Presentation Title

Comparing the Structure of RNA Genomes from Virulent and Avirulent Strains of Coxsackievirus B3

Advisor Information

William Tapprich

Location

UNO Criss Library, Room 107

Presentation Type

Oral Presentation

Start Date

7-3-2014 3:30 PM

End Date

7-3-2014 3:45 PM

Abstract

The study of a viral structure, replication, and evolution is important for understanding how viruses cause disease. Coxsackievirus (CVB3) is a picornavirus that causes inflammation of the heart and pancreas with a particular pathogenicity in infants. Previous research has shown that the structure of the CVB3 RNA genome is responsible for virulence, with clear differences in structure between the genomes of virulent and avirulent strains of the virus. The CVB3 genome is comprised of a well-organized ssRNA beginning with a 5’ untranslated region (5’UTR). This 5’UTR contains an internal ribosome entry site (IRES), which drives translation of viral proteins. This study will determine how structural differences between the virulent and avirulent 5’UTR sequences influence interactions between viral RNA and host proteins. We hypothesize that viral interactions with the host protein, PCBP2, differ in virulent and avirulent 5’UTR sequences. Our lab has previously determined characteristics of PCBP2 interactions with the 5’UTR of a virulent strain (CVB328). We now focus on interactions of PCBP2 with the 5’UTR of an avirulent strain (CVB3GA). This will be done by monitoring PCBP2 affinity using electrophoresis mobility shift assays and PCBP2 influence on RNA structure through chemical probing. Results from this study may lead to new approaches for treating CVB3 infection.

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COinS
 
Mar 7th, 3:30 PM Mar 7th, 3:45 PM

Comparing the Structure of RNA Genomes from Virulent and Avirulent Strains of Coxsackievirus B3

UNO Criss Library, Room 107

The study of a viral structure, replication, and evolution is important for understanding how viruses cause disease. Coxsackievirus (CVB3) is a picornavirus that causes inflammation of the heart and pancreas with a particular pathogenicity in infants. Previous research has shown that the structure of the CVB3 RNA genome is responsible for virulence, with clear differences in structure between the genomes of virulent and avirulent strains of the virus. The CVB3 genome is comprised of a well-organized ssRNA beginning with a 5’ untranslated region (5’UTR). This 5’UTR contains an internal ribosome entry site (IRES), which drives translation of viral proteins. This study will determine how structural differences between the virulent and avirulent 5’UTR sequences influence interactions between viral RNA and host proteins. We hypothesize that viral interactions with the host protein, PCBP2, differ in virulent and avirulent 5’UTR sequences. Our lab has previously determined characteristics of PCBP2 interactions with the 5’UTR of a virulent strain (CVB328). We now focus on interactions of PCBP2 with the 5’UTR of an avirulent strain (CVB3GA). This will be done by monitoring PCBP2 affinity using electrophoresis mobility shift assays and PCBP2 influence on RNA structure through chemical probing. Results from this study may lead to new approaches for treating CVB3 infection.