Page 105 - CSIR-IGIB Annual Report 2020-21
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Pathogens’ Genome Architecture As equal stakes holder in the host-pathogen
Pathogens, irrespective of being with RNA or DNA interaction, host response at genetic and
backbone, are not a monolith. This is best transcriptional level is equally important with
exemplified with spectrum of variants of interest utmost emphasis on disease severity sub-
(VOI) and variants of concern (VOC) of SARS-CoV- phenotypes and clinical outcome. Challenging the
2 which had differential infectivity and global DOGMA of differences in the diseased patients
footprint. The underlying genomic mutations have compared to the healthy individuals and emphasis
been shown to be causal factor for increased on the disease severity sub-phenotypes is the core
immune escape potential and ability to area of focus in the lab. Towards this, our lab is
enter/infect the human host. In this background, working towards understanding the host
it is imperative to discover such functional response:
mutations with reduced sample to sequence time. • Differential gene expression modulating
An enabler towards this would be point-of-care disease sub-phenotypes (mild, moderate,
sequencing with an optimized analysis pipeline for severe and mortality),
inferring the result/s. Our lab has been at the • Differential expression of LncRNAs vis-à-
forefront of the SARS-CoV-2 genomic surveillance vis disease severity sub-phenotypes,
since its first footprint in India. Since then, we AI/ML based identification of clinical
identified important milestones of SARS-CoV-2 parameters important for risk
reinfections, vaccination breakthroughs, stratification,
discovering and tracking different VOCs, mobile • Role of cellular heterogeneity in disease
sequencing at Delhi airport for international severity.
travelers and leading a hub-and-spoke model for
MicroLab based pathogen sequencing. The Co-infections modulating disease severity sub-
genome information has to be threaded with the phenotypes
disease severity sub-phenotypes as well as clinical As pathogens challenge us they also make friends
outcome. with other co-habitants as well as the
microenvironment within the host. As with human
interactions, all co-habitants are not only friends;
some are foes as well with competing interests.
How does this interaction shape the clinical
outcome? Are they beneficial, inconsequential, or
harmful for the host? Can the co-infections be
surrogate for clinical phenotype and clinical
outcome?
We have investigated the role of co-infections in
modulating COVID-19 disease severity sub-
phenotypes of mild, moderate, severe and
mortality. This has advanced the field wherein we
are highlighting the role of co-presence of
bacterial species with observed clinical sub-
phenotypes albeit infected by the same pathogen
Host response (hardware and software) – SARS-CoV-2.
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