COVID-19 immunity 'declines sharply' a month after hospital discharge

COVID-19 immunity 'declines sharply' a month after hospital discharge

Researchers say their study provides information helpful for developing effective treatments and a preventive vaccine.

Published: September 11, 2020 at 9:22 am

The antibody response in patients who have recovered from coronavirus is not typically strong, and declines sharply one month after hospital discharge, a new study suggests.

A better understanding of antibody responses against SARS-CoV-2, the virus that causes COVID-19, will provide fundamental information for developing effective treatments and a preventive coronavirus vaccine, experts say.

In the study, researchers monitored SARS-CoV-2-specific antibody responses in 19 non-severe and 7 severe COVID-19 patients for seven weeks from disease onset. They found that most patients generated antibody responses against SARS-CoV-2.

According to the study published in PLOS Pathogens, although 80.7 per cent of recovered COVID-19 patients had varying levels of antibody neutralisation activity against SARS-CoV-2, only a small portion elicited a potent level of neutralisation activity.

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Researchers say this highlights the importance of carefully selecting blood samples from recovered patients using antibody neutralisation assays prior to transfusion into other COVID-19 patients.

The study indicates that three to four weeks after hospital discharge, the neutralising activity of antibodies from recovered patients declined significantly.

The authors from Nanjing University Medical School in China say: “The world is facing an unprecedented challenge with communities and economies affected by the growing pandemic of [COVID-19].”

The authors add: “The development of antibody response to SARS-CoV-2, the virus that causes COVID-19, started to be reported but remained largely elusive.

“Understanding the adaptive responses where the body makes antibodies that specifically bind to the SARS-CoV-2 among COVID-19 patients provides fundamental information for developing [an] effective treatment and preventive vaccine.”

Once again, evidence shows that the half-life of these antibodies in the blood is not particularly sustained

Professor Danny Altman

Danny Altmann, professor of immunology at Imperial College London, and British Society for Immunology spokesperson, said: “After the initial publications about SARS-CoV-2 antibody assays and levels, important papers are starting to emerge which look at specificity and durability of the response in more detail.

“Studies like this are a vital part of the ‘work-in-progress’ to make sense of who has immunity and how long for.

“This paper makes a number of points: the gold-standard in assessing the antibody response to a virus is measuring ability to neutralise the entry of virus into cells, although this is not one of the routinely available tests.

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He added: “Most convalescent patients show this response, though, importantly, 20 per cent do not. Also, this antibody level declines in most people by the time of their follow-up appointment a month later.

“Once again, evidence shows that the half-life of these antibodies in the blood is not particularly sustained.

“We don’t know to what extent this is bad news unless we know the extent to which the white blood cells that make the antibody (B cells) are up and ready to defend against any repeat attack.”

How do scientists develop vaccines for new viruses?

Vaccines work by fooling our bodies into thinking that we’ve been infected by a virus. Our body mounts an immune response, and builds a memory of that virus which will enable us to fight it in the future.

Viruses and the immune system interact in complex ways, so there are many different approaches to developing an effective vaccine. The two most common types are inactivated vaccines (which use harmless viruses that have been ‘killed’, but which still activate the immune system), and attenuated vaccines (which use live viruses that have been modified so that they trigger an immune response without causing us harm).

A more recent development is recombinant vaccines, which involve genetically engineering a less harmful virus so that it includes a small part of the target virus. Our body launches an immune response to the carrier virus, but also to the target virus.

Over the past few years, this approach has been used to develop a vaccine (called rVSV-ZEBOV) against the Ebola virus. It consists of a vesicular stomatitis animal virus (which causes flu-like symptoms in humans), engineered to have an outer protein of the Zaire strain of Ebola.

Vaccines go through a huge amount of testing to check that they are safe and effective, whether there are any side effects, and what dosage levels are suitable. It usually takes years before a vaccine is commercially available.

Sometimes this is too long, and the new Ebola vaccine is being administered under ‘compassionate use’ terms: it has yet to complete all its formal testing and paperwork, but has been shown to be safe and effective. Something similar may be possible if one of the many groups around the world working on a vaccine for the new strain of coronavirus (SARS-CoV-2) is successful.

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