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 named ‘miPepBase’. This database contains detailed information about mimicry peptides and proteins and autoimmune diseases that might develop due to molecular mimicry between host and pathogen proteins. Our research paper was published in Frontiers in Microbiology in 2018 [PMID: 29109711].
Being a student of biology and biotechnology, I had very little knowledge of programing languages. But when I enrolled myself for a PhD programme in bioinformatics, I learnt as much as I could about scripting languages and webpage designing. It took us months to compile the data on molecular mimicry and almost a year to design miPepBase. But this proved to be a worthy exercise because during this process, I learnt several prospects and aspects of molecular mimicry. One of them was that molecular mimicry was not a random phenomenon; it was a well-planned and carefully orchestrated strategy presented by a number
of pathogenic microbes.
Second, it helped brush up
our school of thought that Mycobacterium tuberculosis
(Mtb), widely believed to
cause the deadly disease
tuberculosis (TB), might also be
involved in several autoimmune
diseases. In this context, an
interesting observation was
reported by some scientists;
while treating patients with
TB, they observed numerous
clinical events associated with
autoimmune diseases. One
of them was Poncet’s disease
an inflammatory polyarthritis
autoimmune disease that was
observed in cured patients with TB. It would be pertinent to mention that recent studies suggest that mycobacterial infections might have driven autoimmunity as an evolutionary
Ms. Anjali Garg || 453
strategy, and proteins involved in molecular mimicry are produced in the host long before the appearance of the symptoms of TB. But the pathology of TB, in terms of autoimmune diseases, is an overlooked event.
This paved way for our another study published in Drug Discovery Today in 2018 (PMID: 30366058) in which we worked on the possibility of using molecular mimicry to discover new drug targets and drug molecules using a pathogen’s molecular- mimicry-inducing proteins. The identification has been made with the use of an interaction network of pathogen (Mtb) mimicry proteins to findoutthepathwaysdirectlyinfluencedbyit. Then, we systematically analyzed each node of the metabolic network to identify points that, if blocked, would lead to choking of that metabolic pathway. Finding targets for Mtb is just like deep-sea salvaging. With the help of this approach, we found many Mtb metabolic
chokepoint proteins that could serve as ideal drug targets. Further, we explored the possibility of drug repurposing, that is, using already available the Food and Drug Administration (FDA)-approved drugs for inhibiting these drug targets. Through rigorous in silico experiments, we were able to find four experimental FDA-approved drugs that could be used against the five metabolic chokepoint proteins identified by us.
In addition, we observed that these drug targets were not involved in any active physiological process or
protein(s) responsible for establishing TB bacteria inside the host. Thus, their disruption can be used as a prophylactic measure against TB before the onset of active TB infection.
   Molecular mimicry can be defined as structural, functional or immunological similarity between the host and pathogen macromolecules. Molecular mimicry can be present in the form of complete identity or homology at the protein level, or as a similarity in the sequences of amino acids or as a structural similarity between the host and pathogen proteins.
  







































































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