this with the literature, and I keep bringing up these articles because people really care. We have a majority of our adult population now vaccinated and people want to know, “Did it work?” A lot of our other vaccines, hepatitis B, even though we don’t think it’s the antibodies that give you the protection, we think of it as a correlate you can measure. A lot of people are asking these questions. A couple of things I’ll say that are encouraging, one is five milligrams of prednisone is actually quite a low dose compared to what we’re seeing in other populations.
As I mentioned my discussion with the oncologist, we are not seeing a lot of individuals like you end up coming in as vaccine breakthroughs that end up in the hospital. We do think that the vaccines continue to be quite effective. Now what about your doctor’s strategy that he’s bringing up? Stopping the prednisone for a period of time, let’s say two or three weeks, getting vaccinated– And this is something we did a lot of times upfront is if we could, we would stop immunosuppressive medicines. We would have a person get vaccinated and then once they had finished the series, then they would potentially be resumed.
I think that’s a reasonable strategy, but again it gets back to this issue, the vaccines are incredibly effective. We are not seeing individuals like you end up in the hospital. Maybe we’re still underselling the vaccines across the board. The incidence is going down, the prevalence is going down. This is getting to be a safer time, at least for the next couple months, you have some time to think about this. If we start seeing rates go up or let’s say you live in an area with a high prevalence, that’s going to be a slightly different metric.
VR: Finally, Mark writes, “I’m a clinician and past clinical researcher who’s been involved with chronic fatigue syndrome since the mid-‘80s. I’ve seen and helped manage around 5,000 to 6,000 people with CFS all the way from near permanently bed-bound patients to impaired Olympic athletes in both inpatient and outpatient settings. The story of many long COVID patients is, to me, indistinguishable from my post-EBV, post-dengue, and post-Ross River viral cases here in Australia. Many of these are specific viral IgM remains raised and abnormalities of t-lymphocytes keep supporting a hypothesis of persistent immune failure to bring the infection to an end.
The few COVID-19 patients with persistent symptoms I have seen show the same immunology changes. Although I know that this is a very small sample and likely selection bias, we’d have very few cases in Australia so far but that will change with opening of our borders and our low vaccination rates.
My question is, ‘Could long COVID be a specific instance of CFS?’ No diagnostic tests or wide range of symptoms and disability, no clear mechanism identified a lack of disease classification impairing care. You raised dysautonomia as one component and this is especially common in young people with CFS. Treatment for postural orthostatic tachycardia syndrome, POTS, is well established and does provide considerable reduction of disability for many while we await deeper understanding of these conditions. Cheers, from Australia.”
DG: These are actually really excellent points all across the board. There certainly are similarities in this population. One of the things we learned from the CFS population was that a subset, if you try to just exercise them up so to speak, rehabilitate them, treat it as issue of deconditioning, you actually can make them worse. We see a very similar pattern in a subset of these patients, the POTS, the dysautonomia, there actually are a lot of similarities between these populations. That might be good. It might be bad.
One of the troubles we realize is that there was a lot of research at one point looking at CFS trying to figure out what was going on, trying to introduce helpful therapies, and we did not make a lot of headway. I know some people are looking at this and saying, “Oh my gosh. Is this the next CFS?”
Here’s the big difference when I have those conversations is, “People got this all at the same time?” I’m actually hoping it’s the other way, is that now since we had a large number of people get infected at the same time, we all know when the onset was that we’re going to get insights into long COVID that can allow us to go back to the chronic fatigue syndrome patients.
I do suspect there at least are certain patients that have similar mechanisms underlying this. I was going to throw chikungunya as another one of those post-viral syndromes that we see. I continue to be optimistic, but I think everything you said there was really insightful.
VR: That’s COVID-19 Clinical Update Number 68 with Dr. Daniel Griffin. Thank you, Daniel.
DG: Thank you, Vincent. Thank you, everyone, and be safe.
[00:38:32] [END OF AUDIO]
