Eric Hickman: 4th-Wave Of COVID-19 Will Push Rates To Zero
Eric Hickman discusses why we should beware of the 4th-Wave of Covid-19.
I know everyone is tired of hearing about the virus. Some think it is overblown by the media, many want to focus on the positives, and others have had their lives upended and want..
Eric Hickman discusses why we should beware of the 4th-Wave of Covid-19.
I know everyone is tired of hearing about the virus. Some think it is overblown by the media, many want to focus on the positives, and others have had their lives upended and want to forget.
There are reasons for optimism. It is a new year with longer days and warmer temperatures. People continue to get inoculated with increasing speed. The approval of new vaccines continues as new cases, deaths, and hospitalizations from the third wave fall (see below). The 1918 Spanish Flu had three waves over about a year; the COVID-19 pandemic has had three over a year as well.
Indeed, this is about over, right?
Tuned Out?
It isn’t over, and financial markets don’t accept that yet. I realize suggesting anything negative about the virus is misanthropic, but the truth matters, and the optics are misleading.
New cases decrease in the third wave because we are past the holidays, not because of vaccinations. It is a common misconception the decrease we’ve seen in the virus is due to vaccinations. The two aren’t related, at least yet.
“The decline in cases is likely a natural drop after record travel followed by indoor holiday gatherings triggered a surge in infections.” – Dr. Sarita Shah, associate professor at Emory University’s Rollins School of Public Health.
“We’ve seen these rises and falls in the COVID case counts now a few times, and they seem to really track along holidays or people’s movements,” Shah said.
To Early
“COVID-19 symptoms take between two to 14 days to appear after exposure, and cases peaked precisely two weeks after the Christmas holidays.” – Brittany Baker, undergraduate program coordinator and clinical assistant professor at North Carolina Central University.
Dr. Wafaa El-Sadr, professor of epidemiology and medicine at Columbia University’s Mailman School of Public Health, said the falling case numbers couldn’t get attributed to the COVID-19 vaccine. Not even a tenth of the population has gotten vaccinated, according to the CDC.
“We’re vaccinating our most vulnerable populations right now, but once we start to move into the broad population, the population that’s driving the numbers. That’s when we’ll start to see an impact on the overall numbers,” Shah said.
She said Americans might start to see the vaccine’s influence on case numbers as early as the summer, but it will be more evident in the fall.
As with all replicating biological entities, viruses change over time with random mutations to their genetic code (genome) when reproducing. Most mutations do not affect or are detrimental. Still, every once in a while, a random change (or series of changes) will alter a trait that increases its biological fitness – its competitive advantage in its environment. Beneficial mutations get carried forward to new generations, which crowd out the inferior older genome. Such is natural selection.
The process happens at a glacial pace in the life-forms we are most familiar with (say mammals) because reproduction takes years. Viruses replicate in a matter of hours to days, and more specifically, single-strand RNA viruses (of which the coronavirus, SARS-CoV-2, is one) replicate faster than other viruses.
Viruses that encode their genome in RNA, such as SARS-CoV-2, HIV and influenza, tend to pick up mutations quickly as they get copied inside their hosts, because enzymes that copy RNA are prone to making errors.
The concerning new Sars-CoV-2 variants emerging from the U.K., South Africa, and Brazil have yet to become dominant in the U.S. On February 7, a study reported that the more transmissible U.K. variant is now “spreading rapidly in the U.S.” It could become the dominant strain by late March. Italy’s health ministry said on February 12 that the U.K. variant makes up 17.8% of cases and will likely become prevalent in the coming months. The vaccine-weakening South African and Brazilian variants got detected in the U.S. in January. There are now several cases dotted around the U.S. They will presumably gain traction as they did in their original countries. This process takes months.
New Variants
The variants detected recently in the U.K. and South Africa have several novel changes in their spike-protein genes.
Scientists think one mutation these variants share could help the virus attach to and enter cells. The recently detected variant from Brazil shares a key spike-protein mutation with the one from South Africa.
