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Viruses are tiny biological entities, much smaller than bacteria. While a bacteria may be made up of a few thousand proteins, most viruses amount to as few as 10 to 100 proteins.

And, unlike bacteria, viruses can’t reproduce themselves on their own. This is why they are not thought of as living things.

Viruses can only reproduce themselves by invading the cells of a host, like us, and that is what makes them dangerous.

WATCH: SARS-CoV-2 has a few tricks up its sleeve that we believe make it more infectious. Video: University of Melbourne

Once inside the body, unless a virus can be quickly killed by our immune system, it will try to break into cells and hijack our proteins to replicate their own genome (the sum total of an organism’s DNA).

This is why it is difficult to develop therapies to kill viruses – antivirals.

We are able to target bacterial infections using antibiotics that attack the proteins in bacteria. But because viruses use our own proteins, antiviral therapies attacking these proteins can cause potentially damaging side effects.

It means that effective antivirals need to be specifically targeted so they attack only those proteins we know are critical for the virus. That way we can minimise any potential harm to the overall health of the patient.

Antiviral researchers also face the ongoing problem of resistance. Just like bacteria, viruses can develop resistance to antivirals over time.

The virus that causes COVID-19, known as SARS-CoV-2, is a type of coronavirus; these are named for the spikes on their surface that give them their crown-like appearance. They commonly attack our respiratory systems.

SARS-CoV-2 is named after the related earlier coronavirus that caused the 2003 outbreak of SARS (Severe Acute Respiratory Syndrome). But unlike SARS, SARS-CoV-2 has a few tricks up its sleeve that we believe make it more infectious and potentially more dangerous.

The ‘spikes’ on SARS-CoV-2 that it uses to break into lung cells, appear to be able to bind more efficiently to the outside of our cells, making it more effective at breaking in.

This means that people can be more easily infected with COVID-19 compared with SARS.

SARS-CoV-2 also uses our own enzymes to trigger its spike action, again making its spread more efficient.

Finally, SARS-CoV-2 causes less immediate symptoms once it has infected someone – meaning an infected person can initially appear asymptomatic, making it easier for SARS-CoV-2 to spread.

On the plus side, our research team showed in March that usually our immune systems are able to launch a robust response to fight SARS-CoV-2, which is good news for vaccine developers.

By tracking blood samples in a COVID-19 patient with mild symptoms, we were able to map how our immune system goes about fighting this coronavirus. We are now trying to understand which parts of the immune system ‘go awry’ in those who develop severe disease.

It means vaccine developers now have a range of areas in our immune system that they can potentially target in creating a vaccine that can head off infection or make it less severe.