The Omicron XBB subvariant of the SARS-CoV-2 virus was a notable stage in the evolution of the COVID-19 pandemic. First identified in the fall of 2022, it is what is known as a “recombinant” variant, unlike predecessors that arose from the accumulation of individual mutations. This distinction contributed to its rapid spread in various parts of the world.
The Origin of Omicron XBB
The genetic makeup of XBB is a result of a process called recombination. This event occurs when two different viral subvariants infect the same cell at the same time. During viral replication, the genetic material of the two parent viruses can be mixed, creating a new hybrid virus that incorporates genetic code from both.
For XBB, the parent sublineages were BA.2.10.1 and BA.2.75, both descendants of the Omicron BA.2 variant. This genetic shuffling created a new variant with a unique combination of mutations. The XBB family of variants quickly demonstrated an ability to evade prior immunity, leading to its rapid increase in prevalence.
The XBB lineage continued to evolve, spawning its own subvariants. One of the most significant was XBB.1.5, first identified in the United States in October 2022. This sublineage contained an additional mutation that enhanced its transmissibility beyond the original XBB. The emergence of these sublineages shows the ongoing evolutionary pressure on the virus.
Symptoms and Clinical Presentation
Symptoms of the Omicron XBB variant are consistent with previous Omicron infections and reflect an infection concentrated in the upper respiratory tract. Commonly reported signs of illness include:
- Sore throat
- Cough
- Fatigue
- Nasal congestion
- Muscle aches
While highly infectious, data has not indicated that XBB inherently causes more severe illness than its Omicron predecessors. Hospitalization rates did increase in some areas during XBB’s ascent, but this was largely attributed to the sheer number of people becoming infected at once, rather than a change in the virus’s intrinsic virulence.
For most people with immunity from vaccination or past infection, an XBB infection resulted in a milder illness. The body’s immune memory, while not always blocking infection, often prevents progression to severe disease. The risk of severe outcomes remains higher for older individuals and those with underlying health conditions.
Transmissibility and Immune Evasion
The Omicron XBB variant and its offshoots like XBB.1.5 are defined by their ability to spread rapidly. This high transmissibility is linked to immune evasion, which is the virus’s capacity to bypass protective antibodies from a previous infection or vaccination. Even people with hybrid immunity were susceptible to infection.
This mechanism lies in the mutations on XBB’s spike protein, the part of the virus that attaches to human cells. These mutations alter the spike protein’s shape. If antibodies are keys designed for a previous variant’s lock, XBB’s mutations change that lock. This makes the old keys less effective at neutralizing the virus.
This enhanced immune evasion was the reason for high rates of breakthrough infections and reinfections during XBB waves. Immunity from an earlier Omicron infection offered limited protection because its genetic makeup was so different. The XBB.1.5 subvariant spread with notable speed, quickly becoming the dominant strain in the United States.
In addition to dodging antibodies, some mutations improved the virus’s ability to bind to the ACE2 receptor on human cells. This stronger binding affinity, particularly in the XBB.1.5 subvariant, made it more contagious than prior Omicron versions. This combination of better cellular binding and immune evasion made XBB an evolutionarily successful variant.
Vaccine and Treatment Effectiveness
Despite XBB’s immune-evasive properties, tools to combat COVID-19 remained useful in preventing serious outcomes. Updated bivalent vaccines, designed to target both the original strain and a later Omicron variant, proved effective in protecting against severe disease, hospitalization, and death from XBB. While less effective at preventing infection, this protection against severe outcomes was a significant benefit.
Laboratory studies confirmed that bivalent boosters generated antibodies that could act against XBB. Although the vaccine was tailored for the BA.5 variant and XBB descended from BA.2, there was enough similarity for an effective immune response. This highlights the value of vaccination in mitigating the public health impact of new variants.
Major antiviral treatments like Paxlovid remained effective against XBB and its sublineages. These treatments target different parts of the viral life cycle, not the heavily mutated spike protein. By inhibiting viral replication through other mechanisms, these drugs provide a durable treatment for those at higher risk of severe disease.