“What we’re seeing is exactly what we expect to see. The surface proteins of the virus are under tremendous pressure to change.” – Sean Whelan, a virologist at Washington University in St. Louis.
“All the virus really cares about is multiplying. If it can get into the cells of the [host] and avoid the immune system of that host, it will multiply. Whether it causes the disease is a different question.”
Some scientists worry that South Africa’s variant could be better at evading antibodies produced in response to natural infection and vaccination. Preliminary estimates suggest the variant from the U.K. is 50%–70% more transmissible than earlier versions of the virus. And U.K. scientists said recently that early data suggested it could also be deadlier.
The variants found in the U.K. and South Africa have become the dominant types in countries where they were first detected.
Chart Source: Wall Street Journal
Parallel Evolution
The variant from the U.K. has spread widely abroad. As of late January, it had been reported in 70 countries and territories. The variant from South Africa has been reported in more than 30, while the U.K. variant was detected in more than two dozen U.S. states through late January. The Centers for Disease Control and Prevention projected it could become the dominant domestic strain by mid- to late March unless steps are taken to slow it. Variants first found in South Africa and Brazil have also been detected in the U.S.
Restricting travel between continents may prevent these variants from getting around, but there is another wrinkle to this. In biology, convergent or parallel evolution is a common yet counter-intuitive phenomenon. Independent lineages of a biological entity can arrive at similar evolutionary fitness solutions without any interaction between them. The similarity between the sugar glider (marsupial from Australia) and the flying squirrel (mammal from North America) is an example of this (image below).
Image Source: Getty/Encyclopedia Brittanica/UIG
Mutants
The same phenomenon is happening with Sars-CoV-2 mutations. Critical mutations from the U.K. variant (N501Y) and the one shared by the South African and Brazilian variants (E484K) emerged independently in a now-deceased Boston COVID-19 patient with a prolonged continuous infection. There are quotes from a National Public Radio story below. But for those interested, it is an interesting read (or listen) found at the link below:
Li and his colleagues published their findings in The New England Journal of Medicine in early November 2020 with little fanfare. Then about a month later, the pandemic took a surprising turn – and this peculiar case in Boston took on a new importance.
Scientists in the U.K. and South Africa announced they had detected new variants of the coronavirus. These variants were causing huge surges of COVID-19 in these countries.
When researchers looked at the genes of these variants, guess what they found? A cluster of mutations that looked remarkably similar to the mutations found in the virus from the Boston patient. The sets of mutations weren’t exactly identical, but they shared important characteristics. They both had about 20 mutations, and they shared several key ones, including a mutation (N501Y) known to help the virus bind more tightly to human cells and another mutation (E484K) known to help the virus evade antibody detection.
The virus may optimize itself to known mutations without spreading geographically, weakening the power of travel restrictions.
New Variants Will Emerge
The virus is just a little over one-year-old on its new metaphorical planet of “humans” and is still trying to find an evolutionary best fit. A safe assumption is that more variants will emerge.
“Look, there is going to be a whole cascade of these new variants. The virus moved between species. It migrated from the back end of a pangolin and to humans. And it’s got to adapt to humans. What we see now is it is getting better and better and more efficient at living in humans. And that we can see a set of other mutations coming down the line. So, I think we mustn’t say ‘ahh, well we now know what the mutations are going to look like.’ We don’t. There’s gonna be a set of other ones.”
Even though vaccination plans for developed-world adults are firming up, the developing world and children are less clear. As long as the virus circulates in humans anywhere, it will find new optimizations that will likely require vaccine alterations.
The more widespread infections remain globally, the more mutations will occur. A lingering pool of cases in poorer countries risks giving birth to resistant strains that force richer economies to lock down and start vaccinating all over again.
Taken together, it is probable that the world will have at least one more severe wave of infections this spring and summer – a fourth wave – before the inoculated and previously infected can crowd out those with no protection. Re-vaccination (booster shots) for new variants add to this timeline.
