What we know and don’t know about COVID-19 rebirth cases

As President Trump claims he is immune to COVID-19, and isolated reports emerge as reintegration, what is the truth about immunity to COVID-19?

To date, there have been six published cases of COVID-19 reinfection, along with various other unverified accounts worldwide. However this is a relatively small fraction of the millions who are known whether we should be concerned? To unpick this puzzle, we must first consider what we mean by immunity.

How does immunity work

When we are infected with any pathogen, our immune system responds quickly to try to prevent danger and minimize any damage. Our first line of defense is from immune cells, known as innate cells. These cells are usually not enough to eliminate a threat, which comes into play where there is a more flexible “adaptive” immune response – our lymphocytes.

Lymphocytes come in two main varieties: B lymphocytes, which make antibodies, and T lymphocytes, which include cells that directly kill germ invaders.

As antibodies are easily measured in blood, they are often used to indicate a good adaptive immune response. However, over time, the antibody levels in our blood levels decrease, but this does not mean that protection is lost. We retain some lymphocytes that know how to deal with danger – our memory cells. Memory cells live remarkably long, patrolling our bodies, ready to spring into action when needed.

Vaccines work by creating memory cells without the risk of potentially fatal infections. In an ideal world, building immunity would be relatively easy, but it is not always straightforward.

Although our immune system has evolved to deal with a large variety of pathogens, these germs have also evolved to hide from the immune system. This arms race means that some pathogens such as malaria or HIV are very difficult to deal with.

Infections from animals — zoonotic diseases — are also challenging for our immune system because they can be completely novel. The virus that causes COVID-19 is a disease that occurs in bats.

COVID-19 is caused by a betacoronavirus. Many betacoronaviruses are already common in human populations – most familiar as the cause of the common cold. Immunity to these cold-causing viruses is not so severe, but immunity is more durable for more severe conditions, mers and sars.

Data to date on COVID-19 suggest that antibodies can be detected up to three months after infection, although, as with Sir and Mers, antibodies gradually decrease over time. .

Of course, antibody levels are not just signs of immunity and do not tell us about T lymphocytes or our memory cells. The virus causing COVID-19 is structurally similar to Sir, so perhaps we can be more optimistic about a more durable protective response – time will tell. Then how worried should we be about the reports of revision with COVID-19?

How worried should we be?

The handful of cases reported on recombination with COVID-19 are not necessarily immune. Testing issues may account for some reports as “viruses” can be detected after infection and recovery. The tests look for viral RNA (the genetic material of the virus), and viral RNAs that cannot cause infection can be shed from the body even after the person is recovered.

Conversely, false-negative results occur when insufficient viral content is detected in the sample used in the test – for example, because the virus is at a very low level in the body. Such obvious negative consequences may occur for cases in which the interval between the first and second infections is short. It is extremely important, therefore, to use additional measures such as viral sequencing and immune indicators.

Regeneration can also occur in immunity, but it will usually be mild or asymptomatic because the immune response protects against the worst effects. Consistent with this is that most verified cases of reinfection have either no or mild symptoms. However, one of the latest verified cases of reinfection – which occurred exactly 48 days after the initial infection – actually had a more severe reaction to reinfection.

What could be the second time round for worse symptoms? One possibility is that the patient did not first mount a strong adaptive immune response and that their initial infection was largely implied by the innate immune response (first line of defense). One way to monitor this would be to assess the response of the antibody because the type of antibody detected can tell us something about the time of infection. But unfortunately, the antibody results in the patient’s first infection were not analyzed until recently.

Another interpretation is that various viral strains caused infections with subsequent effects on immunity. Genetic sequencing showed differences in viral strains, but it is not known whether this is equivalent to altered immune detection. Many viruses share structural characteristics, enabling an immune response to a virus to protect against a similar virus. It has been suggested to take into account the lack of symptoms in children who often suffer from colds due to Betacoronavirus.

However, a recent study, as yet peer-reviewed, found that protection against coronavirus due to cold did not protect against COVID-19. In fact, antibodies recognizing similar viruses can be dangerous – accounting for the rare occurrence of antibody-dependent growth (ADE) of the disease. ADE occurs when antibodies increase viral infection of cells with potentially life-threatening consequences.

However, it should be emphasized that antibodies are only one indicator of immunity and in these cases we have no data of T lymphocytes or memory cells. Emphasizing these matters, robust evaluation of the reinforcement threat requires a standardized approach to capture key information.

We are still learning about the immune response to COVID-19, and every piece of new data is helping us unpick the puzzle of this challenging virus. Our immune system is a powerful ally in the fight against infection, and only by unlocking it can we hope to eventually defeat COVID-19.

Sheena Cruikshank, Professor at Biomedical Sciences, University of Manchester.

This article was originally published by Conversation. Read the original article.