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Here’s What to Know About XBB.1.5

The new Omicron subvariant XBB.1.5 is growing rapidly in the U.S., becoming the most common strain as the proportion of cases for which it’s responsible for doubled in just a week.

XBB.1.5 now accounts for an estimated 41% of COVID cases in the U.S., up from 22% the week prior, according to CDC data.

Just 1 month ago, in the first week of December, XBB.1.5 accounted for only 1% of all COVID cases in the U.S., CDC data show.

It’s particularly prevalent in the Northeast, found in about three-quarters of infections there, according to the agency.

Overall in the U.S., the BA.5 variant has all but disappeared, while BQ.1.1 is the second most common variant, at 27% of cases, followed by BQ.1 at 18%.

XBB.1.5 evolved from XBB.1, which evolved from XBB — an Omicron subvariant that emerged in India in mid-August and quickly became predominant there, as well as in Singapore and other regions in Asia, according to a paper in Cell Reports.

XBB involved a recombination of two descendants of the BA.2 variant, according to virologist Jesse Bloom, PhD, of Fred Hutchinson Cancer Center in Seattle.

Notably, in Singapore, XBB was responsible for a surge in cases, but it didn’t cause an increase in hospitalizations or death, Ali Mokdad, PhD, of the Institute for Health Metrics and Evaluation (IHME) at the University of Washington in Seattle, previously told MedPage Today.

Currently there’s no indication that XBB.1.5 causes more severe illness than other Omicron subvariants, as there hasn’t been a greater increase in hospitalizations in regions hit hardest by the strain.

Still, it remains to be seen whether this variant will drive an overall surge in cases given its increased transmissibility, Bloom said.

Bloom said that while XBB.1.5 is equally as immune evasive as the two other XBB lineages — which had a significant amount of antibody escape, according to a paper in Nature — it has a higher affinity for ACE2, which explains its increased transmissibility.

Driving that higher affinity for ACE2 is a change at site 486, which has been a “major site of antibody escape going back to the earliest variants,” Bloom tweeted.

“It’s easy to understand why it took longer for variants to emerge at site 486: mutations at 486 reduce ACE2 affinity, so benefit they provide in antibody escape comes at cost to receptor binding,” he tweeted. “Difference between XBB.1.5 and its immediate parent XBB.1 is that it has traded the more costly F486S mutation for F486P. Therefore, XBB.1.5 isn’t expected to have more antibody escape than XBB.1 (which already had mutated F486), but it should have greater ACE2 affinity.”

  • Kristina Fiore leads MedPage’s enterprise & investigative reporting team. She’s been a medical journalist for more than a decade and her work has been recognized by Barlett & Steele, AHCJ, SABEW, and others. Send story tips to [email protected]. Follow

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