Why can COVID-19 Omicron rapidly spread worldwide?

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Why can COVID-19 Omicron rapidly spread worldwide?

New Research Sheds Light on the Rapid Spread of SARS-CoV-2 Variants.

Over the past year, the Omicron variants of the SARS-CoV-2 virus have rapidly spread worldwide, demonstrating a remarkable ability to adhere more tightly to our cells, penetrate them more effectively, and evade many of the antibodies induced by previous infections and vaccinations.

These crucial insights stem from a recent study conducted by an international team of scientists, which was recently published in the journal “Nature.”

A multinational research group found that compared to earlier variants, the Omicron variant of SARS-CoV-2 can bind to cells more efficiently and better evade antibodies. The study also suggests that prior exposure to the virus or vaccination still provides some level of protection against the newer variants’ severe illnesses.

The lead authors of this study are Amin Addetia, a graduate student in the laboratory of David Veesler, Professor of Biochemistry at the University of Washington School of Medicine, and Young-Jun Park, a research scientist, along with Luca Picolli, Director at the Swiss-based company Humabs BioMed, and James Brett Case of the Washington University School of Medicine in St. Louis. Veesler, who is also a researcher at the Howard Hughes Medical Institute, spearheaded this research.

Why can COVID-19 Omicron rapidly spread worldwide?

Veesler explains, “The Omicron variants that have dominated over the past year, such as BQ.11 and XBB.1.5, have a high affinity for the host cell receptor angiotensin-converting enzyme 2, allowing them to fuse with the cell membrane and invade much more efficiently than previous SARS-CoV-2 Omicron variants.”

Since the outbreak of SARS-CoV-2 in Wuhan, China, in 2019, the virus has been continually evolving, giving rise to new variants of the original strain. In some cases, these variants have had limited adaptability, constraining their spread. However, in other instances, more efficient variants have triggered waves of infections and fatalities.

Following the initial Omicron lineage called BA.1, a series of subsequent variants emerged, each with mutations that enhanced their infectivity and transmission. These variants include BA.2, BA.4, BA.5, BQ.1.1, XBB, and its derivatives XBB.1 and XBB.1.5.

SARS-CoV-2 also has the capability to reinfect individuals who had previously been infected with earlier variants of the virus, breaking through the immune protection provided by vaccines designed for the earlier variants. Veesler and colleagues discovered that this reinfection and vaccine breakthrough were possible because the new variants could evade antibodies induced by exposure to earlier variants. These antibodies, known as neutralizing antibodies, can rapidly clear the invading virus before it can establish an infection.

However, the researchers also found that prior infection or vaccination does contribute to the production of antibodies that can recognize certain proteins on the newer variants. These antibodies can successfully activate immune cells to eliminate infected cells, preventing severe infections.

Veesler suggests that this immune response might explain why individuals previously exposed to early variants or vaccinated against them seem to have a reduced risk of severe illness, hospitalization, and death after reinfection with newer variants.

While the neutralizing activity of most antibodies generated against early variants has significantly decreased, one antibody known as S309 retains its effectiveness. This antibody targets a region on the virus’s spike protein, a region that tends to remain relatively conserved among different variants, likely because of its critical role in the virus’s function.

Veesler notes, “S309 can still recognize all these variants and neutralize them (albeit less efficiently), promote cellular responses, and prevent disease in animal experiments.”

Scientists explain why vaccines designed for earlier variants, or individuals previously infected with them, may not be as effective at preventing infections with newer variants as they were with early variants: the immune system’s response often generates antibodies induced by previous variants and cross-reacts with newer variants, rather than producing new antibodies customized to the altered proteins on the newer variants.

Veesler suspects that this phenomenon is due to a concept known as “immune imprinting,” where the immune response to a new infection with a similar virus is heavily influenced by the immune system’s previous response. This immune imprinting causes the immune system to focus on what it already knows rather than learning new tricks to combat the mutations found in newer variants.

Veesler suggests that this phenomenon is one reason why vaccines targeting newer variants should not contain components of older variants, as the older variants might favor immune imprinting, making the immune response less effective.