Extracellular Vesicles or EVs are host membrane-bound submicron particles released by cells meant for intercellular communication. They are known to carry proteins, lipids, miRNAs, etc. EVs are classified as exosomes (50-150 nm), microvesicles (200- 1000 nm), and apoptotic bodies (above 1000 nm). RNA Viruses have been observed to hijack the host machinery by which these vesicles are released and utilize them for their egress. By escaping inside EVs help viruses to get packaged inside one vesicle in numbers enhancing their multiplicity of infection (MOI) while invading a new host. Currently, in our laboratory, we are asking questions like what is the molecular mechanism by which the viruses are hijacking the host packaging center to egress out? What is the role of other components like miRNA being packaged along with viruses in viral infectivity?    

Lipid droplets are single membrane-bound organelles with a phospholipid monolayer surrounding a core of neutral lipids, such as triglycerides and cholesterol esters. Unlike the bilayer membranes of most cellular organelles, this monolayer plays a unique role during RNA virus invasion. Upon viral entry, lipid droplet secretion is significantly increased. This phenomenon supports the viral life cycle by providing a surface for replication and modulating the host's interferon responses. Additionally, lipid droplets undergo rapid lipophagy, releasing ATP that viruses utilize for their propagation. We have also observed novel intra-organellar trafficking of viruses during this process.

Our research focuses on modulating lipid droplet secretion to disrupt viral propagation, with the aim of developing new antiviral strategies.

In our research, we delve into the complex interactions between enteric viruses, like Rotavirus, and respiratory viruses, such as Coronavirus, within mammary tissue. We aim to uncover how these viruses engage with the host environment, particularly focusing on their persistence in mucosal tissues. By analyzing transcriptomic differences between infected and uninfected cells, we seek to identify the key factors that enable viral survival and persistence. Understanding these interactions will provide critical insights into how these pathogens evade the immune system and establish long-term presence in mucosal tissues.

Our ultimate objective is to leverage this knowledge to enhance vaccination strategies for neonates, aiming to develop more effective protective measures against these viral infections at the earliest stages of life.