Fluvoxamine reverses PTGS2 gene expression and cellular metabolism changes caused by SARS-CoV-2 N protein

Presenter Major

Biology (Pre-Med Track)

Presentation Type

Poster

Location

Hays Theatre, Wilbur Arts Building

Start Date

26-4-2024 10:45 AM

End Date

26-4-2024 11:30 AM

Description (Abstract)

Statement of the Problem/Background

Patients with long COVID can suffer from neurological problems, such as brain fog, and dizziness.

Research Question/Hypothesis
Fluvoxamine, a selective serotonin-uptake inhibitor can decrease the levels of inflammation in microglia cells protein transfected with the SARS-CoV-2 N protein.

Research Design/Methods Used in the Investigation
Using the protein transfection reagent, Proteojuice (Sigma Aldrich), the SARS-CoV-2 N-protein was transfected into cultured murine microglial BV2 cells (CRL-2469) along with a vehicle control. Cells were analyzed at 2 time points post transfection (48 hrs, ~6/7 days) by MTT assay to measure cellular metabolic activity, and cells were harvested for RT-PCR. At 5 days post transfection a subset of transfected cells were incubated in fluvoxamine, then analyzed by MTT assay and RT-PCR.

Results/Summary of the Investigation
BV2 cells transfected by SAR-CoV-2 N protein showed reduced expression levels of Glyceraldehyde phosphate dehydrogenase (GAPDH) an important enzyme in cellular metabolism, and increased levels of Prostaglandin Endoperoxidase Synthase 2 (PTGS2) a gene involved in inflammation with a more pronounced effect at 6/7 days. MTT assay showed decreased metabolic activity in transfected cells compared to controls at both 2 days and 7 days. Incubation in Fluvoxamine for 24 hours reversed both the gene expression and cellular metabolism effects.

Interpretation/Conclusion of the Investigation
SAR-CoV-2 reduces cellular metabolism and increases inflammation in N-protein transfected cells. This may explain the fatigue that is associated with COVID19. Further, we show that the N-protein alone is sufficient in creating these negative effects. Fluvoxamine should be further investigated as a medication used to alleviate neurological long COVID symptoms.

Keywords

SARS-CoV-2, COVID, Fluvoxamine

Related Pillar(s)

Community, Study

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Apr 26th, 10:45 AM Apr 26th, 11:30 AM

Fluvoxamine reverses PTGS2 gene expression and cellular metabolism changes caused by SARS-CoV-2 N protein

Hays Theatre, Wilbur Arts Building

Statement of the Problem/Background

Patients with long COVID can suffer from neurological problems, such as brain fog, and dizziness.

Research Question/Hypothesis
Fluvoxamine, a selective serotonin-uptake inhibitor can decrease the levels of inflammation in microglia cells protein transfected with the SARS-CoV-2 N protein.

Research Design/Methods Used in the Investigation
Using the protein transfection reagent, Proteojuice (Sigma Aldrich), the SARS-CoV-2 N-protein was transfected into cultured murine microglial BV2 cells (CRL-2469) along with a vehicle control. Cells were analyzed at 2 time points post transfection (48 hrs, ~6/7 days) by MTT assay to measure cellular metabolic activity, and cells were harvested for RT-PCR. At 5 days post transfection a subset of transfected cells were incubated in fluvoxamine, then analyzed by MTT assay and RT-PCR.

Results/Summary of the Investigation
BV2 cells transfected by SAR-CoV-2 N protein showed reduced expression levels of Glyceraldehyde phosphate dehydrogenase (GAPDH) an important enzyme in cellular metabolism, and increased levels of Prostaglandin Endoperoxidase Synthase 2 (PTGS2) a gene involved in inflammation with a more pronounced effect at 6/7 days. MTT assay showed decreased metabolic activity in transfected cells compared to controls at both 2 days and 7 days. Incubation in Fluvoxamine for 24 hours reversed both the gene expression and cellular metabolism effects.

Interpretation/Conclusion of the Investigation
SAR-CoV-2 reduces cellular metabolism and increases inflammation in N-protein transfected cells. This may explain the fatigue that is associated with COVID19. Further, we show that the N-protein alone is sufficient in creating these negative effects. Fluvoxamine should be further investigated as a medication used to alleviate neurological long COVID symptoms.