Rates Will Fall Dramatically
Such isn’t doomsday, but at a minimum, it elongates the time until battered industries (hospitality, entertainment) will have a chance to recover. So far, markets continue to believe the pandemic is a net benefit to bigger businesses globally (all-time highs in public companies, see below).
The explanation for this is that it is only the small, non-public companies that are struggling.
That is far-fetched.
The pandemic will cost the world’s public companies in aggregate at some point. I wrote nine months ago that “COVID-19 Defies Hyperbole.” Even though risk-on markets had gone up when I suggested they would go down, I stand by my prediction. Apt fiscal and monetary injections forestalled a deeper contraction. Still, it is a delusion to think we will get out of this for free – especially in a world economy that was overdue for a retraction anyways.
Even without a fourth COVID-19 wave, the negative impact on jobs, rents, consumer demand, tax revenue, and entire economy segments (hospitality, entertainment) has yet to be considered seriously. As they become so, risk-on markets (stocks, commodities, crypto-currencies, houses, and non-G-7 currencies) will drop, and long-term U.S. Treasury yields will fall dramatically.
Eric Hickman is president of Kessler Investment Advisors, Inc., an advisory firm located in Denver, Colorado, specializing in U.S. Treasury bonds.
Airlines operate in a market that's dictated by supply and demand: If more people want to fly a specific route than there are available seats, then tickets on those flights cost more.
That makes scheduling and predicting demand a huge part of maximizing revenue for airlines. There are, however, numerous factors that go into how airlines decide which flights to put on the schedule.
Every airport has only a certain number of gates, flight slots and runway capacity, limiting carriers' flexibility. That's why during times of high demand — like flights to Las Vegas during Super Bowl week — do not usually translate to airlines sending more planes to and from that destination.
Airlines generally do try to add capacity every year. That's become challenging as Boeing has struggled to keep up with demand for new airplanes. If you can't add airplanes, you can't grow your business. That's caused problems for the entire industry.
Every airline retires planes each year. In general, those get replaced by newer, better models that offer more efficiency and, in most cases, better passenger amenities.
If an airline can't get the planes it had hoped to add to its fleet in a given year, it can face capacity problems. And it's a problem that both Southwest Airlines (LUV) and United Airlines have addressed in a way that's inevitable but bad for passengers.
Southwest Airlines has not been able to get the airplanes it had hoped to.
Image source: Kevin Dietsch/Getty Images
Southwest slows down its pilot hiring
In 2023, Southwest made a huge push to hire pilots. The airline lost thousands of pilots to retirement during the covid pandemic and it needed to replace them in order to build back to its 2019 capacity.
The airline successfully did that but will not continue that trend in 2024.
"Southwest plans to hire approximately 350 pilots this year, and no new-hire classes are scheduled after this month," Travel Weekly reported. "Last year, Southwest hired 1,916 pilots, according to pilot recruitment advisory firm Future & Active Pilot Advisors. The airline hired 1,140 pilots in 2022."
The slowdown in hiring directly relates to the airline expecting to grow capacity only in the low-single-digits percent in 2024.
"Moving into 2024, there is continued uncertainty around the timing of expected Boeing deliveries and the certification of the Max 7 aircraft. Our fleet plans remain nimble and currently differs from our contractual order book with Boeing," Southwest Airlines Chief Financial Officer Tammy Romo said during the airline's fourth-quarter-earnings call.
"We are planning for 79 aircraft deliveries this year and expect to retire roughly 45 700 and 4 800, resulting in a net expected increase of 30 aircraft this year."
That's very modest growth, which should not be enough of an increase in capacity to lower prices in any significant way.
United Airlines pauses pilot hiring
Boeing's (BA) struggles have had wide impact across the industry. United Airlines has also said it was going to pause hiring new pilots through the end of May.
United (UAL) Fight Operations Vice President Marc Champion explained the situation in a memo to the airline's staff.
