Rotavirus Genome Replication and Virion Assembly

NIH Pandemic-Era Grants

Pandemic Era Grants

2024

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Principal Investigator: Deborah F Kelly
Organization: WAKE FOREST UNIVERSITY
Fiscal Year: 2024
Award: $458,225
Funding agency: National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY/ABSTRACT (DESCRIPTION): 
 
RNA viruses can be devastating human pathogens that impart large medical and economic burdens to society 
(e.g.,  SARS-­CoV-­2,  influenza  A  virus,  Ebola  virus,  rotavirus,  etc.).  While  these  viruses  can  differ  quite 
dramatically  in  their  pathogenesis,  they  share  a  common  replication  feature—they  must  synthesize  new  RNA 
molecules from RNA templates. Because host cell enzymes lack this activity, RNA viruses encode a specialized 
RNA-­dependent  RNA  polymerase  (RdRp).  Viral  RdRps  are  structurally-­  and  functionally-­conserved  among 
diverse  RNA  viral  families,  and  they  directly  catalyze  all  stages  of  viral  transcription  and  genome  replication. 
However, these enzymes rarely function alone in the context of infected cells. Instead, the viral RdRps are tightly 
regulated  by  other proteins  in  multi-­subunit  transcriptase/replicase  complexes  so  as  to  maximize  the  type and 
timing of viral RNA synthesis. The overall objective of this application is to gain mechanistic insight into RdRp 
regulation for rotavirus—an 11-­segmented, double-­stranded (ds) RNA virus that causes life-­threatening diarrhea 
in young children. The rotavirus VP1 RdRp functions only when bound beneath the icosahedral VP2 core shell 
layer of intact, or partially intact, particles. Engagement of VP1 by VP2 during early particle assembly activates 
the  RdRp  so  that  it  functions  as  a  replicase,  converting  packaged,  single-­stranded  positive  sense  (+)  RNA 
templates  into  dsRNA  genome  segments.  Early  assembly  intermediates  then  morph  into  double-­layered 
particles,  wherein  the  VP2-­bound,  VP1  RdRp  switches  to  a  transcriptase  activity,  synthesizing  +RNAs  using 
dsRNA  templates.  Still,  major  gaps  in  knowledge  remain  about  the  structure  of  the  VP1  RdRp  as  a  replicase 
during  dsRNA  synthesis  and  its  regulation  by  the  VP2  core  shell  protein.  Here,  well-­established  in  vitro 
biochemical and genetic techniques are combined with state-­of-­the-­art structural approaches to close these gaps 
in knowledge and inform a deep understanding of rotavirus RdRp regulation. AIM 1 will elucidate VP2 core shell 
determinants critical for VP1 replicase activity, and AIM 2 will determine the first-­ever in situ 3D atomic structures 
of VP1 as a replicase in both ice (using cryo-­EM) and liquid (using a microfluidics system). The work outlined in 
this application is significant, as it is expected to reveal detailed structure-­function information about the rotavirus 
RdRp that could be applied to rational antiviral drug design. 
 
 
 
 
 
 

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