Wnt-Independent SARS-CoV-2 Infection in Pulmonary Epithelial Cells

Koval, Alexey; Xu, Jiabin; Williams, Nathalia; Schmolke, Mirco; Krause, Karl‐Heinz; Katanaev, Vladimir L.

doi:10.1128/spectrum.04827-22

Cited by 3 publications

(3 citation statements)

References 42 publications

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“…Chatterjee et al were the first to demonstrate the role of β-catenin in SARS-CoV-2 infection by iCRT-14 treatment and β-catenin silencing in Vero cells, which have both effectively reduced virus infection [ 17 ]. On the other hand, Koval et al had tested several Wnt inhibitors, namely clofazimine, MU17, F2-99 and ICG-001, in Calu-3 and A549-ACE2-TMPRSS2 cells and have shown no significant inhibition in SARS-CoV-2 infection, hence contradicting the initial observations of the possible role of the canonical signaling pathway for SARS-CoV-2 infection [ 18 ]. Nonetheless, our findings agree with those of Chatterjee et al that the canonical Wnt signaling pathway is important for SARS-CoV-2 infection.…”

Section: Discussionmentioning

confidence: 98%

“…Wnt3a has been studied in several viruses, such as influenza virus, Rift Valley Fever virus (RVFV) and pseudorabies virus [ 10 , 11 , 12 , 13 , 14 , 15 , 16 ]. However, conflicting studies made the involvement of Wnt in SARS-CoV-2 infection inconclusive [ 17 , 18 ]. Chatterjee et al showed that silencing β-catenin expression and inhibiting its activity reduced virus infection [ 17 ], whereas Koval et al demonstrated that the addition of several Wnt inhibitors has no effect on SARS-CoV-2 infection [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

“…However, conflicting studies made the involvement of Wnt in SARS-CoV-2 infection inconclusive [ 17 , 18 ]. Chatterjee et al showed that silencing β-catenin expression and inhibiting its activity reduced virus infection [ 17 ], whereas Koval et al demonstrated that the addition of several Wnt inhibitors has no effect on SARS-CoV-2 infection [ 18 ]. In this study, we validated its importance and elucidated its role in SARS-CoV-2 infection.…”

Section: Introductionmentioning

confidence: 99%

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Wnt3a Facilitates SARS-CoV-2 Pseudovirus Entry into Cells

Melano,

Chen,

Ngwira

et al. 2023

IJMS

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How ACE2 functions as the major host receptor of SARS-CoV-2 despite having low expression in the lungs is still unknown. To facilitate the development of therapeutic strategies against coronaviruses, gaining a deeper comprehension of the molecular mechanism of SARS-CoV-2 infection is imperative. In our previous study, we identified several potential host factors of SARS-CoV-2 using an shRNA arrayed screen, one of which was Wnt3a. Here, we validated the significance of Wnt3a, a potent activator of the Wnt/β-catenin signaling pathway, for SARS-CoV-2 entry into cells by evaluating the effects of its knockdown and overexpression on SARS-CoV-2 pseudotyped virus entry. Further analysis revealed that SARS-CoV-2 pseudotyped virus infection activates the canonical Wnt/β-catenin signaling pathway, which we found could subsequently stimulate ACE2 transcription. Collectively, our study identified Wnt3a as an important host factor that facilitates ACE2-mediated virus infection. Insight into the virus entry mechanism is impactful as it will aid in developing novel therapeutic strategies against current and future coronavirus pandemics.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Wnt3a Facilitates SARS-CoV-2 Pseudovirus Entry into Cells

Melano,

Chen,

Ngwira

et al. 2023

IJMS

View full text Add to dashboard Cite

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Clofazimine: A journey of a drug

Xu,

Koval,

Katanaev

2023

Biomedicine & Pharmacotherapy

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1-L Transcription of SARS-CoV-2 Spike Protein S1 Subunit

Nahalka

2024

IJMS

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The COVID-19 pandemic prompted rapid research on SARS-CoV-2 pathogenicity. Consequently, new data can be used to advance the molecular understanding of SARS-CoV-2 infection. The present bioinformatics study discusses the “spikeopathy” at the molecular level and focuses on the possible post-transcriptional regulation of the SARS-CoV-2 spike protein S1 subunit in the host cell/tissue. A theoretical protein–RNA recognition code was used to check the compatibility of the SARS-CoV-2 spike protein S1 subunit with mRNAs in the human transcriptome (1-L transcription). The principle for this method is elucidated on the defined RNA binding protein GEMIN5 (gem nuclear organelle-associated protein 5) and RNU2-1 (U2 spliceosomal RNA). Using the method described here, it was shown that 45% of the genes/proteins identified by 1-L transcription of the SARS-CoV-2 spike protein S1 subunit are directly linked to COVID-19, 39% are indirectly linked to COVID-19, and 16% cannot currently be associated with COVID-19. The identified genes/proteins are associated with stroke, diabetes, and cardiac injury.

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Wnt-Independent SARS-CoV-2 Infection in Pulmonary Epithelial Cells

Cited by 3 publications

References 42 publications

Wnt3a Facilitates SARS-CoV-2 Pseudovirus Entry into Cells

Wnt3a Facilitates SARS-CoV-2 Pseudovirus Entry into Cells

Clofazimine: A journey of a drug

1-L Transcription of SARS-CoV-2 Spike Protein S1 Subunit

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