"As you know, United has hundreds of new planes on order, and while we remain on path to be the fastest-growing airline in the industry, we just won't grow as fast as we thought we would in 2024 due to continued delays at Boeing," he said.
"For example, we had contractual deliveries for 80 Max 10s this year alone, but those aircraft aren't even certified yet, and it's impossible to know when they will arrive."
That's another blow to consumers hoping that multiple major carriers would grow capacity, putting pressure on fares. Until Boeing can get back on track, it's unlikely that competition between the large airlines will lead to lower fares.
In fact, it's possible that consumer demand will grow more than airline capacity which could push prices higher.
Simple blood test could predict risk of long-term COVID-19 lung problems
UVA Health researchers have discovered a potential way to predict which patients with severe COVID-19 are likely to recover well and which are likely to…
UVA Health researchers have discovered a potential way to predict which patients with severe COVID-19 are likely to recover well and which are likely to suffer “long-haul” lung problems. That finding could help doctors better personalize treatments for individual patients.
Credit: UVA Health
UVA Health researchers have discovered a potential way to predict which patients with severe COVID-19 are likely to recover well and which are likely to suffer “long-haul” lung problems. That finding could help doctors better personalize treatments for individual patients.
UVA’s new research also alleviates concerns that severe COVID-19 could trigger relentless, ongoing lung scarring akin to the chronic lung disease known as idiopathic pulmonary fibrosis, the researchers report. That type of continuing lung damage would mean that patients’ ability to breathe would continue to worsen over time.
“We are excited to find that people with long-haul COVID have an immune system that is totally different from people who have lung scarring that doesn’t stop,” said researcher Catherine A. Bonham, MD, a pulmonary and critical care expert who serves as scientific director of UVA Health’s Interstitial Lung Disease Program. “This offers hope that even patients with the worst COVID do not have progressive scarring of the lung that leads to death.”
Long-Haul COVID-19
Up to 30% of patients hospitalized with severe COVID-19 continue to suffer persistent symptoms months after recovering from the virus. Many of these patients develop lung scarring – some early on in their hospitalization, and others within six months of their initial illness, prior research has found. Bonham and her collaborators wanted to better understand why this scarring occurs, to determine if it is similar to progressive pulmonary fibrosis and to see if there is a way to identify patients at risk.
To do this, the researchers followed 16 UVA Health patients who had survived severe COVID-19. Fourteen had been hospitalized and placed on a ventilator. All continued to have trouble breathing and suffered fatigue and abnormal lung function at their first outpatient checkup.
After six months, the researchers found that the patients could be divided into two groups: One group’s lung health improved, prompting the researchers to label them “early resolvers,” while the other group, dubbed “late resolvers,” continued to suffer lung problems and pulmonary fibrosis.
Looking at blood samples taken before the patients’ recovery began to diverge, the UVA team found that the late resolvers had significantly fewer immune cells known as monocytes circulating in their blood. These white blood cells play a critical role in our ability to fend off disease, and the cells were abnormally depleted in patients who continued to suffer lung problems compared both to those who recovered and healthy control subjects.
Further, the decrease in monocytes correlated with the severity of the patients’ ongoing symptoms. That suggests that doctors may be able to use a simple blood test to identify patients likely to become long-haulers — and to improve their care.
“About half of the patients we examined still had lingering, bothersome symptoms and abnormal tests after six months,” Bonham said. “We were able to detect differences in their blood from the first visit, with fewer blood monocytes mapping to lower lung function.”
The researchers also wanted to determine if severe COVID-19 could cause progressive lung scarring as in idiopathic pulmonary fibrosis. They found that the two conditions had very different effects on immune cells, suggesting that even when the symptoms were similar, the underlying causes were very different. This held true even in patients with the most persistent long-haul COVID-19 symptoms. “Idiopathic pulmonary fibrosis is progressive and kills patients within three to five years,” Bonham said. “It was a relief to see that all our COVID patients, even those with long-haul symptoms, were not similar.”
