{"id":290624,"date":"2022-06-13T18:51:56","date_gmt":"2022-06-13T18:51:56","guid":{"rendered":"https:\/\/parasiteswithoutborders.com\/?p=290624"},"modified":"2022-06-13T18:52:01","modified_gmt":"2022-06-13T18:52:01","slug":"twiv-772-covid-19-clinical-update-68","status":"publish","type":"post","link":"https:\/\/parasiteswithoutborders.com\/es\/twiv-772-covid-19-clinical-update-68\/","title":{"rendered":"TWiV 772 COVID-19 Clinical Update #68<\/strong>"},"content":{"rendered":"\n

This Week in Virology<\/strong><\/p>\n\n\n\n

Host: Vincent Racaniello<\/p>\n\n\n\n

Guest: Daniel Griffin<\/p>\n\n\n\n

Aired 26 June 2021<\/p>\n\n\n\n

pdf of this transcript available (link)<\/p>\n\n\n\n

Vincent Racaniello: <\/strong>This Week in Virology,<\/em> the podcast about viruses, the kind that make you sick.<\/p>\n\n\n\n

[music]<\/p>\n\n\n\n

VR: <\/strong>From MicrobeTV, this is TWiV<\/em>, This Week in Virology<\/em>, Episode 772, recorded on June 24, 2021. I\u2019m Vincent Racaniello and you\u2019re listening to the podcast all about viruses. Joining me today from New York, Daniel Griffin.<\/p>\n\n\n\n

Daniel Griffin: <\/strong>Hello everyone.<\/p>\n\n\n\n

VR: <\/strong>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.<\/p>\n\n\n\n

DG: <\/strong>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\u2019re having trouble breathing.<\/p>\n\n\n\n

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\u2019re having an asthma attack or a COPD exacerbation. We\u2019ve been hesitant to use those, but we, actually, we\u2019re saying, \u201cBoy, if a person\u2019s vaccinated, if you\u2019re prevalence is– your test positivity rate is under 1%, you could start thinking about being a little bit more flexible.\u201d We\u2019ve always done that when it\u2019s been really severe, in an emergency.<\/p>\n\n\n\n

One of the people on the call said, \u201cThat\u2019s pretty strict, under 1%,\u201d and I was proud to say, \u201cHere in New York our test positivity rate is under 1%,\u201d and we\u2019re doing a lot of testing. That\u2019s not true everywhere as we sort of bring up, right?<\/p>\n\n\n\n

Let\u2019s start with our quotation, and then let\u2019s get right into the thick of it. The quotation, \u201cPrejudice is a burden that confuses the past, threatens the future, and renders the present inaccessible.\u201d That\u2019s by Maya Angelou. I like that because I feel like we all need to keep being reminded that we don\u2019t want confirmation bias, we don\u2019t 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.<\/p>\n\n\n\n

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\u2019ll get into that as we go forward. The update really hits home with– it\u2019s 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.<\/p>\n\n\n\n

I don\u2019t 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\u2019s difficult.<\/p>\n\n\n\n

For those of us, we talk about how difficult the pandemic has been. We couldn\u2019t go to that bar, we couldn\u2019t 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\u2019s a vaccine shortage, this is about not having food. This is about going to bed hungry.<\/p>\n\n\n\n

Here though in the U.S., today I was covering three of the hospitals and my other partner was covering the other three. There\u2019s two of us covering these six hospitals because one of my partners, Dr. Anuja Lee, was off attending the funeral of her brother\u2019s wife. This, I think was tragic. Anuja\u2019s 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.<\/p>\n\n\n\n

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\u2019s just tragic. I think when people make up stuff like these microchips and all these other crazy things, there\u2019s no science there. This is not a scientific debate. It\u2019s just untrue and that has repercussions and someone\u2019s got to explain to these teenage children that they no longer have a mom.<\/p>\n\n\n\n

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\u2019re seeing high COVID rates and hospitalizations, and deaths. What we\u2019re also seeing, and I\u2019m putting this in right before the children, we\u2019ll get into this, is that we\u2019re actually seeing all those common winter viruses packed into June.<\/p>\n\n\n\n

Now that everyone\u2019s taking off their masks, everyone\u2019s celebrating, everyone\u2019s 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\u2019re 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.<\/p>\n\n\n\n

There is, I have to say, \u201cNo way that a COVID vaccination will give parainfluenza virus or RSV,\u201d 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\u2019re seeing a lot of this. In New York, we\u2019re not seeing much COVID-19, but we are seeing a lot of these URIs, so it\u2019s important for people to realize that.<\/p>\n\n\n\n

