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The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) variant BA.2.86 has over 30 mutations in spike compared with BA.2 and XBB.1.5, which raised the possibility that BA.2.86 might evade neutralizing antibodies (NAbs) induced by vaccination or infection. In this study, we show that NAb titers are substantially lower to BA.2.86 compared with BA.2 but are similar or slightly higher than to other current circulating variants, including XBB.1.5, EG.5.1, and FL.1.5.1. Moreover, NAb titers against all these variants were higher in vaccinated individuals with a history of XBB.1.5 infection compared with vaccinated individuals with no history of XBB.1.5 infection, suggesting the potential utility of the monovalent XBB.1.5 mRNA boosters.

The highly mutated BA.2.86, with over 30 spike protein mutations in comparison to Omicron BA.2 and XBB.1.5 variants, has raised concerns about its potential to evade COVID-19 vaccination or prior SARS-CoV-2 infection-elicited immunity. In this study, we employ a live SARS-CoV-2 neutralization assay to compare the neutralization evasion ability of BA.2.86 with other emerged SARS-CoV-2 subvariants, including BA.2-derived CH.1.1, Delta-Omicron recombinant XBC.1.6, and XBB descendants XBB.1.5, XBB.1.16, XBB.2.3, EG.5.1 and FL.1.5.1. Our results show that BA.2.86 is less neutralization evasive than XBB sublineages. XBB descendants XBB.1.16, EG.5.1, and FL.1.5.1 continue to significantly evade neutralization induced by the parental COVID-19 mRNA vaccine and a BA.5 Bivalent booster. Notably, when compared to XBB.1.5, the more recent XBB descendants, particularly EG.5.1, display increased resistance to neutralization. Among all the tested variants, CH.1.1 exhibits the greatest neutralization evasion. In contrast, XBC.1.6 shows a slight reduction but remains comparably sensitive to neutralization when compared to BA.5. Furthermore, a recent XBB.1.5-breakthrough infection significantly enhances the breadth and potency of cross-neutralization. These findings reinforce the expectation that the upcoming XBB.1.5 mRNA vaccine would likely boost the neutralization of currently circulating variants, while also underscoring the critical importance of ongoing surveillance to monitor the evolution and immune evasion potential of SARS-CoV-2 variants.

Background The World Health Organization announced the end of the Coronavirus Disease of 2019 (COVID-19) global health emergency on May 5, 2023. However, the reports from different countries indicate an elevation in the number of COVID-19-related hospitalizations and deaths through the last months. The subvariant XBB.1.5 (Kraken) was the cause of 49.1% of COVID-19 cases by the end of January 2023. Although, the subvariant EG.5 (Eris) has surpassed the XBB.1.5 recently. EG.5 is a close subvariant descending from XBB.1.9.2 subvariant of Omicron. EG.5.1 is a sublineage carrying two crucial spike mutations F456L and Q52H. Up to now, it is not well-established whether its infectivity, severity, and immune evasion have shown any change or not. Also, BA.2.86 another subvariant of Omicron descending from BA.2 bears over 30 mutations which could affect its infectivity and transmissibility. Methods Scopus, PubMed, Google Scholar, and Google were searched with six keywords up to 20 November 2023 and highly reliable research and reports were selected to refer to in this article. Purpose This brief review aims to overview the most reliable data about EG.5 and BA.2.86 based on scientific evidence. Conclusion Based on the currently available data these two new subvariants have similar features with currently circulating variants of Omicron and are less immune evasive than ancestral SARS-CoV-2.

The study advances our understanding of the roles of immune evasion and replication fitness in driving the evolution of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) from the BA.2.86 sublineage to its descendants (JN.1, KP.2, and KP.3). Through head-to-head comparisons of the replication fitness of recombinant SARS-CoV-2 strains containing spike sequences from BA.2.86 and its descendants in primary human airway epithelium cells, alongside assessments of their neutralization sensitivity to human sera, we revealed how recurrent mutations R346T, L455S, F456L, and Q493E in the receptor-binding domain (RBD) fine-tune immune evasion and viral replication fitness, underscoring the critical need for updated countermeasures to combat newly emerged SARS-CoV-2 variants. Additionally, our analysis showed that the L455S and Q493E mutations in the RBD can influence spike cleavage, offering new insights into SARS-CoV-2 spike biology.

The severe acute respiratory syndrome corovirus 2 (SARS-CoV-2) is a single-stranded, positive-sense R virus. The SARS-CoV-2 virus is evolving continuously, and many variants have been detected over the last few years. SARS-CoV-2, as an R virus, is more prone to mutating. The continuous evolution of the SARS-CoV-2 virus is due to genetic mutation and recombition during the genomic replication process. Recombition is a turally occurring phenomenon in which two distinct viral lineages simultaneously infect the same cellular entity in an individual. The evolution rate depends on the rate of mutation. The rate of mutation is variable among the R viruses, with the SARS-CoV-2 virus exhibiting a lower rate of mutation than other R viruses. The novel 3′-to-5′ exoribonuclease proofreading machinery is responsible for a lower rate of mutation. Infections due to SARS-CoV-2, influenza, and respiratory syncytial virus have been reported from around the world during the same period of fall and winter, resulting in a “tripledemic”. The JN.1 variant, which evolved from the predecessor, the Omicron variant BA.2.86, is currently the most domint globally. The impact of the JN.1 variant on transmissibility, disease severity, immune evasion, and diagnostic and therapeutic escape will be discussed.

