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expert reaction to latest update from PHE on the Delta variant

Public Health England (PHE) has released more information on the Delta variant first discovered in India (B.1.617.2).


Dr Leon Danon, Associate Professor in Infectious Disease Modelling and Data Analytics, University of Bristol, said:

“We have been seeing trends in the variant now known as Delta for some weeks, and PHE’s reports confirm these trends. Currently, the numbers remain low, but if the growth rate of the new variant continues at the current levels, we will continue to see a rise in cases. The growth rate has increased partly due to the apparent increased transmissibility of the Delta variant, and partly due to a return to ‘normal’ behaviour, as people’s social contacts increase with the relaxation of control measures and the perceived reduction of the threat of COVID-19. The evidence on hospitalisations is still emerging and needs further, careful analysis, as it takes time for cases to show up in hospital. The most important question to answer in the coming days is how sensitive Delta is to vaccine-derived immunity. Recently published experimental studies from the Crick Institute suggest a slightly lower amount of protection against Delta, but this remains to be confirmed in population level studies.”


Dr Julian Tang, Honorary Associate Professor/Clinical Virologist, University of Leicester, said:

“We’ve been here before with the Kent (alpha) B.1.1.7 variant – where there was an initial belief that it was more transmissible (which eventually turned out to be true) and more clinically severe (which eventually turned out to be false):

“Generally, from an evolutionary viewpoint, if a virus is more transmissible, it tends to be less severe – those infected still have to be well and mobile enough to spread the infection to others.

“The Indian (delta) B.1.617.2 variant seems to be at least, if not more transmissible than the previous predominant Kent (alpha) variant – not just based on case numbers in the UK – but elsewhere also – particular in some Asian countries where natural infections have been well-controlled, and where very few  COVID-19 vaccines have so far been given.

“I am not sure how good the data is on clinical severity for the delta variant – particularly in children where some observations may suggest more rapid spread with more symptomatic infections (e.g. the Bristol school clusters) – if the virus is causing more ‘severe’ symptomatic infections, making them easier to identify, then this may also give the impression of more rapid spread.

“Also a virus that is more transmissible than it is severe – and spreads more quickly will increase the ‘denominator’ of cases identified (if the testing can keep up), so you might see an increase of, say, 10% in daily cases due to the delta variant which may decrease the overall percentage of hospitalisations if these numbers (the ‘numerator’) do not increase, i.e. whilst there may be more symptomatic cases, these symptoms (e.g. like the common cold) are not severe enough to require hospitalisation.

“However, I would say that given the predominance and still increasing numbers of COVID-19 cases caused by the delta variant now, we need to be cautious about the extent of the further relaxations planned on 21 June – especially with recent data showing some reduced effectiveness of the current generation of COVID-19 vaccines against this variant:

On transmissibility of the delta variant:

“If the delta variant escapes existing immunity (whether vaccine- or naturally-induced) – better than the alpha variant – which it can – then in the current population, it may give the impression of being more transmissible – but it may not intrinsically be so, from a virus genetics viewpoint.

“From one angle, the degree of transmissibility of any pathogen depends on the level of population immunity.

“But it depends on what you mean by a virus being more transmissible.

“For an epidemiologist/modeller – the above scenario might qualify as a higher relative transmissibility in this current population – even if the virus may not contain a genetic mutation that raises its intrinsic transmissibility in humans.

“For a virologist, this is not necessarily a true case of enhanced genetic transmissibility – a good example is from influenza

– avian A/H5N1 influenza preferentially uses 2,3 sialic acid as a receptor – which is more common in birds than humans

– human influenza uses the 2,6 sialic acid receptor in preference to the 2,3 sialic acid.

– but if the avian H5N1 influenza virus can be altered to use the human 2,6 sialic acid receptor – then you would have a potentially pandemic version of avian A/H5N1 – which has a mortality of 60%.

– and this has been done already in gain of function studies:

“So it really depends on how different research specialties define ‘increased transmissibility’ – not everyone defines this the same way.”


Prof Ian Jones, Professor of Virology, University of Reading, said:

“The suggestion that the Indian variant is more pathogenic needs to be taken with a big dose of salt. The same was initially suggested for the Kent variant but was later shown not to be true. From a virus point of view there is an advantage in being more transmissible, you reach more people, but there is no advantage in making people sicker. It is possible, but not yet proved. Its current dominance is partly explained by its introduction into a relatively vaccine naive population when the circulation of existing variants was already in decline. However, the recent Zoe data, and the current case reductions in India, suggests it is also controlled by vaccination, so the key message remains unaltered. This is not a sudden change for the worse; rather it illustrates that the immune status of the population in the affected areas is key and that this needs to be as high as can be realistically achieved.”      


Prof Paul Hunter, Professor in Medicine, UEA, said:

“The Public Health England variant report states that “there was a significantly increased risk of hospitalisation within 14 days of specimen date …., for Delta cases compared to Alpha cases after adjustment for confounders (age, sex, ethnicity, area of residence, index of multiple deprivation, week of diagnosis and vaccination status)”.

“I think we need to be a little cautious about assuming that the delta (Indian) variant is intrinsically more virulent than the alpha (Kent) variant. We know from a recently published preprint that the delta variant is a little more resistant to vaccine after two doses and moderately more resistant after a single dose. So this variation in hospitalisation rates may in part be down to the fact that over 13 million people are still waiting for their second dose of vaccine. It is not clear from the Technical briefing document whether the relative increase in risk of hospitalisation was similar in people who have had no, one or two doses of vaccine. This is important because apparent differences in severity of disease could be due to either increased virulence or increase immune escape and simple adjustment for vaccination status may not be sufficient to illustrate such an effect.

“So with the information available it is too early to say for certain whether the delta variant does indeed cause more severe disease needing hospitalisation or not. What we can be confident about with available data is that if you have had one or preferably two doses of vaccine you are rather less likely to catch either alpha or delta variants and even if you do become infected you are less likely to need hospital admission.”



PHE press release: Delta (VOC-21APR-02) variant now dominant in the UK:

COVID-19 variants: genomically confirmed case numbers:

Investigation of SARS-CoV-2 variants of concern: technical briefings:



All our previous output on this subject can be seen at this weblink:



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