A news analysis
More than a year into the SARS-CoV-2 pandemic, doctors in England finally took the bold step of intentionally exposing 36 young and healthy volunteers to the virus in what is called a “challenge study” to monitor how the disease develops.
- Just less than half of their group of 18 to 29 years olds had a high natural resistance to the virus and never developed Covid-19, the disease caused by the SARS-CoV-2. This was not a huge surprise. When passengers aboard the cruise ship Diamond Princess were locked up with the virus for more than a week in early 2020, much the same thing happened, and a similar situation that developed aboard the aircraft carrier USS Theodore Roosevelt infected only about a quarter of the crew of 4,085 in close proximity to the virus for three weeks.
- None of those who caught the disease – all of them blessed with being healthy at the start and still young – encountered any “serious adverse events.” “Symptoms were present in 89 percent of infected individuals but, despite high viral loads (those) were consistently mild to moderate, transient and predominantly confined to the upper respiratory tract.” This was not a surprise either. Globally the number of deaths of people under 30 from Covid-19 is tiny. From an ecological standpoint, Covid-19 might be considered to have been kind to humans in following a path that mimics the mythical idea that nature in its untampered state only kills the weak and old. The reality is nature mainly kills the young, but that’s a whole other story.
- Only 37 percent of the SARS-CoV-2 infected developed a noticeable fever, an indication all the fever checking to spot Covid-19 infections might not have been very effective.
- Viral load – the amount of the virus with which individuals were infected – did not alter the nature of the illness. People with high viral loads displayed the same symptoms as those with low viral lands.
- The viral loads of the asymptomatic participants in the study, the people who were infected but never got sick – were as high as in those who got sick. But only two people in the small group ended up asymptomatic. That put this study’s number way out of sync with estimates that have suggested that up to 50 percent of people who get Covid-19 could remain asymptomatic, but one can possibly blame the small sample size for this difference.
- “Viral shedding,” the attempt by the infected to rid themselves of the virus which thus puts more virus in the air to infect others, began “within two days of exposure, rapidly reaching high levels with viable virus detectable up to 12 days after inoculation and significantly higher viral loads in the nose than the throat despite its later onset” in the nose. There is quite a bit there that differs from what everyone believed before. So much so that it will be discussed further down in the story.
- Viral replication with Covid-19 starts in the throat, but quickly spreads to the nose from which much of the resulting viral shedding follows with “viral loads…significantly higher in nasal samples.” Now think about all those people walking around with their noses poking out around their maks blowing virus everywhere. This is a troubling vision if you’re a masking believer. Not so troubling if you are of the opinion the whole masking exercise was largely about social signaling.
- Viral shedding from Covid-1`9 seriously declines within 10 days, but people remain viral carriers for two weeks or longer. “At day 28…six of 18 participants (33 percent) remained qPCR positive – ie. still infected according to the results of a quantitative polymerase chain reaction (qPCR) test – in the nose and two of 18 (11 percent) in the throat.”
- Humans gear up their natural defenses as soon as Covid-19 takes hold. All of those who came down sick displayed antibody responses indicating their natural immune systems were battling the disease. But again, the sample size was small and involved fundamentally healthy people, thus no conclusions can be drawn as regards those who might be immune-compromised in any way.
- Remdesivir, a broad-spectrum anti-viral drug thought to offer some protection against SARS-CoV-2 infection, did nothing for nobody. Other studies have indicated it might help lessen the symptoms of Covid-19.
- Viral loads, in this study, did not sync with reported symptoms and there was “no difference in symptoms between remdesivir-treated and untreated participants.” The difference between viral loads and reported symptoms does, however, make it hard to develop an objective conclusion on remdesivir. For Covid-19 as with so many other diseases, part of how we feel lives in our bodies and part in our heads.
- And lastly, there was no evidence of pulmonary disease in infected participants based on clinical and radiological assessments.”
Cue the debates
Other studies have linked pulmonary diseases to both Covid-19 and some of the vaccines against Covid-19 with the consensus at this time being that infection poses a greater risk of heart problems than the vaccines.
This study raises the question of whether either should be of much concern to those under the age of 30.
The English authors of the study noted the liabilities of their small sample size, but argued their challenge study added some very important information to the discussion of SARS-CoV-2 and Covid-19.
One could probably start with the nasal spread of the virus which red flags all those who were running around with their noses hanging out of their face coverings when face coverings were mandated, and could possibly generate some new discussion on the danger of fomites, the microscopic particles that can carry a virus from, say, a speck of dust on that mask under someone’s nose to the hand that adjusts the mask and from there to a countertop, door handle or who knows what.
Fomites were an early concern during the pandemic, and thus the early advice to wash your hands, wash your hands, wash your hands. They were later discounted in the belief that airborne spread through human spittle, ie. those often unseen droplets of moisture that spew from our mouths when we talk or sing, was the major form of transmission.
That has finally now given way to the acceptance that most transmission is from aerosols, the tiniest particles of dust and moisture we emit when we breathe. Government officials in the U.S. were painfully slow to accept this idea, despite the early data on the unusually high infections rates among people habitually visiting bars and restaurants.
Bars have historically been smoke-filled spaces due to bad ventilation, all of which is why smokers were kicked to the curb years ago. This should have been a red flag for scientists, but many were so focused on fancy photos showing how much normally unseen spittle emerges from our mouths when we talk that they refused to recognize this and focused on droplets, which can be disrupted by face coverings.
The new data on nasal emissions should now underline the need to fix the ventilation in buildings to prevent the build-up of SARS-CoV-2, and other viruses, in indoor environments.
