The story so far:COVID-19 , which has affected over 1.5 million globally and killed more than 100,000 people, is not different from how influenza viruses, or even the coronaviruses responsible for the common cold, attack the body. Therefore, the immune system has a predictable response. It is the degree to which this response is tolerated by the body that determines mortality rates.
How does the immune system respond to a coronavirus attack?
A cascade of viral particles enters the body through the nose, eyes or mouth. Breathing carries some of these particles to the lower respiratory tract where the spike proteins of the coronavirus, acting like a key, lock into epithelial cells that line the respiratory tract as well as those in the the airsacs in the lungs. SARS-CoV-2 is able to stay undetected longer than many flu or coronaviruses and its spike proteins are able to gain entry by unlocking the ACE2 protein on the lung cells. Once in, they hijack the cell’s machinery, replicate and multiply and infect adjoining cells. Like the defining ACE2 proteins on the epithelial cells, viruses too have a tell-tale signature on their surface called antigens and spotting these is what kicks the immune system into action by producing antibodies.
The signals they generate trigger another class of chemicals — cytokines and chemokines — and they alert the immune system to send an array of different kinds of cells that specialise in destroying viral particles. However, these cytokines and chemokines trigger inflammation in the cells. In the nose and upper regions of the respiratory system, this inflammation produces mucus and a runny nose to trap viral particles and prevent their ingress. This also triggers sneezes to expel them. When the sinuses are inflammed we get a headache and the general stuffiness that we associate with a cold. When a gland called the hypothalamus is inflamed, it results in a fever.
However, in the case of SARS-CoV-2, the virus seems better at penetrating deeper. The inflammation triggers a fluid build-up in the lungs. The fluids also contain the residue of a host of specialised cells — including T cells — that carpet bomb and damage many of the body’s own cells as well as the viral particles. It is in expelling this fluid that a dry cough, characteristic of the coronavirus infection, begins. As more airsacs are infected, the lungs find it harder to perform their core job of extracting oxygen from the air, and eventually, this aggravates breathlessness.
Why are some infections mild and others life-threatening?
Depending on the degree of infection in the lungs, the inflammation and the fluid build-up can lead to pneumonia. A patient will require hospitalisation to treat the breathlessness and ventilator support to artificially provide oxygen if the condition worsens. However, massive levels of cytokines can cause extensive lung damage and a condition called Acute Respiratory Distress Syndrome. The unsustainable cytokine storm can cause organ damage far beyond the lungs and spread to the kidneys as well as the heart. If the infection is acute, it can also lead to a depletion of the frontline white blood corpuscles tasked with fighting the infection and making the body vulnerable to other secondary infections, which may lead to death.
How have the elderly reacted to the virus?
The elderly, especially those with existing conditions such as diabetes and cardiovascular disease, already have an inherent malfunctioning in the immune system. In many ways, it is the reaction of the body in trying to combat the virus that ends up being suicidal. The different kinds of drugs, whether it is hydroxycholoroquine or anti-HIV drugs, deployed to treat serious COVID-19 infection, also work in some way to moderate the immune-system’s aggressive defence.
Mortality statistics globally suggest that men are twice more likely than women to succumb to a COVID-19 infection. This follows from studies that show women, on average, have a better-regulated immune response than men in pathogenic infections. Estrogen is said to be an immune-system modulator and the ability to deal with a pregnancy — which also begins as a foreign body growing within — primes women to better deal with infections, say experts.
What about children?
The response of the immune system is in many ways a mystery. For instance, so far, there have been few deaths reported in children from COVID-19. Given that children’s immunity systems are still maturing and learning to adapt to a galaxy of infectious agents, why they seem to be relatively better protected from severe COVID-19 disease is not known.
Will a vaccine help?
There are several vaccine candidates but it will be months before we know if any of them will be viable. The bulk are aimed at developing a molecular construct, in some cases a weakened version of the coronavirus, that mimics the antigens of the virus and triggers an appropriate antibody response. There are complications — such as an antibody-dependent enhancement — in which insufficient levels of antibodies can actually end up aggravating an infection as in the case of dengue. However, in the case of COVID-19, that’s a problem for another day.