While coronavirus spreads across the globe, a major question has emerged: Are people immune after recovering from an infection? This topic is important for understanding who can safely return to work, and for understanding how long the pandemic’s worst effects are expected to last. The response is not completely known, since the virus is so new. Yet it looks like SARS-CoV-2 potentially induces immunity like other coronaviruses so far, scientists suggest.
“We do not have any reason to assume that the immune response would be significantly different” from what’s seen with other coronaviruses, said Nicolas Vabret, an assistant professor of medicine at the Mount Sinai Icahn School of Medicine who specializes in virology and immunology.
However, so far research on SARS-CoV-2 has shown that in some people the immune response to the virus also contributes to the devastating effects of the disease.
The immune response to coronavirus
Benjamin tenOever, a biology professor at the Mount Sinai Icahn School of Medicine, said that when a virus infects its first cell in the body, that cell has two jobs to do before it dies. The infected cell must issue a call for reinforcements, sending out a cascade of chemical signals to activate an army of immune cells to fight the foreign invaders. When interferons land on neighboring cells, those cells are activated into defensive mode. When interferons land on neighboring cells, those cells are activated into defensive mode.
The cells slow down their metabolism, interrupt transportation of proteins and other molecules around their interiors, and slow down transcription, which is the method by which genetic instructions become proteins and other molecules. (Transcription is the method hijacked by viruses to make more of themselves.)
TenOever and his colleagues found in a study approved by the journal Cell that SARS-CoV-2 appears to block this interferon signal, indicating that it is interfering with the second job of the cell. So the first job— the call for immune system reinforcement— works well, but the cells in the lungs don’t really enter defensive mode and therefore remain vulnerable to viral infection.
“It just keeps replicating in your lungs, and replicating in your lungs and all the while you keep calling in for more reinforcements,” tenOever told Live Science.
Even this compromised immune response is enough in many individuals to fight back the virus. But some individuals enter a vicious cycle for reasons which are not yet completely understood.
While the virus continues to spread, the immune army that comes to fight it begins doing its job: destroying infected cells, digesting debris and chemicals spewed out by dying cells, even killing surrounding cells in an effort to staunch the damage.
Sadly this army will do more harm than good if the virus continues to enter lung cells. The lung tissue becomes hopelessly inflamed; the blood vessels start leaking fluids into the lung; and the patient begins drowning on dry land. That seems to be the reason why some people get severely ill a few weeks after their initial infections, tenOever said.
“At that point, it’s not about what the virus has done,” he said. “At that point, it’s about controlling the severe inflammation.”
This cycle represents really bad news. But the findings do provide a glimmer of hope. Since the system that calls in the army of immune cells works just fine, COVID-19 survivors will retain immunity to the virus. Moreover, research in newly recovered patients has found high levels of antibodies to SARS-CoV-2. Antibodies are proteins formed by immune system cells, and they’re called B cells.
The B cells stick around in the blood post-infection and can connect to the virus, either directly or marking it with other immune cells for destruction. For example, the blood of 14 COVID-19 patients who had experienced relatively mild COVID-19 symptoms was examined 14 days after hospital discharge in a study led by researcher Chen Dong of the Institute for Immunology and the School of Medicine at Tsinghua University, Beijing.
They found that 13 of them showed high levels of SARS-CoV-2 antibodies which suggested immune protection from immediate reinfection. The results were accepted for publication in the journal Immunity. These findings coincide with results from other recovered patient studies and are the main reason why scientists are not worried about occasional reports of people recovering from COVID-19, testing negative for the virus through a nasal swab PCR test that detects the viral genome, and then testing positive again in a few weeks ‘ time.
These individuals are not being reinfected, said tenOever. Their antibody levels are high, and they are protected against further attacks by their immune system. The PCR tests actually pick up pieces of inert viral genetic debris leftover from the previous infection, instead.
How long will COVID-19 immunity last?
The SARS-CoV-2 has only been circulating in human hosts for five to six months, indicating that there is absolutely no way to tell whether immunity to the disease lasts longer than that.
“Per our findings, we can only confirm that COVID-19 patients can maintain the adaptive immunity to SARS-CoV-2 for 2 weeks post-discharge,” Tsinghua’s Dong said.
Evidence from other coronaviruses indicates immunity is likely to last longer, Vabret said. Together with Mount Sinai colleagues Robert Samstein and Miriam Merad, Vibrat led more than two dozen doctoral students and postdoctoral researchers to study the avalanche of immunology work on coronavirus in newspapers and on preprint repositories hosting scientific papers prior to peer review.
Studies of the proteins and genetics of SARS-CoV-2 show that the virus is likely to cause a long-term immune response close to that of other coronaviruses, like SARS 1 from 2002, or Middle Easter Respiratory Syndrome (MERS), which appeared in 2012. Research on SARS 1 and MERS indicates that for at least two or three years some level of antibody immunity remains, starting strong and slowly diminishing as time goes by, Samstein explained.
In response to coronavirus infection, the immune system often produces a type of immune cell, called virus-specific T cells. Compared with antibodies, less is known about T cells, Vabret and Samstein said, since they’re more difficult to identify in the blood and study. Yet other coronaviruses tend to cause their production and in some cases, these T cells seem to live for years.
None of the SARS 1 studies published in the Vaccine journal revealed that these T-cells last up to 11 years after infection. Overall, researchers are still unsure as to what level of long-term immune memory is sufficient to protect against potential infection with coronavirus, and how long it takes for the immune system to fall below that.
If someone with immunity could transmit the coronavirus to others while fighting off a second infection is not clear yet, Vabret and Samstein said. If the immune response were powerful enough to quickly kill the virus, they said the individual would probably not be transmitting it any further.
However, a weaker response that enabled some viral replication might not prevent transmission, particularly because people with no symptoms are known to pass the coronavirus around.
“We’re taking lessons from the older viruses, but we don’t know how much for sure how much is similar,” Samstein said.
Nevertheless, this confusion does not reduce vaccine expectations. One benefit of vaccines is that scientists can mimic the viral proteins that cause the most powerful immune response. Therefore, vaccination can also induce immunity which lasts longer than getting ill.
“You can aim at inducing protection that would be better than what you would get from an infection,” Vabret said.
