Alcohol Consumption Modulates the Development of Chronic Pain in COVID-19 Patients: A Network Meta-Analysis

Figures

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  Figure 1. Impact of alcohol exposure on discomfort. (A) Venn diagram showing 138 molecules, which are commonly shared between EtOH and discomfort. (B) EtOH simulation of activation of the overlapping molecules between EtOH and discomfort that participate in the inhibition of discomfort or pain. Orange connecting lines indicate activation, blue indicate inhibition, and gray indicate that the z-score is zero and no prediction can be made.

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  Figure 2. Impact of alcohol and SARS-CoV-2 infection on discomfort. (A) Venn diagram showing 134 molecules were found to be commonly shared between EtOH (859 molecules) and SARS-CoV-2 infection (1035 molecules). (B) EtOH simulation activation of the overlapping molecules between EtOH and COVID-19 resulted in increased discomfort. Orange connecting lines indicate activation, blue indicate inhibition, and gray indicate that the z-score is zero and no prediction can be made.

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  Figure 3. Summary of the core analysis: the figure shows the top signaling pathways and functions and the upstream regulators that mediate the observed activation (orange) or inhibition (blue) of the signaling pathways and functions in the (A) PFC, (B) Amygdala of COVID-19 patients.

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  Figure 4. SARS-CoV-2 infection triggers upstream regulator IFNAR results in the activation of the DEGs in the data set and modulates the activation of immune response of cells in the PFC.

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  Figure 5. SARS-CoV-2 infection triggers upstream regulators, which results in the activation of the DEGs including CSF1, RNF213, SMD, PSM8, IF135, MX1, ISG15, OAS3, EPST1, TRIM5, IRF7, and RELB, and inhibition APP, IGF1, and DNM3, these activation and inhibition of the DEGs modulates progressive neuromuscular disease, and motor neuron disease, progressive neuropathy, and neuromuscular disease with neuropathy in the amygdala of the COVID-19 patients.

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  Figure 6. Impact of EtOH exposure on various pain nodes in IPA. (A) EtOH and SARS-CoV-2 infection induced DEGs commonly shared molecules in the PFC. Enhancement of EtOH in simulation results in increased (B) discomfort, (C) neuropathic pain, and (D) inflammatory pain remained unchanged.

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  Figure 7. Impact of EtOH exposure on various pain nodes in IPA. (A) EtOH and SARS-CoV-2 infection induced DEGs commonly shared molecules (A) commonly in the amygdala. Enhancement of EtOH in simulation results in an increase in (B) discomfort and (C) inflammatory pain but (D) neuropathic pain remained unchanged.