Under most conditions, the virus that causes COVID-19 accumulates around one to two mutations per month. Most don’t amount to anything and are 'viral dead-ends'. Some are important and can increase the ability of the virus to spread.

The UK variant has far more changes than expected (as do the South African and Brazilian variants). This could be from a patient with a chronic infection where the virus has accumulated changes over time.

It could also be from antibody treatment in someone that is chronically-infected, where pressure is placed on the virus and what survives is better adapted and may evade an antibody response.

An alternative theory is re-infection, where the virus appears in someone with a SARS immune response they may have had in the past.

The fact is we do not know, but the rapid appearance of these changes is faster than expected. It’s the consequence of a biological event, but we do not know what that event or collection of events that would be.

With the accumulation of more changes to the virus we need to be aware that we don’t fully know what the virus is up to.

Many countries have taken a cautious approach to the new variant.

If the UK variant does transmit far better than the previous variants, then we need to inform the public of the increased risk of transmission.

If the virus evades the immune response, we need to think through vaccine design, treatment and the message that re-infection could increase.

Our measures and strategies have done us well in Australia. The virus appears to have raised the bar.

Through testing, tracing and linking infections back to the source, it will inform if changes need to take place.

In most cases, it will be hard-hit countries such as the UK that will globally inform us with respect to increased risk of a newly emerging variant.

We are in a good space with respect to the pandemic as we have limited community spread and will follow this story from a distance.

The cluster of changes in what we refer to as the receptor-binding domain suggest the virus is trying to move around something or just simply grab on better to its target.;

As for immune escape or resistance to a current vaccine response, there is evidence now by several groups that the two particular changes can challenge the ability of antibodies to neutralise the virus.

One is s477n (the one circulating last year in Melbourne), the second is e484k. Both have been observed in what are referred to as antibody escape studies, where viruses are placed under pressure in the lab and accumulate changes to be resistant to antibodies.

Whilst some of this data comes from research that is yet to be peer-reviewed, it is being observed in other independent studies.

Whilst, fortunately, the UK variant does not have this change, the South African and Brazilian variants have both accumulated the e484k change.

Fortunately, the s477n variant in Australia is no longer observed in the community (we can thank our response in Victoria to getting rid of that one here).

Whilst antibody binding may be reduced, it must be noted the vaccine responses are higher than those observed in people who have had COVID-19 (a good thing). Strong responses give good breadth and, to-date, most antibodies generated from a vaccine response can still bind the new mutants to good levels.

If there are breakthrough infections in vaccinated patients, then we will need to work through what we need to change in vaccine preparations to [tackle] these new variants (not unlike seasonal vaccinations).

If they found patient zero, very strong.

However, like patient zero in Wuhan, we may never find these things out.

As seen in South Africa and Brazil, more changes in a short period do not appear unique to the UK experience.

The fact they have only turned up now is probably more related to the fact we are seeing over half a million infections per day globally.

So, rarer viral events now may be occurring with increasing frequency.

A longer infection in someone who is immunocompromised could have occurred. Coronaviruses recombine as well, so the rapid accumulation of changes could reflect someone infected (superinfection) with two viruses and the progeny is the sum of its parts.

Many platforms can be re-engineered in a manner to cover new viral variants. At this point, as we do not know how vaccination programs will work against the newly-emerging variants such as the UK one. To change it, you would need significant datasets to show that a particular one is breaking through and infecting people. After that, you may need to then ask if the change would lead to a response that would confer vaccine protection.

At this point, the data coming out in various labs does not point to the UK variant being of significant concern in terms of the vaccine response.

The South African and Brazillian variants, on the other hand, both have a change that can reduce antibody binding (e484k). This change has also been linked to re-infection.

Re-infection is evidence that immunity generated in the first infection is not strong enough to prevent a second infection.

Whilst this could relate to a person having a poor immune response in their first infection (which is common), increasing rates of re-infection may serve as an indicator that these mutations could have the potential to break through a vaccine response.

We have seen viruses with changes that benefit them before.

The variants that would be of significant concern would be those that cause increases in mortality rates.

Fortunately, current evidence in the UK does not support a case for increased mortality with this or any other variant. There may never be one.

We will see viruses mutate to evade antibody responses, we may see them become better adapted as the virus adjusts to its new host. This is what viruses can do.

Whilst many may take the edge off an antibody response or a vaccine response, none to date can completely evade the immune response.

We will see how vaccines will deal with each variant in real-time in places such as the UK.

A key observation will be what viruses breakthrough and infect those vaccinated. We may see very few breakthroughs or we may see a cluster of vaccinated patients appearing with a similar viral variant.

To date, we have yet to see a single virus mutant with complete immune evasion that would make a vaccine useless.

Many articles are yet to be peer-reviewed, but many point to the vaccines having enough breadth to deal with all of the virus variants. We will see subtle differences with certain viral variants. One might take the edge off a vaccine response and in a small group of people it could lead to infection (if the vaccine response was mediocre, for instance).

Fortunately, the vaccine responses so far have been strong in many studies and this level of strength will hopefully translate to cover many different viral flavours (ie. It will have sufficient breadth). We are yet to see a virus that can evade a vaccine response to a degree where it would be of significant concern.

The global response to the virus and amazing efforts like those from the UK to track viral variants and link them to patients at the clinic will enable many of us to witness this real-world experiment in real-time.

Key for us will be to look at their data with respect to who gets infected post-vaccination and with what. In addition, we may be able to see how different vaccines line up.