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PXD019113-2 The Global Phosphorylation Landscape of SARS-CoV-2 Infection [Reanalysis: PXD019113]

ABSTRACT: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the coronavirus disease 2019 (COVID-19) pandemic, has infected over 3 million people worldwide and caused over 200,000 deaths since it emerged in late 2019. There is an urgent need to develop therapies that can limit SARS-CoV-2 infection, replication, and pathogenesis. Due to the rapid emergence of SARS-CoV-2, there currently exists a lack in the knowledge of the host cellular pathways that sustain infection and contribute to pathogenesis. Here, we present a quantitative proteomics and phosphoproteomics survey of SARS-CoV-2 infection in Vero-E6 cells. [Original project description]

ORGANISM(S): Cell Culture

SUBMITTER: Yasushi Ishihama

PROVIDER: RPXD034684 | JPOST Repository | Sat Mar 25 00:00:00 GMT 2023

REPOSITORIES: jPOST

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			Action	DRS
	LP1_03_phos_DDA_111.maxq.txt	Txt
	LP1_03_phos_DDA_111.txt	Txt
	LP1_05_phos_DDA_114.maxq.txt	Txt
	LP1_05_phos_DDA_114.txt	Txt
	LP1_07_phos_DDA_122.maxq.txt	Txt

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The Global Phosphorylation Landscape of SARS-CoV-2 Infection

Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the coronavirus disease 2019 (COVID-19) pandemic, has infected over 3 million people worldwide and caused over 200,000 deaths since it emerged in late 2019. There is an urgent need to develop therapies that can limit SARS-CoV-2 infection, replication, and pathogenesis. Due to the rapid emergence of SARS-CoV-2, there currently exists a lack in the knowledge of the host cellular pathways that sustain infection and contribute to pathogenesis. Here, we present a quantitative proteomics and phosphoproteomics survey of SARS-CoV-2 infection in Vero-E6 cells.

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PXD019113-1 The Global Phosphorylation Landscape of SARS-CoV-2 Infection [Reanalysis: PXD019113]

2023-03-25 | RPXD034683 | JPOST Repository

The Global Phosphorylation Landscape of SARS-CoV-2 Infection

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Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been identified as the cause of the Coronavirus disease 19 (COVID-19), which was initially reported in December 2019 in China and has since rapidly spread worldwide. Since then, the COVID-19 pandemic has caused a detrimental effect of the national health care system, causing a drastic reduction of the screening programs for colorectal cancer and requiring the redistribution of the hospital resources from elective surgery to the care of patients with SARS-Cov_2 infection requiring admission.

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Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the ongoing coronavirus disease 19 (COVID-19) pandemic. Despite the urgent need, we still do not fully understand the molecular basis of SARS-CoV-2 pathogenesis and its ability to antagonize innate immune responses. Here, we use RNA-sequencing and ribosome profiling along SARS-CoV-2 infection and comprehensively define the mechanisms that are utilized by SARS-CoV-2 to shutoff cellular protein synthesis. We show SARS-CoV-2 infection leads to a global reduction in translation but that viral transcripts are not preferentially translated. Instead, we reveal that infection leads to accelerated degradation of cytosolic cellular mRNAs which facilitates viral takeover of the mRNA pool in infected cells. Moreover, we show that the translation of transcripts whose expression is induced in response to infection, including innate immune genes, is impaired, implying infection prevents newly transcribed cellular mRNAs from accessing the ribosomes. Overall, our results uncover the multipronged strategy employed by SARS-CoV-2 to commandeer the translation machinery and to suppress host defenses.

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Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of the coronavirus disease-19 (COVID-19) pandemic, was identified in late 2019 and went on to cause over 3.3 million deaths in 15 months. To date, targeted antiviral interventions against COVID-19 are limited. The spectrum of SARS-CoV-2 infection ranges from asymptomatic to fatal disease. However, the reasons for varying outcomes to SARS-CoV-2 infection are yet to be elucidated. Here we show that an endogenously activated interferon lambda (IFNλ) pathway leads to resistance against SARS-CoV-2 infection. Using a well-differentiated primary nasal epithelial cell (WD-PNEC) model from multiple adult donors, we discovered that susceptibility to SARS-CoV-2 infection, but not respiratory syncytial virus (RSV) infection, varied. One of four donors was resistant to SARS-CoV-2 infection. High baseline IFNλ expression levels and associated interferon stimulated genes correlated with resistance to SARS-CoV-2 infection. Inhibition of the JAK/STAT pathway in WD-PNECs with high endogenous IFNλ secretion resulted in higher SARS-CoV-2 titres. Conversely, prophylactic IFNλ treatment of WD-PNECs susceptible to infection resulted in reduced viral titres. An endogenously activated IFNλ response, possibly due to genetic differences, may be one explanation for the differences in susceptibility to SARS-CoV-2 infection in humans.

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RNA-Seq of Human iPSC-cardiomyocytes infected with SARS-CoV-2

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