A 44-Nucleotide Region in the Chikungunya Virus 3′ UTR Dictates Viral Fitness in Disparate Host Cells

Author:

Ander Stephanie E.1,Carpentier Kathryn S.1,Sanders Wes2,Lucas Cormac J.1,Jolly Austin J.1ORCID,Johnson Cydney N.1,Hawman David W.1ORCID,Heise Mark T.3,Moorman Nathaniel J.2,Morrison Thomas E.1ORCID

Affiliation:

1. Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA

2. Department of Microbiology & Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA

3. Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA

Abstract

We previously reported that deletion of a 44-nucleotide element in the 3′ untranslated region (UTR) of the Chikungunya virus (CHIKV) genome enhances the virulence of CHIKV infection in mice. Here, we find that while this 44-nucleotide deletion enhances CHIKV fitness in murine embryonic fibroblasts in a manner independent of the type I interferon response, the same mutation decreases viral fitness in C6/36 mosquito cells. Further, the fitness advantage conferred by the UTR deletion in mammalian cells is maintained in vivo in a mouse model of CHIKV dissemination. Finally, SHAPE-MaP analysis of the CHIKV 3′ UTR revealed this 44-nucleotide element forms a distinctive two-stem-loop structure that is ablated in the mutant 3′ UTR without altering additional 3′ UTR RNA secondary structures.

Funder

National Institute of Allergy and Infectious Diseases

Publisher

MDPI AG

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