Immunoinformatics Study of Potential Molecular Mimicry between Viral T-Cell Epitopes and Human Peptides as an Underlying Mechanism of Autoimmunity

Abstract

There have been reports regarding the autoimmunity induced by SARS-CoV-2 in COVID-19 patients, such as: GBS, SLE, multiple sclerosis, demyelinating neuropathies, and orthostatic tachycardia syndrome, narcolepsy, even vaccine-induced. However, the exact mechanism is still unclear. One of possible reason is molecular mimicry, a condition in which the T-cell epitopes come from the virus antigens are similar with the peptide from human body proteins, hence the HTL and CTL recognizes them and perform the appropriate process to the cells, which result in destruction of normal tissues, leading to autoimmune condition. This study is a full computational biology (in-silico) approach to analyze the similarity between predicted SARS-CoV-2 proteins with human antigens by checking the affinity of the epitopes to bind with the MHC molecules. Several immune-informatics tools will be applied: NetCTLpan-1.1, NetMHCIIpan-4.0, IEDB, IFN-gamma epitope, and BLASTP.