Opinion by Harry Rakowski • Thursday - National Post
After three painful years, COVID-19, while not over, is finally a manageable, endemic disease, yet debates surrounding its origin and how it’s being managed are still highly politicized. It is therefore not surprising that there is an ongoing, politicized debate about the cause of the unusually frequent viral mutations that are now occurring and the value of ongoing bivalent boosters.
There are two important issues at play here: Why are the new bivalent boosters not performing as well as hoped in reducing the number of new infections? And is vaccination somehow driving the evolution of the virus to more easily evade antibody neutralization?
Allysia Finley, a member of the Wall Street Journal editorial board, recently wrote a column stating that, “Growing evidence … suggests that repeated vaccinations may make people more susceptible to XBB and could be fuelling the virus’s rapid evolution.” She concludes that, “The Biden administration’s monomaniacal focus on vaccines over new treatments has left the highest-risk Americans more vulnerable to new variants.”
Yet this not an accurate description of the present situation. Boosters aren’t fuelling the pandemic. They don’t cause the virus to mutate, the virus just outsmarts the antibodies produced and new mutations lead to more breakthrough infections.
There are important lessons to be learned from understanding how this virus is unique. The SARS‑CoV‑2 virus is a never-before-encountered coronavirus belonging to a large family of viruses named after the crown-like spikes on their surface.
Previous coronaviruses generally caused colds, but rarely resulted in death. Only twice before have coronaviruses caused much more serious disease, namely in the SARS outbreak of 2002 and MERS, which was identified in the Middle East in 2012.
In neither case was vaccination available, nor was rapid viral mutation a worrisome feature that might facilitate frequent reinfections or ongoing worldwide spread. To get a sense of why SARS‑CoV‑2 is different, it is helpful to understand the course of the 1918 Spanish Flu pandemic and how it ended.
The U.S. Centres for Disease Control and Prevention estimates that the 1918-19 Spanish Flu pandemic infected about one-third of the world’s population and resulted in 50-million deaths worldwide, including 675,000 in the United States. A unique feature was its high mortality rate in healthy people.
The Spanish Flu was caused by an H1N1 influenza virus. With no available vaccines, the pandemic lasted two years and finally petered out as the high number of infected people led to herd immunity. The virus simply ran out of people it could continue to infect who could then spread it further. As well, cellular immunity from previous infection protected against future bad outcomes. The virus never went away , it simply became one of the causes of the much more benign seasonal flu.
Every so often, new variants, perhaps as the result of cross-infection from animal hosts, has led to more severe, but limited, flu outbreaks. This is what happened with the H1N1 virus that caused the swine flu pandemic of 2009.
Jeffery Taubenberger, one of the scientists who studied the Spanish Flu virus, determined through genetic sequencing of preserved pathology specimens from 1918 that, “Every single human infection with Influenza A in the past 102 years is derived from the one introduction of the 1918 flu.”
While this pattern will likely also eventually happen with SARS‑CoV‑2, there are still questions over how vaccines have influenced new variants.
Allysia Finley, a member of the Wall Street Journal editorial board, recently wrote a column stating that, “Growing evidence … suggests that repeated vaccinations may make people more susceptible to XBB and could be fuelling the virus’s rapid evolution.” She concludes that, “The Biden administration’s monomaniacal focus on vaccines over new treatments has left the highest-risk Americans more vulnerable to new variants.”
Yet this not an accurate description of the present situation. Boosters aren’t fuelling the pandemic. They don’t cause the virus to mutate, the virus just outsmarts the antibodies produced and new mutations lead to more breakthrough infections.
There are important lessons to be learned from understanding how this virus is unique. The SARS‑CoV‑2 virus is a never-before-encountered coronavirus belonging to a large family of viruses named after the crown-like spikes on their surface.
Previous coronaviruses generally caused colds, but rarely resulted in death. Only twice before have coronaviruses caused much more serious disease, namely in the SARS outbreak of 2002 and MERS, which was identified in the Middle East in 2012.
In neither case was vaccination available, nor was rapid viral mutation a worrisome feature that might facilitate frequent reinfections or ongoing worldwide spread. To get a sense of why SARS‑CoV‑2 is different, it is helpful to understand the course of the 1918 Spanish Flu pandemic and how it ended.
The U.S. Centres for Disease Control and Prevention estimates that the 1918-19 Spanish Flu pandemic infected about one-third of the world’s population and resulted in 50-million deaths worldwide, including 675,000 in the United States. A unique feature was its high mortality rate in healthy people.
The Spanish Flu was caused by an H1N1 influenza virus. With no available vaccines, the pandemic lasted two years and finally petered out as the high number of infected people led to herd immunity. The virus simply ran out of people it could continue to infect who could then spread it further. As well, cellular immunity from previous infection protected against future bad outcomes. The virus never went away , it simply became one of the causes of the much more benign seasonal flu.
Every so often, new variants, perhaps as the result of cross-infection from animal hosts, has led to more severe, but limited, flu outbreaks. This is what happened with the H1N1 virus that caused the swine flu pandemic of 2009.
Jeffery Taubenberger, one of the scientists who studied the Spanish Flu virus, determined through genetic sequencing of preserved pathology specimens from 1918 that, “Every single human infection with Influenza A in the past 102 years is derived from the one introduction of the 1918 flu.”
