Ajit Chande

We strive to understand how retroviruses evolve and what makes some (like HIV-1) highly pathogenic to humans. The overarching goal is to comprehend how various cellular processes control retrovirus replication at [i] protein levels and [ii] RNA levels and how this knowledge can be translated into [iii] developing efficient gene delivery vehicles and gene regulatory circuits.

Circular RNAs (circRNAs) are formed by back-splicing events that occur in both coding and non-coding linear transcripts. The back-splice junction connects two ends and distinguishes circRNAs from their linear counterpart. CircRNAs are abundant in immune cells, and several of them are deregulated during immunological signaling, inflammation, and viral infection. However, only a few circRNAs have been functionally characterized in the context of viral infection. During pathogenic conditions, circRNAs appear to assert a complex interplay between the host and the viruses. We employ high-throughput and modern sequencing technologies to explore the roles of circRNAs during HIV-1 infection. Our studies identified a significant role for a host-encoded circRNA that is hijacked by the virus for successful transmission.