Because of the small numbers of participants in UVA’s study, and because they were mostly male (for easier comparison with IPF, a disease that strikes mostly men), the researchers say larger, multi-center studies are needed to bear out the findings. But they are hopeful that their new discovery will provide doctors a useful tool to identify COVID-19 patients at risk for long-haul lung problems and help guide them to recovery.
“We are only beginning to understand the biology of how the immune system impacts pulmonary fibrosis,” Bonham said. “My team and I were humbled and grateful to work with the outstanding patients who made this study possible.”
Findings Published
The researchers have published their findings in the scientific journal Frontiers in Immunology. The research team consisted of Grace C. Bingham, Lyndsey M. Muehling, Chaofan Li, Yong Huang, Shwu-Fan Ma, Daniel Abebayehu, Imre Noth, Jie Sun, Judith A. Woodfolk, Thomas H. Barker and Bonham. Noth disclosed that he has received personal fees from Boehringer Ingelheim, Genentech and Confo unrelated to the research project. In addition, he has a patent pending related to idiopathic pulmonary fibrosis. Bonham and all other members of the research team had no financial conflicts to disclose.
The UVA research was supported by the National Institutes of Health, grants R21 AI160334 and U01 AI125056; NIH’s National Heart, Lung and Blood Institute, grants 5K23HL143135-04 and UG3HL145266; UVA’s Engineering in Medicine Seed Fund; the UVA Global Infectious Diseases Institute’s COVID-19 Rapid Response; a UVA Robert R. Wagner Fellowship; and a Sture G. Olsson Fellowship in Engineering.
To keep up with the latest medical research news from UVA, subscribe to the Making of Medicine blog at http://makingofmedicine.virginia.edu.
After having moved from Canada to the United States, partly to be wealthier and partly to be freer (those two are connected, by the way), I was shocked,…
After having moved from Canada to the United States, partly to be wealthier and partly to be freer (those two are connected, by the way), I was shocked, in March 2020, when President Trump and most US governors imposed heavy restrictions on people’s freedom. The purpose, said Trump and his COVID-19 advisers, was to “flatten the curve”: shut down people’s mobility for two weeks so that hospitals could catch up with the expected demand from COVID patients. In her book Silent Invasion, Dr. Deborah Birx, the coordinator of the White House Coronavirus Task Force, admitted that she was scrambling during those two weeks to come up with a reason to extend the lockdowns for much longer. As she put it, “I didn’t have the numbers in front of me yet to make the case for extending it longer, but I had two weeks to get them.” In short, she chose the goal and then tried to find the data to justify the goal. This, by the way, was from someone who, along with her task force colleague Dr. Anthony Fauci, kept talking about the importance of the scientific method. By the end of April 2020, the term “flatten the curve” had all but disappeared from public discussion.
Now that we are four years past that awful time, it makes sense to look back and see whether those heavy restrictions on the lives of people of all ages made sense. I’ll save you the suspense. They didn’t. The damage to the economy was huge. Remember that “the economy” is not a term used to describe a big machine; it’s a shorthand for the trillions of interactions among hundreds of millions of people. The lockdowns and the subsequent federal spending ballooned the budget deficit and consequent federal debt. The effect on children’s learning, not just in school but outside of school, was huge. These effects will be with us for a long time. It’s not as if there wasn’t another way to go. The people who came up with the idea of lockdowns did so on the basis of abstract models that had not been tested. They ignored a model of human behavior, which I’ll call Hayekian, that is tested every day.
That wasn’t the only uncertainty. My daughter Karen lived in San Francisco and made her living teaching Pilates. San Francisco mayor London Breed shut down all the gyms, and so there went my daughter’s business. (The good news was that she quickly got online and shifted many of her clients to virtual Pilates. But that’s another story.) We tried to see her every six weeks or so, whether that meant our driving up to San Fran or her driving down to Monterey. But were we allowed to drive to see her? In that first month and a half, we simply didn’t know.
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