Originally published by Newsroom
How should we interpret the reported increased transmissibility of variants of the virus that causes COVID-19?
It is important to note that phenomena like this are commonly observed in infectious diseases. Strain differences in transmission (the proportion of contacts infected), the ability to cause disease (the proportion of those infected who develop disease) or the ability to cause severe disease causing death (proportion of those with disease who die), have been observed for many pathogens. For example, our work in tuberculosis (TB) has shown the Mycobacterium africanum ‘strain’ of Mycobacterium tuberculosis is just as likely to transmit, but is a lot less likely to cause TB disease than other strains. It is also possible for some strains to respond differently to vaccines. For example, we have shown recently that Beijing strains of Mycobacterium tuberculosis have the ability to avoid the protection induced by BCG vaccine against TB.
Careful review of the data from the UK does point to a real increase in transmissibility of at least one variant of the virus that causes COVID-19. It is not entirely clear how much, but somewhere between a 10% and 70% increase seems likely. While on average around 15% more close contacts of cases are infected than usual, modelling suggests the overall percentage increase in cases is 50-70%, because of the compounding effect of increased interpersonal transmissibility on both the number of contact networks infected and the number becoming infected within each network. It does not appear that the incubation period (which is crucial with respect to the effectiveness of contact tracing) is affected, but increased transmissibility may be achieved through higher loads of virus in the throat.
Given that human behaviour can dramatically change the ability of this virus to transmit between humans, human behavioural factors should always be considered when interpreting COVID-19 trends. While human behaviour could be playing a role here, the consistency of the data across different regions of the UK and age groups and time periods, suggests it does not explain the increased incidence.
There are a number of reasons to be cautious about the findings from the UK, however. First, the UK only sequences the virus from less than 10% of all COVID-19 cases. On the one hand, this is still a large number of cases to analyse. On the other hand, we usually would like to see at least 50% of cases sequenced when doing in-depth analyses linking sequencing data with epidemiological data. Low percentages of sequenced virus genomes put the data at risk of being interpreted wrongly because of unknowns.
Second, the vast majority of countries, including the USA, do little or no sequencing of the virus. Therefore, rather than singling out the UK and South Africa as having variant strains of concern, we should interpret the finding from the UK as demonstrating that strain variation in transmission occurs for this pathogen, and there are almost certainly more variants that have the same ability around the world, but remain unidentified. We do not actually know where this variant originated from – it could well have been imported into the UK, rather than have evolved there. Therefore, we need to be suspicious of any strain from anywhere.
Third, interestingly, the rapid rise in the proportion of COVID-19 cases due to the new variant in the UK is levelling off. We do not know what this means. It could be that other variants are not able to infect everybody, for reasons such as having cross-immunity from endemic coronaviruses, and that once this ‘niche’ is filled, then a levelling off occurs. It could be that the levelling off will progress to a decrease. We see this with some ‘serotype’ strains of the pneumococcus bacteria that cause pneumonia – some serotypes engage the population in particular ways – causing mini, severe, but short-lasting epidemics and then they disappear for a while.
Fourth, in the UK, they are not seeing what we call classic “strain replacement”. Both the new variant and other strains are growing COVID-19 case numbers exponentially. If this variant is able to infect a different set of people, then initially at least it can co-exist with the other strains and both grow exponentially. The variant strain could be infecting “different people” or it might just mean they are moving in different contact networks and when they do meet up the variant strain will out-compete. This could indicate either different susceptibilities (e.g. the variant strain is able to infect people that the non-variant can’t) or different transmission routes (e.g. the variant strain is able to survive longer in the environment). Overall, we would suggest this variant is able to thrive because of certain conditions – be they environmental, social or individual.
Fifth, there has been some speculation about how the new UK variant came about. It has an unusually high number of mutations. One thought is that it evolved through enhanced mutation in someone or some people with chronic infection – ie. the virus mutates more if under long-term pressure from engagement of the human immune system. The virus would then have had to be transmitted from such individuals, which is rare. One concern is that some vaccines may not protect well against infection, but rather protect more against the development of disease. It is possible that this would promote chronic infection and more rapid mutations, fast-tracking the adaptability of the virus.
So how do these findings influence our approach in New Zealand? First, we should continue to strengthen our infection controls at the border and increase our capacity to respond to an outbreak utilising the full combined force of all the tools we now have at our disposal. These things are already happening. Second, we should be careful about banning people entering NZ from specific countries based on the presence of the UK or other known variants, given there is so little sequencing being done in other parts of the world. We just don’t know enough about the global distribution of variants to treat people from some countries as more or less safe to come to NZ on that basis. Third, we should make sure that our approvals process for new vaccines, and our vaccine distribution planning, are in place as quickly as possible, so they do not inhibit decision-making about when our vaccine programme can commence. Fourth, we should be very careful to choose the right vaccine, so as not to precipitate conditions that promote the emergence of new virus variants. A vaccine that has relatively low protection against infection, and/or has relatively low protection against disease, should be avoided if a vaccine that protects better against infection and disease is available, even if it is more expensive.
We would like to thank Professor Graham Medley at the London School of Hygiene and Tropical Medicine for interactions related to this article.