The human immune system is designed in a way to defend against different types of pathogen. Viruses have evolved to trick, bypass and evade these defences. Our immune systems have in turn, learn to recognise the tactics of the virus. In COVID-19, the enemy is a tiny piece of genetic material wearing a lipid coat and a protein crown.
How does this apply to COVID-19? The virus that causes COVID-19 is called severe acute respiratory syndrome coronavirus 2 (Sars-Cov-2) and was first detected in humans around five months ago. It is a coronavirus. “Corona”, in Latin, means crown. The virus is adorned with an outer layer of protein covered in spikes, like a crown. These spikes help the virus attach itself to target cells. A scientist is fast learning about immunity to COVID-19, and we are also applying our knowledge of similar respiratory viruses to predict what to expect in this infection.
Importantly, COVID-19 cannot gain entry to our homes or bodies by itself – we have to let it in
It cannot reproduce so it needs a factory of materials – proteins, lipids and nucleotides – to build copies of itself. The coat allows the virus to attach itself to the target cell’s membrane.
The first job of a virus that enters our bodies is to invade target cells so that it can comfortably remove its coat and deploy its RNA.
Once inside, the virus seizes the cell and borrows cellular machinery to build more viruses before immune cells detect the intruders and raise the alarm. Antibody proteins that can stick to the virus-spike proteins, and prevent attachment to the target cells, are called neutralising antibodies: generating them is often the goal of protective vaccination.
Our infected cells make the ultimate sacrifice and invite their destruction by displaying distress signals for T-cells, which swiftly detect and kill them. T-cells are cytotoxic – powerful serial killers that can recognise peptide fragments of virus displayed on the infected cell surface. When they do, they release a payload of toxic enzymes that kill the infected cell in a “kiss of death”.
This strategic martyrdom is organised by the immune system to deprive the virus of its replication factories and can lead to the reduction of viral load in the patient. It takes several days for antiviral T-cells to expand and antibodies to be generated.
Here’s the silver lining: memory cells ensure that if we encounter the same virus again, we can react immediately with pre-existing defences. Sars-Cov-2 is new to humanity so we have no protective immunological memory. Vaccines prepared using harmless parts of the virus can help us build protective memory.
People are already trialling all sorts of medications and we’re hopeful that we might discover that there are various combinations of viral and anti-viral medications that could be effective. At the moment there isn’t any established treatment apart from supportive treatment, which is what we give people in intensive care.