Like other viruses, COVID-19 mutates as it spreads between people. These new versions of the virus are called variants, and they can be identified by studying their genetic material (known as RNA). The most common variants causing disease in humans are Delta, Kappa and Omicron.
Variants differ in their ability to bind and infect cells. Their virulence is affected by mutations in the spike protein and other non-spike proteins. Some mutations increase transmissibility, while others allow the virus to evade vaccine or infection-acquired immunity. The relative importance of these different traits depends on the complexity of human immune system and the environment in which the virus circulates.
The most serious COVID-19 variants acquired mutations that made them more able to infect ACE2 receptors, which are the key targets of current treatment strategies. The most significant of these was the D614G mutation, which increased the virulence of the virus and the intensity with which it infects ACE2 receptors.
In addition, a missense mutation L452R in the spike protein of the Delta and Kappa variants increases their binding to ACE2 receptors, reducing the effectiveness of vaccine-stimulated antibodies. This is a key reason why those two variants have caused more deaths and severe disease.
More recently, a new strain of the virus has emerged and is spreading globally. It is a recombination of two previously isolated subvariants of the virus: LP.1.8.1 and LF.7. The new strain is circulating in many regions around the world and is responsible for a majority of cases. This variant is characterized by increased transmissibility, virulence and escape from vaccine-stimulated antibodies.