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Potential role of mitochondria-eating protein (MIEAP) in regulating H1N1 pathogenesis and replication Clinical Relevance Globally, influenza A virus (IAV) infects approximately 1 billion people every year, resulting in more than 3 million cases of severe clinical manifestations and more than 290 thousand respiratory deaths. IAV is an enveloped, negative-sense, segmented single-stranded RNA virus with a wide range of hosts including humans, birds, swine, horses, and marine mam

Rapid replication of RNA viruses requires substantial cellular energy and effective mechanisms to evade cellular immunity. To meet these demands, many RNA viruses manipulate mitochondrial dynamics, including mitochondrial fragmentation and mitophagy. In the upcoming hypothesis, I propose a potential role for mitochondria-eating protein (MIEAP, also known as SPATA18), a novel regulator of non-canonical mitophagy, in the cellular pathogenesis and replication of H1N1 influenza v

Using computational approaches and a custom chemical structure database, I designed several novel indole derivatives that may target orthoflavivirus NS1 protein and alleviate NS1-associated pathology. Several unpublished in vitro and in vivo findings supporting this hypothesis are presented.

Using computational approaches, I have designed novel indole derivatives that may target the orthoflavivirus non-structural NS1 protein.