The emergence of XBB.1.16 has gained rapid global prominence. Previous studies have elucidated that the infection of SARS-CoV-2 induces alterations in the mitochondrial integrity of host cells, subsequently influencing the cellular response to infection. In this study, we compared the differences in infectivity and pathogenicity between XBB.1.16 and the parental Omicron sublineages BA.1 and BA.2 and assessed their impact on host mitochondria. Our findings suggest that, in comparison with BA.1 and BA.2, XBB.1.16 exhibits more efficient spike protein cleavage, more efficient mediating syncytia formation, mild mitochondriopathy, and less pathogenicity. Altogether, our investigations suggest that, based on the mutation of key sites, XBB.1.16 exhibited enhanced infectivity but lower pathogenicity. This will help us to further investigate the biological functions of key mutation sites.
Keyphrases
- sars cov
- biofilm formation
- respiratory syndrome coronavirus
- induced apoptosis
- oxidative stress
- cell cycle arrest
- cell death
- hiv infected
- staphylococcus aureus
- pseudomonas aeruginosa
- reactive oxygen species
- antiretroviral therapy
- cell proliferation
- hiv infected patients
- endoplasmic reticulum stress
- case control
- signaling pathway
- coronavirus disease
- quantum dots