Mumbai Covid-19 case: Why panic over XE is premature
The confirmed Indian infection was in a 50-year-old woman who was asymptomatic and tested positive on March 2, before testing negative a day later. Union health ministry officials separately told HT that the variant sequenced in Mumbai is not XE and may have been misclassified.
Officials in Mumbai announced on Wednesday that they detected a Covid-19 case caused by the Omicron variant’s lineage XE a month ago. The announcement appeared to trigger some concern, although the timing of the discovery and clinical features of the particular case and studies in other countries show that there is little of note about the XE variant as of now.

The confirmed Indian infection was in a 50-year-old woman who was asymptomatic and tested positive on March 2, before testing negative a day later. Union health ministry officials separately told HT that the variant sequenced in Mumbai is not XE and may have been misclassified.
XE – one among many
Whether or not the variant found is indeed XE, there are now several viruses that are a further mutation of the Omicron variant, which swept through most of the world over the last winter. The XE appears to be the result of a recombination of the BA.1 and BA.2, the first two Omicron variant lineages that spread widely. Such recombinations are common.
In terms of its genetic makeup, XE has the Spike protein and other key structural features of the BA.2, with a smaller portion of its genome coming from BA.1, Imperial College virologist Tom Peacock said in a tweet on March 16, shortly after the variant first began popping up on genome surveillance.
The variant was first sequenced in the UK on January 19.
XE is not the only BA.1-BA.2 recombinant. As of March 16, there are, in fact, 11 such variants with a genome that is a varying mix of the genes of the two parental viruses. The others have been classified as XR, XL, XN, XP, XQ, XG, XH, XJ, XK and XM.
No notable concern
Peacock explained that recombinant viruses that contain Spike and structural proteins from a parental virus (which in this case happens to be BA.2) are likely to behave in the same manner. The Spike protein is responsible for the virus’s ability to latch on and infect a host cell. In other words, the XE is no likely to be any more different than the BA.2, which has already spread widely across the country during the winter wave.
This is further supported by epidemiological studies in the UK, where XE was first found. According to the UK Health Security Agency’s variant technical briefing on March 25, preliminary data suggested it had a growth advantage of about 10% compared to BA.2, which means it may be 1.1 times more transmissible, although the trend was not consistent and “it cannot yet be interpreted as an estimate of growth advantage for the recombinant”.
Similar assumptions also likely hold true for the variant’s resistance to antibodies, vaccines and therapeutics since, as noted above, its key structural features are similar to BA.2’s.
The other clue that supports that the variant is not worrying is the Mumbai case (if it indeed is of XE): the infection was detected more than a month ago on March 2. If it were particularly worrying, more cases would have been inevitable – as was the case when Omicron first took hold in India, triggering a sharp spike within a fortnight of first samples being detected.
(With inputs from Rhythma Kaul)