Or everyone could go on wearing masks forever and argue over their effectiveness.
The science of the mask still isn’t settled, and as with so many things in the U.S. today, that has left room for a debate between the believers and the non-believers over whether masks work, how much they work if they do, and which styles are more about social signaling than actually doing anything to control the spread of SARS-CoV-2.
No matter what one believes there, this study does make clear that if masking is going to be mandated some standards need to be established for how people wear masks.
As the authors put it, “with virus present at significantly higher titers in the nose than the throat, these data provide clear evidence that emphasizes the critical importance of wearing face coverings over the nose as well as the mouth.”
You’re going to catch it
Mainly, though, what the study does is underline the efficiency with which SARS-CoV-2 moves among us, and thus reinforces the growing reality that as with the common cold and the flu almost everyone is likely to become infected at some time.
“Our data clearly show that SARS-CoV-2 viral shedding occurs at high levels irrespective of symptom severity,” they wrote, “thus explaining the high transmissibility of this infection and emphasizing that symptom severity cannot be considered a surrogate for transmission risk in this disease.”
You could catch the disease from someone who is infected with SARS-CoV-2, but will never know it. Or someone who has Covid-19 now, but won’t have a clue as to that fact until the day after tomorrow. Or maybe even from someone who had it and felt fully recovered but continued shedding virus.
The researchers probably best exposed their thoughts as to how widespread Covid-19 is likely to become in observing how useful it would be to conduct further studies “with larger numbers of participants for sufficient power to identify biomarkers that have less marked differential expression and/or are more inconsistent than viral load and symptoms. However, although globally there are groups that remain naive to SARS-CoV-2 vaccination and infection, it is unlikely that a larger study in seronegative volunteers (ie. never infected people) will be achievable going forward, and this study may, therefore, remain the only one of its kind.”
That said, they strongly argued for continuing experiments with human volunteers, a somewhat touchy ethical issue given that it raises concerns about taking advantage of the poor. The “volunteers” in this study were paid or “given a donation,” as the study calls it, “of up to £4,565 (about $6,000) to compensate for the time and inconvenience of taking part in the study, including at least a 17-day quarantine). This was calculated using the National Institute for Health Research formula and the UK national living wage.”
The mean age of participants was 22. Six-thousand dollars is not a lot of money, but it is probably enough to tempt an out-of-work 22-year-old to invest a month in participation in a study with limited risks.
Then again, the risks of serious Covid-19 in young people are very, very low despite U.S. mainstream media efforts to hype the idea that the disease is an equal opportunity killer. It’s not.
The latest data from the U.S. Centers for Disease Control (CDC) reports deaths among those age 50 or older are more than 100 times greater than deaths among those under age 30. An even clearer picture of the situation might come from looking at deaths among those over age 85.
These people comprise but 2 percent of the U.S. population. Americans under the age of 30 out number them by nearly 20 to 1, but when it comes to Covid-19 those age 85 and over die at 30 times the rate of those under 30. Nationwide, there have been 7,244 deaths among all of those under age 30 since the pandemic began in early 2020, and there have been 216,722 deaths among those over age 85.
The annualized mortality for Covid-19 among those under age 30 now stands at about 3,600 per year. As a cause of death, this ranks Covid-19 far behind the “unintentional injuries,” many of them preventable, that killed 15,864 Americans under the age of 24 in 2018, according to CDC data; and suicides, which killed nearly 7,000 under 24.
It also ranks Covid-19 behind “congenital anomalies,” which claimed the lives of 4,473 babies in 2018, premature births that resulted in the death of 3,679 babies that year, and homicides which resulted in the deaths of 5,249 under age 24 in 2018.
Homicides that year accounted for 4,607 deaths in the 15-24 age group alone. In America’s inner cities, murder among young blacks is the killing equivalent of Covid-19 among the nation’s aged.
“Thirty-seven percent of gun homicide victims were black males between the ages of 15 and 34 although they made up only 2 percent of the U.S. population,” according to a report from the Educational Fund to Stop Gun Violence. “Their gun homicide rate was more than 20 times higher than white males of the same age group.”
The best protection against that pandemic is to get out of the inner city, but for many young blacks that is not a realistic option just as for many older Americans, the best protection against SARS-CoV-2 – being healthy, fit and under age 30 – is not an option.
The good news is that vaccines have made more progress against Covid-19 than anything has made against inner-city violence but people continue to die from both. Comfortably well-off Americans should feel lucky that what threatens them has received a lot more attention than what threatens young blacks.
The English researchers now argue that given their first challenge study didn’t seriously harm any of it participants, there should be “further development and expansion of this approach. This first report focuses on safety, tolerability and virological responses, but the uniquely controlled nature of the model will also enable robust identification of host factors present at the time of inoculation and associated with protection in those participants who resisted infection.
“Analysis of local and systemic immune markers (including potentially cross-reactive antibodies, T cells and soluble mediators) from this SARS-CoV-2 human challenge study that may explain these differences in susceptibility is, therefore, ongoing. In addition, with the feasibility of this approach having been demonstrated using a prototypic wild-type strain, further challenge studies are now underway in which previously infected and vaccinated volunteers will be challenged with escalating inoculum doses (ClinicalTrials.gov identifier NCT04864548) and/or viral variants to investigate the interplay between virus and host factors that influence clinical outcome.
“Together, these studies will, thus, optimize the platform for potential use in the rapid evaluation of vaccines, antivirals and diagnostics by generating efficacy data early during clinical development and avoiding the uncertainties of studies that require ongoing community transmission.”