Photo: James Pond/Unsplash.
SARS-CoV-2, known colloquially as the novel coronavirus, is of animal origin. Viruses are known to be able to infect some recipients but don’t harm them; such recipients help the viruses survive in their bodies and propagate further. In the case of the novel coronavirus, these recipients are thought to have been bats.
The extent to which a virus can infect a host organism is determined by its virulence – or the severity with which it can infect the host. After being transmitted from a donor to a novel recipient, the virus can undergo a change in virulence.
The novel coronavirus enters the human body through respiratory droplets. Each virus has four major components: S (spike), M (Membrane), E (envelope) and N (nucleocapsid). Upon inhalation, the viral particles use the S protein to latch onto host cells and slowly infiltrate the upper portions of the respiratory tract. Their primary role is to bind to the ACE2 receptor, which is present on the epithelial cells, vascular epithelial cells and macrophages in the lungs. As a result, the lung loses pulmonary ACE2 function and becomes injured. This event also affects blood pressure and fluid and electrolyte balance. In severe cases, multiple organs can be affected and the person can die.
When our body encounters foreign microorganisms, it activates the immune system, which provides non-specific defences against any invading pathogen. This is usually in the form of neutrophils, macrophages and mast cells. After this step of preliminary elimination, the body mobilises the adaptive immune system, which consists of components that can initiate an immune response that it will be able to recollect in future, if the same pathogen invades the body again. This is achieved with the help of antibodies called immunoglobulins. How long these antibodies last in our bodies is what determines the period of immunity towards a particular pathogen.
For example, in the case of the Varicella-zoster virus, the corresponding antibodies last in our system for nearly a lifetime. So once you get chickenpox, you are not likely to get it again. However, in the case of the common cold coronavirus or the norovirus, the antibodies don’t last in our system long enough to guarantee life-long immunity. In some cases like that of hepatitis C or HIV, the antibodies remain in our body long after the infection but the viruses find a way to stay a step ahead, robbing the antibodies of their neutralising abilities.
A vaccine is a technology that allows the body to develop the ‘memory’ of fighting a pathogen by using a dysfunctional form of the pathogen.
Fortunately, we know that the novel coronavirus doesn’t prevent antibody neutralisation, which suggests it may not have any strong mechanisms to escape the human body’s antibody-mediated defence. But on the flip side, some antibodies can bind to the pathogen the second or third time it infects the body and ‘smuggle’ it into the body’s cells, so to speak. Such antibody-dependent enhancement happens with the MERS virus: patients who develop neutralising antibodies earlier during the infection die from it as opposed to people who develop it later and recover.
There have been a few reports of people being reinfected by the novel coronavirus after the first recovery. We need more research ensure these reports weren’t the result of defective tests.
Studies of patients who recovered from MERS and SARS also showed that antibodies persisted in their system for three years and two years respectively. Based on this, scientists are making an educated guess that antibodies against the novel coronavirus could persist in the body for at least a year.
Also read: Why Is It so Difficult to Fight HIV?
From individual to herd
Herd immunity is the situation in which a high percentage of people in a given population are immune against an infectious pathogen. This ‘status’ can in turn lower the chances of infection among those people who are still susceptible to an infection but don’t yet have immunity.
Now, if the presence of antibodies represents the state of being immune, herd immunity might only last a year. So we’ll need to be receiving vaccine shots every year to replenish our immune system’s memories of fighting this infection.
In addition, even if the body develops antibodies against SARS-CoV-2, we know that the severity of COVID-19 can vary from ‘not at all’ (asymptomatic) to severe between people. Ergo, the level of immunity will also vary among people, and might distort the perfect herd-immunity hypothesis.
So while we can rely on herd immunity to protect us in the long run, especially after we have an effective vaccine, we still have a long way to go to ridding ourselves of the virus – if at all.
It’s still unclear if SARS-CoV-2 will be a seasonal virus. Even viruses need to survive and propagate. So if a virus has infected a certain fraction of the population and doesn’t have any more hosts to infect, it mutates to improve its pathogenicity. This is why the H1N1 influenza virus mutates every season. It’s only a clever prediction mechanism together with a good vaccine and herd immunity that help us keep the flu at bay.
SARS-CoV-2 has also been reported to mutate but these mutations don’t necessarily affect its functions. Researchers usually design a vaccine in a way that targets a region of the virus that’s crucial to its function as well as which is not prone to mutations. This is why a vaccine developed against measles in the 1960s is effective to this day.
There are many open questions about COVID-19 that need to be answered before we can claim to understand what recovery from this pandemic will really look like. While we wait for a vaccine and research to make better sense of this virus and its effects, we also need to strictly implement public health measures and practice physical distancing for now.
Shravanti Suresh is a graduate student pursuing a PhD in biochemistry at Iowa State University.