Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1997 Apr;71(4):2959-69.
doi: 10.1128/JVI.71.4.2959-2969.1997.

Evolution of mouse hepatitis virus: detection and characterization of spike deletion variants during persistent infection

C L Rowe  1 , S C Baker, M J Nathan, J O Fleming
Affiliations

Evolution of mouse hepatitis virus: detection and characterization of spike deletion variants during persistent infection

C L Rowe et al. J Virol. 1997 Apr.

Abstract

High-frequency RNA recombination has been proposed as an important mechanism for generating viral deletion variants of murine coronavirus. Indeed, a number of variants with deletions in the spike glycoprotein have been isolated from persistently infected animals. However, the significance of generating and potentially accumulating deletion variants in the persisting viral RNA population is unclear. To study this issue, we evaluated the evolution of spike variants by examining the population of spike RNA sequences detected in the brains and spinal cords of mice inoculated with coronavirus and sacrificed at 4, 42, or 100 days postinoculation. We focused on the S1 hypervariable region since previous investigators had shown that this region is subject to recombination and deletion. RNA isolated from the brains or spinal cords of infected mice was rescued by reverse transcription-PCR, and the amplified products were cloned and used in differential colony hybridizations to identify individual isolates with deletions. We found that 11 of 20 persistently infected mice harbored spike deletion variants (SDVs), indicating that deletions are common but not required for persistent infection. To determine if a specific type of SDV accumulated during persistence, we sequenced 106 of the deletion isolates. We identified 23 distinct patterns of SDVs, including 5 double-deletion variants. Furthermore, we found that each mouse harbored distinct variants in its central nervous system (CNS), suggesting that SDVs are generated during viral replication in the CNS. Interestingly, mice with the most severe and persisting neurological disease harbored the most prevalent and diverse quasispecies of SDVs. Overall, these findings illustrate the complexity of the population of persisting viral RNAs which may contribute to chronic disease.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Virology. 1995 Apr 1;208(1):67-74 - PubMed
    1. Immunity. 1996 Sep;5(3):253-62 - PubMed
    1. Neurology. 1981 Jan;31(1):38-44 - PubMed
    1. Virology. 1982 Jun;119(2):358-71 - PubMed
    1. Infect Immun. 1983 Mar;39(3):1316-24 - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources