COVID-19 Infection as a Trigger for Seronegative Autoimmune Hepatitis: A Case Report

The patient denied any history of alcohol intake, substance abuse, over-the-counter or herbal medications, or family history of liver or autoimmune disease. The proposed mechanism of AIH development after COVID-19 infection is the molecular mimicry between spike protein S1 and multiple human tissue proteins. See PDF] Table 1. shows extensive hepatitis workup Laboratory test result Reference ALT 271 0-40 U/L AST 175 0-37 U/L ALP 38.9 40-129 U/L Antinuclear ab Negative Negative Anti Mitochondrial ab Negative Negative Anti Mitochondrial M2 ab Negative Negative Anti Smooth Muscle ab Negative Negative Anti Liver Kidney Microsomes Negative Negative Hepatitis B Core ab Reactive non-reactive Hepatitis B Core Ab IgM non-reactive non-reactive Hepatitis B Surface Antigen Non-reactive Non-reactive Hepatitis B e Ab Non-reactive Non-reactive Hepatitis B e Antigen Non-reactive Non-reactive Hepatitis A Ab IgM Non-reactive Non-reactive Hepatitis C Ab Non-reactive Non-reactive Hepatitis E IgG Reactive Non-reactive Hepatitis E IgM Non-reactive Non-reactive Herpes Simplex virus Ab IgM Non-reactive Non-reactive Parvovirus Ab IgM Non-reactive Non-reactive Alpha-1 anti-trypsin 37 20-53 µmol/L Ceruloplasmin 33 14 to 40 mg/dL CMV PCR Negative Negative EBV PCR Negative Negative HBV PCR Negative Negative

Prognostic tools and candidate drugs based on plasma proteomics of patients with severe COVID-19 complications.

COVID-19 complications still present a huge burden on healthcare systems and warrant predictive risk models to triage patients and inform early intervention. Here, we profile 893 plasma proteins from 50 severe and 50 mild-moderate COVID-19 patients, and 50 healthy controls, and show that 375 proteins are differentially expressed in the plasma of severe COVID-19 patients. These differentially expressed plasma proteins are implicated in the pathogenesis of COVID-19 and present targets for candidate drugs to prevent or treat severe complications. Based on the plasma proteomics and clinical lab tests, we also report a 12-plasma protein signature and a model of seven routine clinical tests that validate in an independent cohort as early risk predictors of COVID-19 severity and patient survival. The risk predictors and candidate drugs described in our study can be used and developed for personalized management of SARS-CoV-2 infected patients.