Research offers insight into swift spread of SARS-CoV-2 variants

These variants exhibit a stronger attraction to human cells, enhanced invasion capabilities, and the ability to circumvent a significant portion of antibodies developed from earlier infections and vaccines.

The study published in Nature, was led by Amin Addetia and Young-Jun Park, both from the laboratory of David Veesler, a biochemistry professor at the University of Washington School of Medicine. Veesler expounded that omicron variants like BQ.11 and XBB.1.5, which have come to the forefront in the past year, show a heightened affinity for the receptor on host cells known as angiotensin-converting enzyme 2. Additionally, these variants efficiently merge with cell membranes and infiltrate cells compared to their predecessors.

Since the initial outbreak in Wuhan, China, in 2019, SARS-CoV-2 has continuously evolved, leading to new variants. Some of these have demonstrated reduced viability, limiting their transmission. Nevertheless, others, like the more proficient omicron variants, have prompted upsurges in infections and fatalities.

The study highlighted that the newer variants have managed to re-infect individuals who had previously contracted earlier variants and even surpass the immune defenses induced by vaccines targeting the initial variants. These instances of breakthrough infections and reinfections happen due to the variants’ capacity to elude the neutralising antibodies prompted by earlier exposure, a vital component of the immune response that thwarts the virus from initiating an infection.

However, the research also revealed that individuals with a history of prior infection or vaccination manifested antibodies that recognised specific proteins on the newer variants. These antibodies activated immune cells capable of eliminating infected cells, which could elucidate why prior exposure or vaccination mitigates the severity of illness, hospitalisation, and mortality when encountering a new variant.

Although the neutralising efficacy of most antibodies against the older variants decreased, an antibody named S309 sustained its effectiveness. This antibody targets a section of the virus’ spike protein that remains relatively constant across variants, probably due to its crucial role in the virus’ functioning.

A factor impeding the protective effect of prior infection or vaccination against newer variants is the immune system’s propensity to rely on pre-existing antibodies and cross-reactivity rather than generating tailor-made antibodies that address the modified proteins of the new variants. This phenomenon, referred to as immune imprinting, indicates that the immune system concentrates on what it already knows instead of adapting to address the mutations present in the new variant.

Veesler suggests that this phenomenon underscores the importance of crafting vaccines for new variants that avoid incorporating components from older variants, which might encourage immune imprinting and hinder the immune system’s capacity to adapt and combat the alterations in the virus.