Children and COVID. Children are at low-risk, but they\u2019re not at no risk. Never miss an opportunity to test. I\u2019m going to jump right forward here. I don\u2019t think this will shock anyone, but it\u2019s going to tie right into the kids again. This was the article, \u201cAssessing the Association Between Social Gatherings and COVID-19 Risk Using Birthdays,\u201d and this was published in JAMA Internal Medicine<\/em>.<\/p>\n\n\n\n

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.<\/p>\n\n\n\n

Now, what I will say here is, this really was significant in areas where there was a high incidence of COVID. If there\u2019s a high incidence of COVID and you have a birthday party, that\u2019s what\u2019s 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\u2019s the common coronaviruses, it\u2019s RSV, it\u2019s the rhino-enteroviruses. It\u2019s the other common colds that are spreading.<\/p>\n\n\n\n

I think that this is critical. As people are making decisions, it\u2019s really– prevalence issue is important as you\u2019re making decisions about what to do. The other thing that is coming up here, I\u2019m going to– a subtlety, a nuance here, so we\u2019re back in the times of low prevalence and poor positive predictive value in many parts of our country.<\/p>\n\n\n\n

People may remember that word, orthogonal or orthogonal testing, so if an individual comes in maybe it\u2019s a screening, they\u2019re asymptomatic, they need a negative test for some reason, it comes back positive. I]If your prevalence is less than 1%, that\u2019s 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\u2019ve got to wait those 10 days of isolation. We\u2019ll see where that goes going forward.<\/p>\n\n\n\n

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\u2019s of interest to everyone. Another article was published, \u201cSafety and Immunogenicity of a Third Dose of SARS-CoV-2 Vaccine in Solid Organ Transplant Recipients: A Case Series,\u201d published in the Annals of Internal Medicine<\/em>. 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.<\/p>\n\n\n\n

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\u2019re looking at.<\/p>\n\n\n\n

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.<\/p>\n\n\n\n

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\u2019s 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.<\/p>\n\n\n\n

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, \u201cWhat does it mean if you are vaccinated and your antibody test is negative?\u201d We still, across the board, say in general, don\u2019t rush out and get your serology test after vaccination. These vaccinations are incredibly effective.<\/p>\n\n\n\n

Conversation I was having with one of the oncologists today is we\u2019re not seeing all these transplant patients, all these people with hematological malignancies, who\u2019ve been vaccinated ending up in the hospital. We\u2019re actually getting an experience that supports the efficacy of these vaccines.<\/p>\n\n\n\n

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, \u201cRe-infection with SARS\u2010CoV\u20102 in Patients Undergoing Serial Laboratory Testing.\u201d This was published in CID<\/em>. Here, the authors analyzed 9,119 patient with SARS\u2010CoV\u20102 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.<\/p>\n\n\n\n

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 \u201cSARS\u2010CoV\u20102 infection rates of antibody-positive compared with antibody-negative healthcare workers in England: a large, multicentre, prospective cohort study (SIREN)\u201d that had been published in The Lancet <\/em>back in April.<\/p>\n\n\n\n

I did find it interesting that the infection fatality rate was higher than most of us think, right? Most of us are thinking, \u201cWell, if you get re-infected, it\u2019ll be more mild.\u201d 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\u2019ve been previously infected and vaccines are available.<\/p>\n\n\n\n

I know the authors use the word, \u2018only,\u2019 but my interpretation is that in about four to five months after infection, we\u2019re already seeing re-infections, we\u2019re already seeing deaths. I think the data has continued to support that vaccines are a little bit better than just natural infection.<\/p>\n\n\n\n

The period of detectable viral replication, the viral symptom phase. What I like to say, \u201cThe time for monitoring and monoclonals.\u201d And I like to add, \u201cWhere you get your test is where you should get your monoclonals.\u201d 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, \u201cEfficacy and safety of azithromycin in COVID-19 patients: A systematic review and meta-analysis of randomized clinical trials,\u201d was published in Reviews of Medical Virology<\/em>.<\/p>\n\n\n\n

Now, the author\u2019s 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.<\/p>\n\n\n\n

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, \u201cWe already know this and this doesn\u2019t add much to the literature.\u201d Unfortunately, as I\u2019ve pointed out, 88% of people with COVID have ended up getting antibiotics. Unfortunately, no, people seem not to know this.<\/p>\n\n\n\n

I recently had a conversation with someone taking care of a patient in India and the comment was, \u201cWe really had nothing to give them except for antibiotics,\u201d and I said, \u201cWhat do you mean except for antibiotics?\u201d They\u2019re like, \u201cWe didn\u2019t have oxygen. We didn\u2019t have steroids. All we had on-hand was antibiotics and we wanted to give them something.\u201d Don\u2019t give them antibiotics, that is not giving them something, that\u2019s not helpful. By giving them HCQ, Hydroxychloroquine, you\u2019re 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.<\/p>\n\n\n\n

