SARS-CoV-2 XEC variant exhibited a higher pseudovirus infectivity and immune evasion compared to KP.3, indicating that XEC will be a predominant SARS-CoV-2 variant in the near future.
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Some features of the SARS-CoV-2
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The SARS-CoV-2 spike protein acts as an allosteric agonist of β-adrenergic receptors and contributes to sympathetic hyperactivity
This study is the first to show that the SARS-CoV-2 spike protein activates β-adrenergic receptors in cardiomyocytes, contributes to cardiac sympathetic hyperactivity and increases activation of downstream β-adrenergic receptor signaling induced by epinephrine.
Histamine receptor H1 binds directly to the N-terminal domain on the SARS-CoV-2 S1 protein and acts as an ACE2-independent receptor for SARS-CoV-2, but also synergistically interacts with ACE2 and facilitates ACE2-dependent viral entry (antihistamines could be a potential treatment for COVID-19)
Histamine receptor H1 acts as an independent receptor for SARS-CoV-2. The antihistamine drugs effectively inhibited the binding of H1R to the S protein and viral infection.
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SARS-CoV-2 variant KP.2 (JN.1.11.1.2) exhibits increased immune resistance
This study showed an increased immune resistance of KP.2 variant and its ability to evade neutralizing antibodies to a greater extent than previous variants, including JN.1.
Prion-like domains in the SARS-CoV-2 spike protein
Different beta-coronaviruses (β-CoVs) contain prion-like domains in the S proteins. However, SARS-CoV-2 is the only β-CoV with prion-like domains identified within the receptor-binding domain (RBD) of the S protein.
The receptor binding domain of SARS-CoV-2 S1 subunit binds to kidney injury molecule-1, which is highly expressed upon kidney injury
The receptor binding domain (RBD) of SARS-CoV-2 binds to kidney injury molecule-1 (KIM1), which is highly expresed only upon kidney injury.
SARS-CoV-2 spike protein activates the epidermal growth factor receptor (EGFR), its downstream signaling pathways and the anti-apoptotic protein survivin
SARS-CoV-2 S1 subunit and RBD activate the EGFR and its downstream signaling pathways and increase the expression and activation of the anti-apoptotic protein survivin.
The classification of SARS-CoV-2 variants into five serotypes based on the antigenicity of the receptor-binding domain
Chinese researchers propose the classification of SARS-CoV-2 variants into five serotypes based on the antigenicity of the receptor-binding domain
The bacterial lipopolysaccharide binds to the SARS-CoV-2 spike protein and drives the formation of large S protein aggregates
These findings have established a significant link between excessive inflammation during SARS-CoV-2 infection and comorbidities associated with increased levels of bacterial endotoxins. This synergism between LPS and the S protein is of clinical and therapeutic importance.
Omicron variants may have been artificially synthesized rather than naturally formed
The authors emphasized that the Omicron isolates BA.1, BA.1.1, and BA.2 are formed by a completely new mechanism that cannot be explained by previous biology and that it is highly unlikely that these viruses arose spontaneously.
TMEM106B protein can serve as an alternative receptor for SARS-CoV-2 entry into ACE2-negative host cells
TMEM106B, a lysosomal transmembrane protein, can serve as an alternative receptor for the entry of severe acute respiratory syndrome coronavirus 2 into the angiotensin-converting enzyme 2 receptor-negative cells.
The “bacteriophage-like” behavior of SARS-CoV-2 (the SARS-CoV-2 genome can replicate outside the human body)
The interaction between fecal bacteria and the SARS-CoV-2 suggests a ‘bacteriophage-like’ behavior of SARS-CoV-2.
Delta variant of the SARS-CoV-2 increased the volumes of environmental biofilms and remained viable for up to five days
The virus was viable for up to five days with and without an environmental biofilm on all surfaces tested. The SARS-CoV-2 viability was highly correlated with the microorganisms forming the biofilms.
SARS-CoV-2 S1 protein is electrically conductive and reacts with gold, silicon, copper, and platinum electrodes and denatures. A method of coronavirus deactivation?
These findings provide new opportunities for developing coronavirus-capturing materials that are capable of irreversibly trapping the virus via strong covalent bonds.
