Immunity to COVID-19

Dr Jayaprakash Muliyil, Chairman of the Scientific Advisory Committee of the National Institute of Epidemiology, India, has explained in multiple interviews to media that widespread immunity could be a good way to get out of the pandemic.

Widespread immunity is different from herd immunity in two significant ways. One, to confirm herd immunity, scientists tend to know what percentage of people need to be immune to a pathogen to protect the community.

For example, herd immunity for the measles virus is triggered when at least 95% of the community is immune to it. For the virus that causes polio, this percentage is 80-85%. For SARS-CoV-2, which causes COVID-19, we do not yet know what percentage of the population needs to be immune to protect everybody. That said, early estimate place this figure at 75%.

Two, usually the only safe way to ensure herd immunity is through an effective vaccine that has been given to most people in the community - there is currently no vaccine to protect against COVID-19.

How to safely ensure immunity at scale?

COVID-19 tends to manifest with severe symptoms in older people. Since nearly 90% of India's population is under 60 years of age, Dr Muliyil says immunity among India's young and healthy can be achieved through controlled transmission of the disease in the community. (Read more: COVID-19 prevention in the elderly and those with chronic diseases like diabetes)

However, at least 60% of a population in any area would need to be immune to ward off COVID-19 according to Dr Muliyil. Achieving that number would undoubtedly come at a cost of more lives unless the high-risk groups are kept safe and the disease spread rate in the safer population is kept significantly low.

Vaccines also work on the concept of immunity: when a weak form of the antigen - the microbial protein - is injected into the blood, the body's immune system makes antibodies to fight it off. Once the body makes antibodies for anything, it gains the tools to fight the infection (and win) for many years. (Read more: Why is it taking so long to develop a vaccine for COVID-19?)

There is one caveat that should be mentioned here, though: it is still unknown whether the generation of antibodies against the COVID-19 causing virus is enough to provide long-term immunity against the disease. There have already been some cases of relapse, where a patient who was already treated for COVID-19 again tested positive for it. (Read more: Can you get coronavirus infection twice?)

Our immune system comprises a complex set of cells and molecules that work together to protect us against pathogenic microbes. We have an innate immune system that we are born with and an acquired immune system which we develop as we are exposed to various pathogens over the years.

Specific antibodies are formed in our body against specific antigens (microbes). So every time a new microbe shows up, it takes some time for our immune system to recognise it and develop antibodies against it (adaptive immune response).

There are two arms of the adaptive immune response:

• Humoral immunity: Triggered by B-cells, it leads to the production of antibodies specific to antigens. There are about five different types of antibodies (immunoglobulins, a type of proteins):
  • IgD: These immunoglobulins are usually found on the surface of B-cells; one of their jobs is to alert the immune system to the presence of an antigen or foreign body.
  • IgM: IgM is usually the first antibody to show up whenever the immune system encounters an antigen. The rest of the antibodies show up soon after.
  • IgA: IgA is found in mucosal surfaces (oral and nasal cavity and gut lining, for example).
  • IgG: IgG is present in the serum or blood. The presence of IgG antibodies against a pathogen indicate a previous infection against the pathogen and the presence of IgM antibodies indicates an active infection.
  • IgE: IgE antibodies are produced in case of allergies and are present in the skin, mucous membranes and lungs.
• Cell-mediated immunity: Triggered by T-cells, it usually helps to destroy infected cells in case of viral infection.
  • T-cells also work against cancer cells.
  • Memory cells: Once our immune system has identified and fought against a microbe, it develops specific cells called memory cells which remember the said pathogen. The next time the same pathogen attacks the body, these memory cells quickly develop antibodies against the pathogen and neutralise it. Both B and T cell memory cells are formed in the body after an infection.

Viruses are intracellular parasites (they live inside healthy cells). Once they enter healthy cells, they become invisible to the humoral arm of immunity. The infected cells then use special receptors on their surface to present the viral antigen to the cell-mediated branch of the immune system. The latter activates killer T-cells, which then go and kill the infected cells along with the virus.

Viral interferons are special chemicals that are produced inside infected cells and which neutralise the virus inside the cells. These interferons also send signals to nearby cells and warn them about the presence of the virus in the body. These cells then make sure that the T-cells can easily identify the virus-infected cells by showing their own surface molecules as normal.

Antibodies can neutralize viruses when they show up outside the healthy cells or when they haven’t yet entered into cells. Antibodies work in one of these ways to neutralise viruses:

• They can interfere with the viral binding to the healthy cells
• They can bind with the virus and neutralise them
• They can engulf and kill the virus.

IgG, IgA and IgM antibodies have antiviral properties.

Even though the basics of our immune response are known, in reality, all is not as perfect as the textbook explanation. Our immune system reacts differently to different microbes.

• For instance, once you get chickenpox, you are protected against this disease for life. Though the chickenpox virus (varicella virus) stays dormant (asleep) in your spinal nerves and if it reactivates, it can cause shingles.
• Similarly, if you get typhoid fever, there is a chance that you may become a carrier of the disease. Carriers are those who can shed the typhoid bacteria in their urine and faeces but who themselves don’t have symptoms of the disease.
  You could also be a convalescent carrier, those who shed the bacteria for a while after being treated for the disease or a chronic carrier, shedding the typhoid bacteria long after the infection.
• For tetanus, our immune system does not develop immunity. This is because the amount of toxin required to cause the disease is really low. And tetanus is life-threatening.
• The HIV virus attacks the immune system cells themselves.
• Since COVID-19 is such a new disease and not much is known about the body’s immune response against it, it would be hard to say if getting the infection once can make you immune to the disease, and if yes, then for how long.
  The absence of a strong immune response is being considered one of the causes of relapse (where it is happening) in patients. On the other hand, a small study showed that specific IgM antibodies can be seen in COVID-19 patients within nine days of disease onset and IgG antibodies are seen within two weeks.
  The antibodies showed cross-reactivity with the SARS-CoV-2 virus. In earlier studies, antibodies against this SARS virus have been found in the patient’s serum even after 2 years after the infection.
  Though what actually happens in the body to fight COVID-19, and what kind of immunity can recovered patients expect to have against this disease, only time and further research will tell.