Key questions remain about how quickly B.1.617 variants can spread, their potential to evade immunity and how they might affect the course of the pandemic.

Since the SARS-CoV-2 variant known as B.1.617 was first reported in India late last year, it has spread to dozens of other countries — including the United States, Singapore and the United Kingdom, where it has become dominant in some regions.

Researchers have since identified three subtypes, known as B.1.617.1 (the ‘original’ B.1.617), B.1.617.2 and B.1.617.3, each with a slightly different genetic make-up.

They are now rushing to investigate these variants and work out how they might affect the trajectory of the pandemic in countries where they have gained a foothold. Key questions remain about how quickly the variants can spread, their potential to evade immunity and whether they cause more severe disease.

A lot of this research takes the form of standard epidemiology — confirming COVID-19 cases through testing, identifying the variants responsible for infections and cross-referencing these data to people’s clinical symptoms and vaccination statuses. Scientists can also glean insights from genomic-sequencing data, identifying which mutations are present in the B.1.617 subtypes and comparing these with mutations in earlier variants whose behaviour is better understood.

More transmissible

“I look at individual mutations because they each have individual properties that we think might confer higher transmissibility,” says Julian Tang, a consultant virologist at the Leicester Royal Infirmary, UK. Increased transmissibility — a measure of how quickly variants can spread from person to person — could accelerate outbreaks, which could put more pressure on health-care systems and counter-measures such as vaccination programmes. For example, the B.1.617.2 variant has mutations called 452R and 478K, which Tang says are both linked to increased transmissibility. Both mutations alter the spike protein, which the virus uses to enter human cells.

Researchers have also been able to rapidly track the spread of B.1.617.2 because its genome contains a marker that the dominant B.1.1.7 variant lacks. The presence of this marker — known as the ‘S gene target’ — can be seen in the results of some of the PCR tests used to confirm cases of COVID-19, so researchers can use positive S-target hits as a proxy to quickly map the spread of B.1.617.2, without needing to sequence samples fully. Both S-gene tests and more detailed sequencing data from UK virus samples indicate that B.1.617.2 is outcompeting the two other B.1.617 subtypes, and replacing B.1.1.7 — a variant identified in southeast England in late 2020 — as the most common variant driving new infections in the country.

“Across all of England now, we would expect that 50% of infections would be the [B.1.617.2] variant,” says Tom Wenseleers, a biologist at the Catholic University of Leuven in Belgium who is tracking the figures. An analysis of UK sequencing data that he shared online suggests that numbers of B.1.617.2 infections could be growing 13% faster than B.1.1.7 infections each day.

In a report published on 12 May, A UK government advisory committee called the Scientific Pandemic Influenza Group on Modelling, Operational subgroup said there is a “realistic possibility” that B.1.617.2 is 50% more transmissible than B.1.1.7, according to the available data.

“The prediction of 50% more transmissible sounds entirely plausible,” says Sharon Peacock, a microbiologist at the University of Cambridge, UK, who leads the COVID-19 Genomics UK consortium. “I think as data goes up more, we’ll get more confidence in that, but you can’t really ignore what’s happening.”

At present, Peacock adds, the surge in B.1.617.2 is not leading to a significant rise in the overall number of cases in the United Kingdom, which remain much lower than during the country’s most recent peak, in January. Instead, people are catching the new variant rather than B.1.1.7. “What we’re seeing here is lineage replacement,” she says.