What is ciTRAN?

Researchers at the Indian Institute of Science Education and Research (IISER) in Bhopal have made a groundbreaking discovery in the realm of HIV-1 research. They have identified a Circular RNA virus, named ciTRAN, the role of which has long remained enigmatic in the context of HIV-1 virus replication. Furthermore, they have developed a molecule with the potential to disrupt viral transcription, opening up new avenues for combating HIV-1.

The Enigmatic World of Circular RNA

Circular RNA, or circRNA, is a crucial player in regulating gene expression and governing various biological processes. Despite its importance, the impact of circRNA expression on HIV-1 replication has largely eluded scientists until now.

Unveiling ciTRAN’s Role in HIV-1 Replication

In a study, researchers at IISER Bhopal deployed a specialized protocol called circDR-Seq, utilizing direct RNA nanopore sequencing. Through this innovative approach, they were able to capture circRNAs from HIV-1-infected T cells (white blood cells) and pinpointed the existence of ciTRAN, a circRNA that exerts influence over HIV-1 transcription.

Potential for Novel Drugs and Therapies

Understanding how ciTRAN modulates the transcription process of the virus could be a game-changer in the fight against HIV-1. This newfound knowledge opens doors to the development of novel drugs and therapies to combat this persistent virus.

The Interplay with HIV-1 VpR

HIV-1 viral protein R (VpR) is a versatile protein that assumes specific roles at various stages of the HIV-1 viral life cycle, impacting the anti-HIV functions of immune cells. The researchers uncovered that HIV-1 infection triggers the expression of ciTRAN, and this process is dependent on Vpr. CiTRAN interacts with serine/arginine-rich splicing factor 1 (SRSF1), a protein known for repressing HIV-1 transcription.

The Intricate Mechanism

The study reveals that HIV-1 capitalizes on ciTRAN, which undergoes alterations during immunological signaling, inflammation, and viral infection. This manipulation prevents SRSF1 from carrying out its repressive function, thereby facilitating efficient viral transcription.

Creating a Molecule to Disrupt Viral Transcription

The research team’s efforts also led to the creation of a molecule inspired by SRSF1. This mimic has the potential to inhibit viral transcription, regardless of ciTRAN induction. This development underscores how HIV-1 exploits a host circRNA, shedding light on a previously unknown aspect of how primate lentiviruses overcome transmission barriers.

A Breakthrough in Overcoming Transmission Barriers

The study’s findings reveal how the HIV-1 virus seizes the host-encoded ciTRAN to multiply efficiently, uncovering a previously undisclosed facet of how viruses like HIV-1 surmount transmission hurdles. This discovery holds immense promise for the development of new strategies to combat HIV-1 and enhance our understanding of viral infections.



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