ABSTRACT:
The Omicron, the latest variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was first detected in November 2021 in Botswana, South Africa. Compared to other variants of SARS-CoV-2, the Omicron is the most highly mutated, with 50 mutations throughout the genome, most of which are in the spike (S) protein. These mutations may help the Omicron to evade host immunity against the vaccine. Epidemiological studies suggest that Omicron is highly infectious and spreads rapidly, but causes significantly less severe disease than the wild‐type strain and the other variants of SARS-CoV-2. With the increased transmissibility and a higher rate of re-infection, Omicron has now become a dominant variant worldwide and is predicted to be able to evade vaccine-induced immunity. Several clinical studies using plasma samples from individuals receiving two doses of US Food and Drugs Administration (FDA)-approved COVID-19 vaccines have shown reduced humoral immune response against Omicron infection, but T cell-mediated immunity was well preserved. In fact, T cell-mediated immunity protects against severe disease, and thus the disease caused by Omicron remains mild. In this review, I surveyed the current status of Omicron variant mutations and mechanisms of immune response in the context of immune escape from COVID-19 vaccines. I also discuss the potential implications of therapeutic opportunities that are independent of SARS-CoV-2 variants, including Omicron. A better understanding of vaccine-induced immune responses and variant-independent therapeutic interventions that include potent antiviral, antioxidant, and anti-cytokine activities may pave the way to reducing Omicron-related COVID-19 complications, severity, and mortality. Collectively, these insights point to potential research gaps and will aid in the development of new-generation COVID-19 vaccines and antiviral drugs to combat Omicron, its sublineages, or upcoming new variants of SARS-CoV-2.
Fuente: Heliyon
Available online 31 January 2023, e13285
In Press, Journal Pre-proof
