The rare reports of reinfection to date have not been accompanied by virus sequencing data, so they could not be confirmed, but they are quite expected and there is no cause for alarm.
Our bodies do not become impervious to viruses when we recover from an infection, on the contrary, in many cases, they become inhospitable hosts. Consider that beyond healing, our bodies often offer the same types of cells – such as airway cells – that viruses cling to and enter a safe haven to strip themselves and start producing more virus. These target cells are not substantially altered to prevent future infections months after the virus has been cleared by the immune response.
However, if antibodies and memory cells (B and T cells) are left behind as a result of a recent infection, the further expansion of the virus is rather short-lived and the infection is brought under control before the host suffers too much. – or not even notice it at all.
This appears to be the case with the patient from Hong Kong, who showed no symptoms of the second infection, discovered following routine tests at the airport. Would he ever know he’d been re-infected if he hadn’t traveled? Probably not. A more interesting question is: was he contagious during his second asymptomatic infection?
There is growing evidence that asymptomatic and presymptomatic people are contagious and that is why the sound official advice is to wear a face mask to avoid infecting other people and to keep our distance to avoid be infected. Coronaviruses from previous colds have endowed some of us with memory T cells that can also mobilize against the new coronavirus, which could explain why some people are spared serious illness.
Three potential outcomes
So how should we receive the news about the reinfection of recovered individuals? There are three possible outcomes of re-infection with a similar virus: worse symptoms that lead to more serious illness, the same symptoms as the first infection, and improvement in symptoms leading to milder or no illness.
The first result is known as improvement of the disease and is noted in patients infected with similar strains of viruses like dengue. There is no evidence of this for the new coronavirus, despite more than 23 million confirmed cases of Covid-19 worldwide.
The second result, where the patient suffers from the same disease twice, indicates that there is not enough immunological memory to protect against reinfection. This could happen if the first infection did not require antibodies or T cells to resolve, perhaps because other rapidly deployed immune defenses were sufficient to control it.
The end result is a milder infection thanks to a healthy immune system that generated antibodies and memory B and T cell responses that persisted long enough to be useful on the second exposure. Given the diversity of antibody and T cell responses reported in different Covid-19 patients, we anticipate that immune protection – if effective – may vary among individuals.
Of course, this has implications for the potency and duration of herd immunity, the idea that when we reach a large number of recovered patients who are immune to reinfection, it will protect the most vulnerable. Therefore, vaccination is essential to induce and maintain long-term protective immune responses.
Vaccination can elicit stronger and longer lasting immune responses than natural infection, and these can be supported with booster vaccinations if needed. That’s why scientists weren’t surprised to hear evidence of reinfection. The absence of symptoms experienced by the Hong Kong patient is very good news.