Since the emergence of the first omicron SARS-CoV-2 variant at the end of 2021, several sub-variants have evolved and become predominant in the human population, showing enhanced transmissibility and ability to (partly) escape the adaptive immune response. The XBB sub-variants (e.g., EG.5.1) have become globally dominant. Besides the XBB sub-variants, a phylogenetically distinct variant, i.e., BA.2.86, is also circulating; it carries several mutations in the spike protein as compared to its parental BA.2 variant. Here, we explored the infectivity of the BA.2.86 and EG.5.1 sub-variants compared to the preceding BA.5 sub-variant in Syrian hamsters. Such preclinical models are important for the evaluation of updated vaccine candidates and novel therapeutic modalities. Following intranasal infection with either variant, throat swabs and lung samples were collected on days 3 and 4 post infection. No significant differences in viral RNA loads in throat swabs were observed between these sub-variants. However, the infectious virus titers in the lungs of EG.5.1- and BA.2.86-infected animals were significantly lower compared to the BA.5-infected ones. The lung pathology scores of animals infected with EG.5.1 and BA.2.86 were also markedly lower than that of BA.5 sub-variant. Together, we show that EG.5.1 and BA.2.86 sub-variants exhibit an attenuated replication in hamsters’ lungs as compared to the BA.5 sub-variant.

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the causative agent of the global COVID-19 pandemic, relies on its spike glycoprotein to mediate host cell entry via binding to human angiotensin-converting enzyme 2 (hACE2). The S2 subunit of the spike protein contains heptad repeat regions (HR1 and HR2) that form a six-helix bundle fusion core, a critical step for viral–host membrane fusion. This study aimed to computationally screen a library of 318 probiotic-derived bacteriocins to identify potential inhibitors targeting the conserved HR1 domain. Evaluation included historical variants (Alpha, Beta, Gamma, Kappa, Epsilon, Omicron) and currently circulating strains (BA.2.86, EG.5.1, HV.1, JN.1). Methodologies included: sequence conservation analysis via Clustal Omega, protein–peptide docking using HADDOCK 2.4 with Ambiguous Interaction Restraints derived from the HR1–HR2 complex (PDB: 6LXT), safety profiling with AlgPred, ToxinPred, HemoPred, TargetAntiAngio, and IL-4Pred, and molecular dynamics simulations (GROMACS 2020) assessing RMSD, RMSF, and hydrogen bonds. Results identified plantaricin K (2KEG) as a high-affinity binder to HR1 across all tested variants, with favorable in silico safety profiles (non-toxic, non-allergenic, non-hemolytic). Simulation data confirmed stable binding of 2KEG to HR1, supporting its role as a fusion inhibitor. These findings suggest the potential of probiotic-derived bacteriocins, particularly 2KEG, as broad-spectrum antiviral candidates against SARS-CoV-2. Further experimental studies are required to validate these computational predictions.

The SARS-CoV-2 Omicron sub-variants BA.2.86 and JN.1 contain multiple mutations in the spike protein that were not present in previous variants of concern and Omicron sub-variants. Preliminary research suggests that these variants reduce the neutralizing capability of antibodies induced by vaccines, which is particularly significant for JN.1. This raises concern as many widely deployed COVID-19 vaccines are based on the spike protein of the ancestral Wuhan strain of SARS-CoV-2. While T cell responses have been shown to be robust against previous SARS-CoV-2 variants, less is known about the impact of mutations in BA.2.86 and JN.1 on T cell responses. We evaluate the effect of mutations specific to BA.2.86 and JN.1 on experimentally determined T cell epitopes derived from the spike protein of the ancestral Wuhan strain and the spike protein of the XBB.1.5 strain that has been recommended as a booster vaccine. Our data suggest that BA.2.86 and JN.1 affect numerous T cell epitopes in spike compared to previous variants; however, the widespread loss of T cell recognition against these variants is unlikely.

Recent efforts in vaccine development have targeted spike proteins from evolving SARS-CoV-2 variants. In this study, we analyzed T cell responses to the XBB.1.5 and BA.2.86 subvariants in individuals who previously received bivalent vaccines containing mRNA for ancestral and BA.5 spike proteins. T cell-mediated cytokine responses to spike proteins from both variants were largely preserved. To determine the mechanism of this preserved recognition, we utilized the functional expansion of specific T cells (FEST) assay to distinguish between the presence of T cells that cross-recognized ancestral and variant epitopes versus distinct populations of T cells that were mono-reactive for ancestral or variant epitopes. We found the majority of spike-specific T cells cross-recognized the ancestral spike and the XBB.1.5 and BA.2.86 subvariants, with less than 10% of T cells being mono-reactive for either variant. Interestingly, immunization with the XBB.1.5 monovalent booster vaccine did not significantly increase the percentage of XBB.1.5 mono-reactive T cells. Our results suggest a potential limitation in the induction of mono-reactive T cell responses by variant-specific booster vaccines.

Discover the shifting landscape of SARS-CoV-2 variants from October to December 2023, with JN.1 dominating South and Southeast Asia wastewater samples, increasing from <10% to >90%. Experience the dynamic evolution of viral strains in this period.