We had another article, \u201cCharacterization of Bacterial and Fungal Infections in Hospitalized Patients With Coronavirus Disease 2019 and Factors Associated with Health Care-Associated Infections.\u201d This was published in Open Forum Infectious Diseases<\/em>. 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\u2019re at this prestigious university, Columbia University, there in New York City. Magda Sobieszczyk, the head of our department, was among the authors.<\/p>\n\n\n\n

I was actually presenting to the group this morning, if anyone\u2019s listening, I\u2019m 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\u2019re ending up in the hospital. 94% did not have an acute bacterial infection that would benefit from antibacterial therapy.<\/p>\n\n\n\n

Later on, and we\u2019ve 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.<\/p>\n\n\n\n

Monoclonals, can\u2019t leave monoclonals out, there\u2019s always a little more data. The article, \u201cEffect of monoclonal antibody treatment on clinical outcomes in ambulatory patients with COVID-19,\u201d also published in Open Forum Infectious Diseases<\/em>. 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.<\/p>\n\n\n\n

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\u2019re still serology negative, meaning they do not yet have detectable antibodies, there may still be some benefit– Not this dramatic benefit we\u2019re seeing in that first week, but still a little bit in some patients.<\/p>\n\n\n\n

Early inflammatory phase. We did get a press release from Gilead, and this was Gilead\u2019s remdesivir. I\u2019ve actually replaced their brand name with remdesivir all throughout this, but \u201cAssociated With a Reduction in Mortality Rate in Hospitalized Patients With COVID-19 Across Three Analyses of Large Retrospective Real-World Data Sets\u2014Real-World Evidence from Nearly 100,000 Hospitalized Patients Provides Clinical Insights on the Use of REMDESIVIR for the Treatment of COVID-19.\u201d Now, this data was presented at the World Microbe Forum. Vincent, I don\u2019t know if you attended World Microbe Forum. I see a shaking head, no. [laughs]<\/p>\n\n\n\n

At that forum, they presented three real-world data analysis that included 98,654 patients hospitalized with COVID-19. Let\u2019s run through the three trials. One was the double-blind, placebo-controlled Adaptive COVID-19 Treatment Trial, so that\u2019s 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.<\/p>\n\n\n\n

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.<\/p>\n\n\n\n

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.<\/p>\n\n\n\n

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).<\/p>\n\n\n\n

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.<\/p>\n\n\n\n

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\u2019m starting to feel a little bit better about all the money and resources we\u2019re putting on remdesivir, but these are huge numbers needed to show a significant impact. I just want to give that as a caveat. [crosstalk]<\/p>\n\n\n\n

VR: <\/strong>Daniel, do you use remdesivir on your patients?<\/p>\n\n\n\n

DG: <\/strong>We still do. There\u2019s 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\u2019ll throw in the caveat, Vincent. If that person is getting better, we\u2019re not keeping them in the hospital for that extra day four, day five. If they\u2019re 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.<\/p>\n\n\n\n

VR: <\/strong>At the same time, you\u2019re probably giving them monoclonals?<\/p>\n\n\n\n

DG: <\/strong>That\u2019s the challenge. Again, it\u2019s all back to our timing. If they show up within the first 7 to 10 days, we\u2019re 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\u2019re still serology negative and have yet to mount an antibody response, monoclonals are still potentially of some benefit. That\u2019s the group that we\u2019re looking at remdesivir. After the first week we\u2019re getting into the second week, they\u2019re starting to get some degree of hypoxemia, that\u2019s when we\u2019re giving the remdesivir.<\/p>\n\n\n\n

VR: <\/strong>Got it.<\/p>\n\n\n\n

DG: <\/strong>It is interesting because you would think we\u2019d want to give it during that first week. It\u2019s an antiviral [laughs]. Let\u2019s give it when they have– Interesting enough, we have not been able to show, and I think it\u2019s because we don\u2019t 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\u2019t need exposure to remdesivir.<\/p>\n\n\n\n

Now, I\u2019m going to jump to the long phase, long COVID. I\u2019m going to try to keep these down to 30 minutes. People have been letting me know we\u2019ve been getting a little long, and then maybe that\u2019s okay, here we got long COVID. A couple things I want to say at the end– This is really important if you\u2019re a clinician, pause it here, get yourself a pen and some paper, be ready to go back to this.<\/p>\n\n\n\n

It\u2019s 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, \u201cHey we\u2019re starting to see a lot of people with long COVID.\u201d 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.<\/p>\n\n\n\n

In the meantime, when you see someone more than four weeks after acute COVID, they\u2019re 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?<\/p>\n\n\n\n

