- Coronavirus antibodies are a hot topic, as more and more studies look at COVID-19 immunity, and how it can be achieved with the help of vaccines and other drugs.
- A team of researchers published a theory in BMG Global Health that suggests antibodies could also play a negative role in COVID-19 via an immunological mechanism known as Antibody-Dependent-Enhancement that can actually lead to severe COVID-19 cases.
- The evidence we have so far indicates that antibody-based therapies can work with COVID-19, and vaccine candidates and monoclonal antibody drugs have offered promising results.
I’ve found myself explaining more than once why the coronavirus is much worse than the flu and any other infectious disease that modern medicine can fight right now. We thought initially it’s a different version of the flu because of the way it can impersonate the flu with its unspecific symptoms, but the reality is that COVID-19 spreads faster, it can infect everyone under the right condition, and it’s a lot more difficult to shake off for patients who fit in certain at-risk categories. That’s why it kills more people than the flu as well.
Unlike other contagious pathogens, we have no specific drugs to neutralize the virus and reduce life-threatening complications. That’s something else that’s unlike the flu. We’ll have to keep washing our hands as often as possible, stay away from others for as long as possible, and wear face masks for a while. These are our only weapons against COVID-19 while we wait for drug research to be finalized. Several vaccines are approaching the final phase of testing, as are brand new monoclonal antibodies drugs. Other researchers are studying existing meds to see whether any of them can be turned into effective COVID-19 treatments. The point of most of these drugs is to help the body gain immunity to the virus and/or get rid of the infection. But a startling hypothesis tells us that the very thing some of these drugs are trying to obtain could be a risk factor for a more severe COVID-19 case upon reinfection.
Vaccines will teach the body to create the same neutralizing antibodies that COVID-19 survivors have developed while fighting the illness. Some of them will also induce a T cell response that will deliver a longer-lasting immunity, before the short life of antibodies. Monoclonal antibodies will lend the body potent antibodies that can protect against infection and neutralize the coronavirus if it’s already multiplying inside the organism. Other meds will fine-tune the immune response to prevent potentially deadly cytokine storms while allowing the immune system to develop antibodies that can prevent the virus from binding to human cells. One way or another, antibodies are critical for fighting the virus and reaching some sort of immunity.
How long will that immunity be? Many experts said we shouldn’t expect COVID-19 immunity to last longer than 12 months, which is typical of coronaviruses, not just the SARS-CoV-2 pathogen that causes COVID-19. This could mean we’ll need vaccines for the rest of our lives, to continue to help the immune system deal with the virus.
Recent research has shown that antibodies will disappear after two to three months, but that won’t be an indication that immunity is gone and reinfection is possible. The immune system can still remember the virus and recreate new batches of antibodies upon secondary contact.
This brings us to a theory from a team of doctors from several universities in Italy, Switzerland, and the UK that says antibodies can also act as catalysts that would favor a more severe course of COVID-19 upon reinfection.
Attempting to explain the course of the disease in Italy, which was the epicenter of the COVID-19 pandemic in March and April, the researchers say that the virus may have circulated for months before the start of the local epidemic. Some people may have been infected with SARS-CoV-2 or a common coronavirus and survived the cold-like illness only to face the virus again. Upon reinfection, an immunological mechanism known as Antibody-Dependent-Enhancement (ADE) could be responsible for a more severe version of the disease in some people.
“An abnormal humoral response due to ADE, in the early stages of a secondary infection by SARS-CoV-2, may delay the innate antiviral immune response relying on the production of type 1 interferon (IFN-1),” the researchers say. “This would compromise the initial antiviral response of the host, with subsequent elevated influx of proinflammatory cytokines, hyperinflammatory neutrophils and monocytes-macrophages and hypercoagulable state accountable for ARDS and typical pneumonia observed in patients affected by severe/critical COVID-19.”
That’s to say the presence of antibodies, whether they’re specific SARS-CoV-2 antibodies or antibodies coming from other coronaviruses that cause common colds, could actually be a bad thing for the immune system trying to fight an infection with SARS-CoV-2, or second reinfection.
Researchers point out that other studies have confirmed that “non-neutralizing, subneutralizing, or even fully neutralizing antibodies may play a key role in ADE,” including in the other two dangerous coronaviruses, MERS and SARS. The same goes for Dengue fever and West Nile.
The researchers note that the reason why the milder coronaviruses do not have vaccines is partly that “immunized individuals could potentially be at higher risk of ADE sustained by facilitated uptake of viral antigen-antibody complexes by target cells.” If this would apply to COVID-19, then vaccine research might not lead to any results. The promising candidates that have reached Phase 3 did not induce severe side effects according to existing reports, but it will be a while until researchers can prove or disprove whether this ADE phenomenon is of concern or not.
Again, this is just a theory. The researchers aren’t providing any evidence of ADE in COVID-19. It’s all based on what can happen in other infectious diseases. Actual research does show that plasma from COVID-19 survivors works on patients who can mount a similar immune response, therefore antibodies are effective. The researchers do make a not of this type of treatment as well. Monoclonal antibody therapy would work similarly.
Separately, other research on animals proved that COVID-19 survivors develop antibodies that can block a secondary infection. Also, it’s just too early to prove COVID-19 reinfection can occur in animals or humans. A report in The New York Times said earlier this week that it’s very unlikely you can get coronavirus twice. There have been cases of patients around the world that tested positive a second time for SARS-CoV-2 weeks or months after the first bout, but the Korean CDC provided the best answer to this puzzle. These patients aren’t infectious, as the viral RNA detected in tests is a remnant of the original infection.
The months ahead will bring us more definitive answers about treatment options, vaccines included, and immunity. If COVID-19 immunity doesn’t last longer than a year, then hospitals could soon witness the first wave of COVID-19 reinfections.
