Omicron has more than twenty new mutations in the S1 domain of the spike gene as compared to the other previously known variants of SARS-CoV-2. Many of these new mutations, especially those located in the receptor binding domain, are likely to improve binding to the ACE2 receptor and to avoid binding to antibodies induced by a previous infection or by vaccination. Today there are several different hypotheses about the origin of Omicron, for example that it would have arisen in an immunosuppressed individual. Alternatively, a SARS-CoV-2 variant could have infected an unknown animal, and re-infection of humans would then have occurred. Furthermore, Omicron may have picked up a piece of a human common cold coronavirus. The hitherto available data suggest that the rapid spread of Omicron is a combination of properties of the virus replication ability in addition to its ability to avoid pre-existing immune responses.
Omikron har mer än 20 nya mutationer i spikgenens S1-domän. Många av dessa mutationer ökar sannolikt förmågan att binda bättre till ACE-2-receptorn och undvika bindning av antikroppar inducerade av en tidigare infektion eller genom vaccination.
I dag finns det flera hypoteser om omikrons ursprung, till exempel att den skulle ha uppstått hos en immunsupprimerad individ. Alternativt kan en tidigare sars-cov-2-variant ha infekterat en okänd djurpopulation och återinfektion av människor skulle då ha inträffat.
De data som finns talar för att den snabba spridningen av omikron är en kombination av egenskaper hos virusets replikationsförmåga och dess förmåga att undvika preexisterande immunsvar.