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Characterization of a Cytolytic Strain of Equine Infectious Anemia Virus

Characterization of a Cytolytic Strain of Equine Infectious Anemia Virus Characterization of a Cytolytic Strain of Equine Infectious Anemia Virus Wendy Maury 1 , * , Patrick J. Wright 1 , and Sarahann Bradley 2 1 Department of Microbiology, University of Iowa, Iowa City, Iowa 52242 2 Division of Basic Biomedical Sciences, University of South Dakota, Vermillion, South Dakota 57069 ABSTRACT A novel strain of equine infectious anemia virus (EIAV) called vMA-1c that rapidly and specifically killed infected equine fibroblasts (ED cells) but not other infectible cell lines was established. This strain was generated from an avirulent, noncytopathic strain of EIAV, MA-1. Studies with this new cytolytic strain of virus have permitted us to define viral parameters associated with EIAV-induced cell killing and begin to explore the mechanism. vMA-1c infection resulted in induction of rapid cell death, enhanced fusogenic activity, and increased rates of spread in equine fibroblasts compared to other strains of EIAV. The highly cytolytic nature of vMA-1c suggested that this strain might be superinfecting equine fibroblasts. Receptor interference studies demonstrated that prior infection of equine fibroblasts with EIAV did not alter the ability of vMA-1c to infect and kill these cells. In similar studies in a canine fibroblast cell line, receptor interference did occur. vMA-1c infection of equine fibroblasts was also associated with large quantities of unintegrated viral DNA, a well-established hallmark of retroviral superinfection. Cloning of the vMA-1c genome identified nucleotide changes that would result in at least one amino acid change in all viral proteins. A chimeric infectious molecular clone containing the vMA-1c tat , S2 , and env open reading frames recapitulated most of the characteristics of vMA-1c, including superinfection, fibroblast killing, and fusogenic activity. In summary, in vitro selection for a strain of EIAV that rapidly killed cells resulted in the generation of a virus that was able to superinfect these cells, presumably by the use of a novel mechanism of cell entry. This phenotype mapped to the 3′ half of the genome. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Virology American Society For Microbiology

Characterization of a Cytolytic Strain of Equine Infectious Anemia Virus

Journal of Virology , Volume 77 (4): 2385 – Feb 15, 2003

Characterization of a Cytolytic Strain of Equine Infectious Anemia Virus

Journal of Virology , Volume 77 (4): 2385 – Feb 15, 2003

Abstract

Characterization of a Cytolytic Strain of Equine Infectious Anemia Virus Wendy Maury 1 , * , Patrick J. Wright 1 , and Sarahann Bradley 2 1 Department of Microbiology, University of Iowa, Iowa City, Iowa 52242 2 Division of Basic Biomedical Sciences, University of South Dakota, Vermillion, South Dakota 57069 ABSTRACT A novel strain of equine infectious anemia virus (EIAV) called vMA-1c that rapidly and specifically killed infected equine fibroblasts (ED cells) but not other infectible cell lines was established. This strain was generated from an avirulent, noncytopathic strain of EIAV, MA-1. Studies with this new cytolytic strain of virus have permitted us to define viral parameters associated with EIAV-induced cell killing and begin to explore the mechanism. vMA-1c infection resulted in induction of rapid cell death, enhanced fusogenic activity, and increased rates of spread in equine fibroblasts compared to other strains of EIAV. The highly cytolytic nature of vMA-1c suggested that this strain might be superinfecting equine fibroblasts. Receptor interference studies demonstrated that prior infection of equine fibroblasts with EIAV did not alter the ability of vMA-1c to infect and kill these cells. In similar studies in a canine fibroblast cell line, receptor interference did occur. vMA-1c infection of equine fibroblasts was also associated with large quantities of unintegrated viral DNA, a well-established hallmark of retroviral superinfection. Cloning of the vMA-1c genome identified nucleotide changes that would result in at least one amino acid change in all viral proteins. A chimeric infectious molecular clone containing the vMA-1c tat , S2 , and env open reading frames recapitulated most of the characteristics of vMA-1c, including superinfection, fibroblast killing, and fusogenic activity. In summary, in vitro selection for a strain of EIAV that rapidly killed cells resulted in the generation of a virus that was able to superinfect these cells, presumably by the use of a novel mechanism of cell entry. This phenotype mapped to the 3′ half of the genome.

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References (55)

Publisher
American Society For Microbiology
Copyright
Copyright © 2003 by the American society for Microbiology.
ISSN
0022-538X
eISSN
1098-5514
DOI
10.1128/JVI.77.4.2385-2399.2003
Publisher site
See Article on Publisher Site

Abstract

Characterization of a Cytolytic Strain of Equine Infectious Anemia Virus Wendy Maury 1 , * , Patrick J. Wright 1 , and Sarahann Bradley 2 1 Department of Microbiology, University of Iowa, Iowa City, Iowa 52242 2 Division of Basic Biomedical Sciences, University of South Dakota, Vermillion, South Dakota 57069 ABSTRACT A novel strain of equine infectious anemia virus (EIAV) called vMA-1c that rapidly and specifically killed infected equine fibroblasts (ED cells) but not other infectible cell lines was established. This strain was generated from an avirulent, noncytopathic strain of EIAV, MA-1. Studies with this new cytolytic strain of virus have permitted us to define viral parameters associated with EIAV-induced cell killing and begin to explore the mechanism. vMA-1c infection resulted in induction of rapid cell death, enhanced fusogenic activity, and increased rates of spread in equine fibroblasts compared to other strains of EIAV. The highly cytolytic nature of vMA-1c suggested that this strain might be superinfecting equine fibroblasts. Receptor interference studies demonstrated that prior infection of equine fibroblasts with EIAV did not alter the ability of vMA-1c to infect and kill these cells. In similar studies in a canine fibroblast cell line, receptor interference did occur. vMA-1c infection of equine fibroblasts was also associated with large quantities of unintegrated viral DNA, a well-established hallmark of retroviral superinfection. Cloning of the vMA-1c genome identified nucleotide changes that would result in at least one amino acid change in all viral proteins. A chimeric infectious molecular clone containing the vMA-1c tat , S2 , and env open reading frames recapitulated most of the characteristics of vMA-1c, including superinfection, fibroblast killing, and fusogenic activity. In summary, in vitro selection for a strain of EIAV that rapidly killed cells resulted in the generation of a virus that was able to superinfect these cells, presumably by the use of a novel mechanism of cell entry. This phenotype mapped to the 3′ half of the genome.

Journal

Journal of VirologyAmerican Society For Microbiology

Published: Feb 15, 2003

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