Prologue: July 2023
Once upon a time, in a world plagued by a persistent and invisible threat known as pathogens, millions of people found themselves grappling with varying degrees of illness. Though the pathogens causing these diseases were the same, the outcomes ranged from recovery to fatality, leaving scientists and healthcare professionals eager to understand the factors that determined such diversity.
In the realm of scientific research, next-generation sequencing offered a glimmer of hope, providing a glimpse into the vicious battle between the host cells and the invading pathogens. As researchers focused on the fluctuations in gene expressions, they stumbled upon a hidden gem, an essential mechanism known as alternative splicing (AS). This cellular process occurring within the host cell, transforming the pre-messenger RNA (pre-mRNA) cadets into functional mRNA troopers, revealed a world of possibilities.
In this cellular boot camp, different exons (coding regions) of a gene were selectively included and excluded during the formation of mature mRNA. With a robust army of proteins and RNA molecules, the spliceosome took centre stage, orchestrating the splicing process. The result? Multiple protein isoforms from a single gene, with distinct functions, enriching the proteome despite their shared genetic origins. These isoforms became the brave soldiers of the cellular army, ready to face the onslaught of infectious diseases with diverse capabilities.
Alternative splicing took on the role of a key player in controlling gene expression, subtly influencing the function, stability, and subcellular localization of genes. Its importance, however, didn’t go unnoticed by pathogens seeking to infiltrate and conquer host cells.
These microscopic adversaries had developed a keen interest in alternative splicing, developing cunning strategies to manipulate the host’s cellular machinery for their own benefit. Like skilled infiltrators, they learned to exploit the spliceosome, to enhance their replication and promote pathogenesis. Their actions extended to critical host genes involved in immune responses and other vital cellular activities.
In the midst of this captivating tale, a pertinent question emerged—what could these hidden intricacies mean for diverse clinical severities suffered by millions of people? Could they unlock new insights into disease progression and offer novel therapeutic opportunities?
The answers to these questions remained a mystery, waiting to be unraveled by dedicated researchers. Though the significance of alternative splicing in cellular responses during infection was becoming evident, its full clinical implications remained veiled, urging the scientific community to embark on a new journey of discovery.
As the quest for knowledge continued, scientists delved deeper into the nuances of alternative splicing in infectious diseases. They sought to decipher the hidden language of isoforms and understand how they influenced the host’s immune response and other critical cellular functions. Perhaps, within these molecular secrets lay the keys to novel therapeutic avenues, holding the promise of effective treatments to counter the relentless pathogens.Though still in its early chapters, the tale of alternative splicing in infectious diseases was a timeless and ever-evolving narrative. The future held promises of enriched understanding and improved patient outcomes.
Priyanka Mehta
I am Priyanka Mehta, a bioinformatician actively pursuing my Ph.D. in Dr. Rajesh Pandey's lab. My research focuses on elucidating the role of alternative splicing in modulating the severity of infectious diseases. Besides my scientific endeavors, I am deeply passionate about creating captivating data visualizations that can tell compelling stories about complex datasets. With an artist's heart and a curious mind, I envision bridging the gap between science and art to effectively communicate my research findings. My goal is to contribute valuable insights that will advance bioinformatics research and enhance our understanding of infectious diseases.