Our immune systems can cope with COVID-19; it’s our politicians who can’t Our immune systems can cope with COVID-19; it’s our politicians who can’t
November 20, 2020
The psychological impact of the virus is profound, but there is nothing to suggest its physical effects can’t be overcome, writes ANGELA RASMUSSEN*
A great deal of conflicting information has emerged about the immune response that develops in patients who have recovered from COVID-19.
A recent study in the UK showed declining antibodies in more than 350,000 people, leading to headlines that immunity wanes rapidly just months after infection.
The next day, another study concluded the opposite: in more than 30,000 patients in New York City, the majority showed high levels of IgG antibodies, which are the type of antibodies that typically neutralise Sars-Cov-2, the virus that causes COVID-19.
Naturally this is very confusing. Is Sars-Cov-2 a superpowered virus that can subvert the immune systems that protect us so effectively against many other pathogens? Can people who have recovered from COVID-19 expect to have long-lasting protective immunity or not?
The good news is that we are unlikely to be reinfected with Sars-Cov-2 repeatedly until it eventually wipes us all out. Most of the evidence in both COVID-19 patients and animal models shows that the immune response to this is quite typical for an acute viral infection.
Initially, the body ramps up high levels of IgG antibodies, but after the infection is cleared, those antibodies drop to a baseline level, which may be below the limit of detection of some serological tests.
Antibodies are produced by B-cells, a specialised type of immune cell that recognises a specific antigen, or viral target. When an infection is cleared, B-cells producing antibodies convert from being plasma cells, which are specialised to pump out massive quantities of Sars-Cov-2-specific antibodies, to being memory B-cells. These cells produce lower levels of IgG antibody; but, importantly they persist in the body for years. If they are re-exposed to Sars-Cov-2, they rapidly convert to plasma cells and begin producing high levels of antibody again.
There is no indication that most COVID-19 patients are not developing immune memory, and animals experimentally infected with Sars-Cov-2 are protected against rechallenge with high doses of virus. Most people who recover from COVID-19 have detectable neutralising antibodies months after infection.
This suggests that Sars-Cov-2 infection does produce an immune response that is protective, at least for several months. To determine how long this protection lasts, unfortunately, we have no choice but to wait. Sars-Cov-2 has been circulating in the human population for less than a year, and there is no way to study immune durability other than to wait and see.
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Furthermore, antibodies are not the only important part of the immune system. T-cells are also a key component to the immune response. They come in two flavours: helper T-cells, which coordinate immune responses and facilitate immunological memory, and killer T-cells, which kill infected cells. Previous studieshttps://6e9a26471aa5a043cd0b77803a30981a.safeframe.googlesyndication.com/safeframe/1-0-38/html/container.htmlhave shown that Sars-Cov-2 infection induces robust T-cell responses.
Interestingly, some people who have never had Covid-19 have memory T-cells from prior common-cold coronavirus infections that cross-react with Sars-Cov-2, suggesting that there may be some existing protection in the population . It’s important to note that the role of T-cells in protecting against Sars-Cov-2 is largely unknown and this is an active area of research. T-cells alone are unlikely to provide complete immune protection, but they are a key contributor to immune memory, and illustrate that antibody levels alone do not tell the full story of protective immunity.
The responses of these cells further underscore that Sars-Cov-2 is not an anomalous virus capable of miraculous feats of immune evasion. Sars-Cov-2 can certainly suppress some antiviral responses, which is probably how it causes severe COVID-19 in some people, but it is not invulnerable to our immune defences.
While there have been some reported cases of reinfection, there is currently no evidence that this is common. It is also possible that reinfection in people with partial immunity may result in milder disease, although that is still an untested hypothesis. There needs to be more research into reinfection to understand how common it is, but we should not regard it as evidence that immunity is useless and there is no hope for preventing Sars-Cov-2 in the future.
On the contrary, there are promising findings in animal studies and clinical trials that candidate vaccines elicit antibody levels equivalent to recovering patients with the highest levels of antibodies and these antibodies endure. This is true of the Pfizer vaccine that was recently announced to be protective against symptomatic COVID-19 cases after an interim analysis of the phase three trial data. This suggests that vaccines may provide more potent, durable protection than natural infection.
Our search for functional immunity to Sars-Cov-2 is less a biological quandary than a psychological one. To explain the widespread transmission and death, the chronic debilitating illness that has resulted in many COVID-19 patients who have cleared the infection but not recovered from the disease, and the severe disruption to our everyday lives, it is tempting to think that the virus is a singular pathogen the likes of which we have not seen before.
In reality, it is our inadequate policies and lack of evidence-based public health strategy that has gotten us to where we are today in the US, the UK and most of the rest of Europe. Our immune systems are mostly responding to this virus the way we’d expect; it is our leadership whose responses have failed. (Guardian UK)
*Angela Rasmussen is a virologist and affiliate of the Georgetown Center for Global Health Science and Security
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