Severe acute respiratory syndrome coronavirus 2 strain:Omicron BA.1
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA888402 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21848564.fastq.gz | Fastqsanger.gz | |||
| SRR21848565.fastq.gz | Fastqsanger.gz | |||
| SRR21848566.fastq.gz | Fastqsanger.gz | |||
| SRR21848567.fastq.gz | Fastqsanger.gz | |||
| SRR21848967_subreads.fastq.gz | Fastqsanger.gz |
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Project description:The Coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains a global threat, exacerbated by the emergence of viral variants. Two recent variants of SARS-CoV-2, Omicron BA.2.75 and BA.5, have been reported globally, yet their precise characteristics are not well understood. In this study, we compared these two Omicron sub-lineages with the previously dominant Delta variant using a hACE2 knock-in mouse model. As expected, Delta exhibited higher viral replication in the lung and brain than both Omicron sub-lineages that induced less severe lung damage and immune activation. In contrast, the Omicron variants especially BA.5 showed a propensity for cellular proliferation and developmental pathways. Both Delta and BA.5 variants, but not BA.2.75, led to decreased pulmonary lymphocytes, indicating differential adaptive immune response. Neuroinvasiveness was shared with all strains, accompanied by vascular abnormalities, synaptic injury, and loss of astrocytes. However, Immunostaining assays and transcriptomic analysis showed that BA.5 displayed stronger immune suppression and neurodegeneration, while BA.2.75 exhibited more similar characteristics to Delta in the cortex. Such differentially infectious features could be partially attributed to the weakened interaction between Omicron Spike protein and host proteomes decoded via co-immunoprecipitation followed by mass spectrometry in neuronal cells. Our present study supports attenuated replication and pathogenicity of Omicron variants but also highlights their newly infectious characteristics in the lung and brain, especially with BA.5 demonstrating enhanced immune evasion and neural damage that could exacerbate neurological sequelae.
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Project description:The Omicron variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), first identified in November 2021 in South Africa, has initiated the 5th wave of global pandemics. Here, we systemically examined immunological and metabolic characteristics of Omicron variants infection. We found Omicron resisted to neutralizing antibody targeting receptor binding domain (RBD) of wild-type SARS-CoV-2. Omicron could not be neutralized by sera of Corona Virus Disease 2019 (COVID-19) convalescent individuals who were infected with the Delta variant. Through mass spectrometry on MHC-bound peptidomes, we found that the spike protein of the Omicron variants could generate additional CD8+ T cell epitopes, compared with Delta. These epitopes could induce robust CD8+ T cell responses. Moreover, we found booster vaccination increased the cross-memory CD8+ T cell responses against Omicron. Metabolic regulome analysis of Omicron-specific T cell showed a metabolic profile that promoted memory T cell responses. Consistently, a higher fraction of memory CD8+ T cells were found in Omicron stimulated peripheral blood mononuclear cells (PBMCs). In addition, CD147 was also a receptor for the Omicron variants, and CD147 antibody inhibited infection of Omicron. CD147-mediated Omicron infection in a human CD147 transgenic mouse model induced exudative alveolar pneumonia. Taken together, our data suggested that vaccination booster and receptor blocking antibody are two effective strategies against Omicron.
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