As the daughter of an air force officer and a nurse, I am fascinated by defence systems. There is none more impressive than the human immune system, equipped as it is with a rich arsenal to defend against different types of pathogen. Viruses have evolved to trick, bypass and evade these defences. Our immune systems have, in turn, learned to recognise and deter these virus stealth tactics. In Covid-19, the enemy is a tiny piece of genetic material wearing a lipid coat and a protein crown.

So how is our immune system able to defend against viral infections, and 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. The research community 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

Think of a virus as a robot; 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 virus then fuses with the cell and releases a shopping list of instructions on how to build and assemble new viruses. This shopping list, the virus genome, is written in nucleotides (RNA). 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 commandeers the cell and borrows cellular machinery to build more viruses before immune cells detect the intruders and raise the alarm. Antibody proteins that are able to 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 own 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.

The virus’s enemy superpower is spreading. The virus achieves this through “shedding” from infected patients. Sars-Cov-2 is expert at hopping from person to person, and in some people, it achieves a stealthy existence with mild or no symptoms. Once many copies of the virus are made, it needs to jump to another host. It hitches a ride on droplets that can be coughed or sneezed to a distance of up to two metres. Droplets can survive on surfaces for several hours enabling pick-up by a new host, or they can be directly inhaled if another person is in close proximity. Studies are emerging into animal hosts – so far the virus has been detected in a few ferrets, cats, tigers and dogs. No animal deaths have yet been reported, and we don’t know if animals can transmit back to humans.

The age differential in fatalities for Covid-19 suggests, with some exceptions, that a healthy immune system is usually able to control infection. Meanwhile, an ageing or weakened immune system may struggle to deploy a protective arsenal. Importantly, Sars-Cov-2 cannot gain entry to our homes or bodies by itself – we have to let it in. This is why official advice has centred around cleaning our hands and avoiding touching our faces.

We know that a healthy immune system is usually able to eliminate infection in a couple of weeks. However, we have no understanding of the components of our immune arsenal that contribute to this feat: some vaccines work by creating potent neutralising antibodies; other vaccines generate powerful memory T-cells. Antiviral antibodies emerge as early as three to four days after virus detection, but are they protective against future reinfection? We believe that antibodies to other coronaviruses (Sars, Mers) last from one to three years. Because this is a new virus, we don’t yet know the answer to this question. Public Health England is recruiting 16,000 to 20,000 volunteers to monitor antibodies once a month for six to 12 months to confirm whether we can generate long-lasting antibody responses to Sars-Cov-2. Determining the quality of these antibodies will be important to understanding long-term protection.

What is our most potent immune weapon against Covid-19? Cytotoxic T-cells may play an important role. Immunologists and virologists are working together to discover the correlates of protection, to design vaccines that offer long-term defences against Covid-19. Years of investment in research means that we can use existing approaches to respond to this new threat, and early mobilisation of research funders, philanthropists and academics are diverting resources to bolster these efforts on an unprecedented scale. Experience has taught us that vaccines are able to eradicate infections from this planet (for instance, smallpox), and medicines against viruses that don’t embed their genetic material to our own (for example, hepatitis C) can also achieve this.

Our secret weapon is research. Scientists are working hard on understanding Covid-19, and collaboration is key to this effort. But until a vaccine or treatment is available, we ought to work hard to protect ourselves and our families: isolate and prevent transmission by using physical distancing, face masks and sensible hygiene. If we all do our part, this little virus holding the world to ransom won’t stand a chance.

• Zania Stamataki is a senior lecturer and researcher in viral immunology at the University of Birmingham