This is really a huge issue. It\u2019s a huge issue for the millions of people that are still suffering. It\u2019s a huge issue for the employers, it\u2019s a huge issue for us as a society, so it\u2019s really important that we\u2019re 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.<\/p>\n\n\n\n

I do want to offer a bit of hope to all these individuals suffering with long COVID. It\u2019s 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\u2019s a tremendous amount of research and medical attention being put on this topic, so I\u2019m really optimistic in the coming months.<\/p>\n\n\n\n

We\u2019ll be shifting some of our discussion away from vaccinations and monoclonals to, \u201cWhat are the therapeutics for these individuals who got COVID before we could prevent it?\u201d Or even, \u201cWho got COVID after we could prevent it, and are still suffering from long COVID?\u201d 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.<\/p>\n\n\n\n

When you\u2019re planning that big celebration, maybe take a moment and send a few dollars to Parasites Without Borders so we can continue to help FIMRC.<\/p>\n\n\n\n

VR: <\/strong>Daniel, what happened to the observation in the long COVID patients that vaccination seemed to help some of them?<\/p>\n\n\n\n

DG: <\/strong>We are still seeing that in about 40% of patients. I should mention that they are doing a study up at Yale, COVIDRecovery@yale.edu. I\u2019m waiting for a little bit more science, but we just keep seeing this, clinically, we\u2019re 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\u2019ve had heart damage, if you had a stroke, the vaccine isn\u2019t going to undo the permanent damage but it continues to be encouraging seeing patients that have had this.<\/p>\n\n\n\n

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\u2019m 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\u2019m looking forward to some more insights into this.<\/p>\n\n\n\n

VR: <\/strong>Time for some email questions. If you\u2019d like to send one to Daniel it\u2019s Daniel@mirobe.tv. Jenny writes, \u201cI 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\u2019m wondering if I should consider getting a second dose Pfizer, Moderna to increase my protection against delta variant from 60% to 80%?\u201d<\/p>\n\n\n\n

DG: <\/strong>I have to say that\u2019s a great question and a lot of people are asking it. The party line, I\u2019m going to give the party line, first, but then we\u2019ll 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.<\/p>\n\n\n\n

The subtleties would be if you said, \u201cOh, but I\u2019m 80-years-old and I have multiple comorbidities and I\u2019m homebound and I don\u2019t have a good care network.\u201d Then you start thinking about– In general, the vaccines are all incredibly effective. We\u2019re not recommending that someone who is vaccinated with J&J go ahead and get an mRNA vaccine.<\/p>\n\n\n\n

VR: <\/strong>David writes, \u201cI\u2019m 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.<\/p>\n\n\n\n

My doctor informs me that I probably still have some protection through other mechanisms, but there\u2019s 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?\u201d<\/p>\n\n\n\n

DG: <\/strong>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, \u201cDid it work?\u201d A lot of our other vaccines, hepatitis B, even though we don\u2019t think it\u2019s 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\u2019ll say that are encouraging, one is five milligrams of prednisone is actually quite a low dose compared to what we\u2019re seeing in other populations.<\/p>\n\n\n\n

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\u2019s strategy that he\u2019s bringing up? Stopping the prednisone for a period of time, let\u2019s 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.<\/p>\n\n\n\n

I think that\u2019s 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\u2019re 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\u2019s say you live in an area with a high prevalence, that\u2019s going to be a slightly different metric.<\/p>\n\n\n\n

VR: <\/strong>Finally, Mark writes, \u201cI\u2019m a clinician and past clinical researcher who\u2019s been involved with chronic fatigue syndrome since the mid-\u201880s. I\u2019ve 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.<\/p>\n\n\n\n

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\u2019d have very few cases in Australia so far but that will change with opening of our borders and our low vaccination rates.<\/p>\n\n\n\n

My question is, \u2018Could long COVID be a specific instance of CFS?\u2019 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.\u201d<\/p>\n\n\n\n

DG: <\/strong>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.<\/p>\n\n\n\n

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, \u201cOh my gosh. Is this the next CFS?\u201d<\/p>\n\n\n\n

Here\u2019s the big difference when I have those conversations is, \u201cPeople got this all at the same time?\u201d I\u2019m actually hoping it\u2019s 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\u2019re going to get insights into long COVID that can allow us to go back to the chronic fatigue syndrome patients.<\/p>\n\n\n\n

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.<\/p>\n\n\n\n

VR: <\/strong>That\u2019s COVID-19 Clinical Update Number 68 with Dr. Daniel Griffin. Thank you, Daniel.<\/p>\n\n\n\n

DG: <\/strong>Thank you, Vincent. Thank you, everyone, and be safe.<\/p>\n\n\n\n

[00:38:32] [END OF AUDIO]<\/strong><\/p>\n","protected":false},"excerpt":{"rendered":"

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