The pandemic has been here for almost 2 years, and scientists are still trying to understand the long term effects of the viral infection with COVID-19 while also working on more effective vaccines and medication.
After all, the virus has killed over 5 million people and infected around 256 million worldwide and many of those who healed are still struggling with so-called “long COVID.”
Furthermore, the vaccines have been helping with keeping the pandemic under control but researchers are still learning how they work and how well.
This is the case especially with new variants emerging but also with some more serious, but rare side effects of the vaccine such as heart inflammation, allergic reactions and blood clotting.
As mentioned before, long COVID poses a lot of questions as well for the experts.
About one in four patients experience long haul symptoms even after healing from COVID-19.
Based on some new research, it appears that both long COVID and some side effects of the vaccines are caused by one’s immune system response.
More precisely, in an article published in The New England Journal of Medicine earlier this month, Professor of Medicine from Harvard Medical School, Dan Longo, and the UC Davis Vice Chair of Research and Professor of Dermatology and Internal Medicine, William Murphy, state that a possible explanation to the many immune responses to the vaccines and to COVID itself can be antibodies mimicking the virus!
The two experts draw on some classic immunological concepts and conclude that the Network Hypothesis by Nobel Laureate Niels Jerne offers some useful insight into the phenomenon.
Niels Jerne’s theory is that the immune system looks for a way to regulate antibodies.
Therefore, it initially launches a protective antibody response to an antigen which can then trigger another antibody response towards themselves later on, causing them to disappear as time goes on.
These antibodies are known as anti-idiotype antibodies and can grab onto and deplete the original antibody responses meant to protect you from the virus.
Not only that but they are also able to act just like the initial antigen, mirroring it perfectly and sometimes causing adverse effects.
Whenever the virus that causes COVID-19, SARS-CoV-2, enters the body, its spike protein grabs onto the ACE2 receptor and is able to enter the cell.
The immune system’s response is by creating antibodies that grab onto the virus, neutralizing its effects.
Furthermore, just as a means of down-regulation, these antibodies may also cause immune responses with anti-idiotype antibodies and as time goes on, they can get rid of the original antibodies, resulting in some limited efficacy of therapies that utilize antibody-based methods to combat the infection.
Murphy explains that “A fascinating aspect of these newly formed anti-idiotype antibodies is that some of their structures can also be a mirror image of the initial antigen and they can act like it in binding to the same receptors the viral antigen binds. This binding can then lead to unwanted actions and pathology, particularly in the long term.”
The research’s authors also think that the anti-idiotype antibodies might even target the same ACE2 receptors and affect some of their functions by triggering or blocking these receptors.
Murphy goes on to say that “Given the critical functions and the wide distribution of ACE2 receptors in numerous cell types, it would be important to determine if the regulatory immune responses could potentially be responsible for some of the long-lasting or off target effects being reported. These responses could also explain why such long-term effects occur long after the viral infection has passed.”
When it comes to the available vaccines, the main antigen used is the spike protein SARS-CoV-2 features.
Longo and Murphy suggest that new studies on antibody responses to the vaccines mostly focus on just the initial protective responses as well as on virus neutralizing efficacy, but not so much on different long term effects.
Murphy comments that “With the incredible impact of the pandemic and with our reliance on vaccines as our primary weapon, there’s an immense need for some more basic research to understand the complex immunological pathways that are at play. This need follows to what it takes to keep the protective responses going, and to the potential unwanted side effects of the infection and the different SARS-CoV-2 vaccines, especially as boosting is applied now. The good news is that they are all testable questions that can be addressed partially in the lab, and in fact, have been used with other viral models.”