While this pattern will likely also eventually happen with SARS‑CoV‑2, there are still questions over how vaccines have influenced new variants.
Related video: Are vaccines holding up against the new COVID variant XBB.1.5? Here's what we know. (USA TODAY) Duration 1:37 View on Watch
The mRNA vaccines produced by Moderna and Pfizer initially appeared to work well in preventing infection. The antibodies produced in response to two vaccine shots could bind to, and neutralize, invading viruses, thus reducing the chance of infection by 95 per cent, in human trials.
The story didn’t end as expected, though. Antibody levels produced by either vaccine, or in response to an infection itself, waned over a period of around six months. Then new, more contagious variants arose and spread rapidly. Yet the initial variants that fuelled new outbreaks didn’t just arise from countries with high levels of vaccination.
Influenza viruses commonly mutate and evade the benefit of annual flu shots. In a similar way, the original Wuhan strain also evolved and mutated in an attempt to infect more people. While many mutations had a neutral effect, those in the spike protein allowed easier cell entry and viral replication and thus dominated.
As new variants of concern developed, they were assigned Greek letters. The first variant of concern, the Alpha variant, which originated in England, was associated with more infections, even in vaccinated people, but memory cell-based immunity continued to protect against hospitalization and death.
Then the Delta variant, which originated in India before many people there were vaccinated, quickly became dominant. It was both more contagious and more deadly. During this phase of the pandemic, Delta became COVID on steroids and a disease of the unvaccinated. The response was to give booster shots of the original vaccine to bump up antibody levels. Yet as the virus continued to mutate, booster protection from infection again fell dramatically.
In the fall of 2021, the Omicron variant, which was first detected in South Africa, a country with low vaccination rates, became dominant, since it was the most contagious variant yet. This led to most people in North America becoming infected, or re-infected, regardless of vaccination status. The response was to produce Omicron-specific boosters, initially targeting the BA.1 Omicron variant, then the BA.4/5 variants that arose.
The hope was that these boosters would produce antibodies both for the original viral strain and the rapidly mutating Omicron variants and would thus provide significant protection from infection. Unfortunately, the ability of the boosters to prevent human infection proved to be dramatically lower than with previous strains. The benefit became even smaller as newer Omicron variants sprung up, especially now with the dominating XBB.1.5 mutation.
The reason for the continuing decline in bivalent boosters limiting infection is likely due to “immune imprinting,” the idea that the immune response to either previous infection or to receiving a vaccine limits an individual’s future response to new variants. The immune system thus prefers to recall existing memory cells rather than produce new responses when the old and new variants are closely related. We produce antibodies that fight the older strains more effectively than the evolving ones that now dominate.
Thus, new strains that develop will continue to rapidly evade the antibodies produced by repeated vaccinations and we will continue to get diminishing returns. The more we try and prevent new infections with more and more booster shots, the less effective they will likely become in preventing infections themselves.
What is critically important, however, is that vaccination continues to greatly decrease the risk of hospitalization or death, despite the rise of ever-mutating new Omicron sub-variants. Despite what Finley suggests, viral mutations happen naturally and are not directly caused by vaccines.
The XBB family of mutations likely originated when two forms of the virus combined in an individual to form a new strain. This new strain started to dominate because it was more immune-evasive. Vaccination is unlikely to have played a major role in this process, as evasion from immunity can come from both the declining benefits of vaccination and natural infection.
We can’t panic when the press hypes every new variant. While they cause more infections, only a small percentage of people have bad outcomes. In healthy people who have been infected in the past, or previously vaccinated, most will now only develop cold- or flu-like symptoms.
We have to now accept that ongoing vaccination will have limited benefit in preventing infection from ever-mutating viruses and hope that they continue to provide protection against bad outcomes. Hopefully, the lesson from the end of the Spanish Flu is that this virus will eventually become little more dangerous than a common cold or a typical flu. Ongoing vaccination for those older people or those at higher risk is reasonable. Ongoing vaccination for younger, healthier people is of limited value.
We need to focus on improving the capacity and resilience of our health-care system, rapidly develop new antiviral therapies to protect the vulnerable once infected and take the fear and politics out of the process.
National Post
Dr. Harry Rakowski is an academic Toronto cardiologist and commentator.
The XBB family of mutations likely originated when two forms of the virus combined in an individual to form a new strain. This new strain started to dominate because it was more immune-evasive. Vaccination is unlikely to have played a major role in this process, as evasion from immunity can come from both the declining benefits of vaccination and natural infection.
We can’t panic when the press hypes every new variant. While they cause more infections, only a small percentage of people have bad outcomes. In healthy people who have been infected in the past, or previously vaccinated, most will now only develop cold- or flu-like symptoms.
We have to now accept that ongoing vaccination will have limited benefit in preventing infection from ever-mutating viruses and hope that they continue to provide protection against bad outcomes. Hopefully, the lesson from the end of the Spanish Flu is that this virus will eventually become little more dangerous than a common cold or a typical flu. Ongoing vaccination for those older people or those at higher risk is reasonable. Ongoing vaccination for younger, healthier people is of limited value.
We need to focus on improving the capacity and resilience of our health-care system, rapidly develop new antiviral therapies to protect the vulnerable once infected and take the fear and politics out of the process.
National Post
Dr. Harry Rakowski is an academic Toronto cardiologist and commentator.
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