Recommendable! Another step towards defeating disease causing viruses!
"Distinguishing between self and non-self is a critical ability of the immune system. Some pathogens have evolved proteins that resemble those of their host, a mechanism called molecular mimicry, in an attempt to evade this surveillance system. However, immune training isn’t perfect, so host cells that recognize self-proteins occasionally slip into the milieu.
Previous work on molecular mimicry focused on the 3D structure of proteins, which is important for antibody-mediated immune recognition, but T cells typically recognize short, linear peptide sequences. Studies of mimicry in these short sequences often focus on a subset of viruses or suspected proteins.
Now, researchers have performed a more comprehensive analysis, screening more than 100 human-infecting viruses for mimicry in short, linear peptide sequences. They demonstrated that this phenomenon is widespread across the virome. These findings ... could help researchers explore novel autoimmune triggers and potential interventions. ..."
From the abstract:
"Mimicry of host protein structures, or ‘molecular mimicry’, is a common mechanism employed by viruses to evade the host’s immune system. Short linear amino acid (AA) molecular mimics can elicit cross-reactive antibodies and T cells from the host, but the prevalence of such mimics throughout the human virome has not been fully explored.
Here we evaluate 134 human-infecting viruses and find significant usage of linear mimicry across the virome, particularly those in the Herpesviridae and Poxviridae families.
Furthermore, host proteins related to cellular replication and inflammation, autosomes, the X chromosome, and thymic cells are enriched as viral mimicry targets.
Finally, we find that short linear mimicry from Epstein-Barr virus (EBV) is higher in auto-antibodies found in patients with multiple sclerosis than previously appreciated.
Our results thus hint that human-infecting viruses leverage mimicry in the course of their infection, and that such mimicry may contribute to autoimmunity, thereby prompting potential targets for therapies."
Fig. 1: Molecular mimicry across human infecting viruses.
No comments:
Post a Comment