Thesis
Immunoinformatics Study of Potential Molecular Mimicry between Viral T-Cell Epitopes and Human Peptides as an Underlying Mechanism of Autoimmunity
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.
No other version available