Coevolution of Virulent Virus and Resistant Cells as a Mechanism of Persistence of Herpes Simplex Virus Type 1 in a Human T Lymphoblastoid Cell Line

Cummings, Patrick J.; Rinaldo, Charles R.

doi:10.1099/0022-1317-70-1-97

Cited by 8 publications

(4 citation statements)

References 22 publications

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“…The ability of herpesviruses to establish persistent infection has been well documented (10,13,14,31,39,48). Numerous studies from our laboratory have demonstrated that DIPs of EHV-1 mediate persistent infection (2,3,8,11,26,35,41).…”

Section: Discussionmentioning

confidence: 99%

Transcriptional and translational analyses of the UL2 gene of equine herpesvirus 1: a homolog of UL55 of herpes simplex virus type 1 that is maintained in the genome of defective interfering particles

Harty

Holden

O’Callaghan

1993

J Virol

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Defective interfering particles (DIPs) of equine herpesvirus 1 (EHV-1; Kentucky A strain) mediate persistent infection. DNA sequences at the L terminus, which contain the UL2 gene (homolog of ULS5 of herpes simplex virus type 1 and open reading frame 3 of varicella-zoster virus) of standard EHV-1, have been shown to be highly conserved in all clones of the EHV-1 DIP genome. The UL2 mRNA was characterized by Si nuclease analyses, which mapped the 5' and 3' termini of the 0.9-kb early UL2 mRNA to approximately 26 and 16 nucleotides downstream of a TITAAA box and polyadenylation signal, respectively. The UL2 open reading frame, present within both the EHV-1 standard and DIP genomes, was inserted into the transcription expression vector pGEM-3Z to yield constructs pGEML2 and pDIL2, respectively. After in vitro transcription and translation, both constructs yielded a comigrating 23-kDa protein, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Polyclonal antiserum was raised against the UL2 protein by injecting rabbits with a TrpE/UL2 fusion protein expressed from plasmid pATH23L2 in Escherichia coli. The UL2-specific antiserum reacted in Western immunoblot and immunoprecipitation analyses with a 23-kDa polypeptide synthesized in cells infected with standard EHV-1 or DIP-enriched virus. These data also indicated that the UL2 polypeptide was more abundant in DIP-infected cells than in standard EHV-1-infected cells. Results from time course and pulse-chase analyses suggested that the UL2 polypeptide has a rapid turnover rate in DIP-infected cells.

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Section: Discussionmentioning

confidence: 99%

Transcriptional and translational analyses of the UL2 gene of equine herpesvirus 1: a homolog of UL55 of herpes simplex virus type 1 that is maintained in the genome of defective interfering particles

Harty

Holden

O’Callaghan

1993

J Virol

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“…Coevolution of cells and virus has been described in the course of persistence of several animal viruses in cell culture (Takemoto & Habel, 1959;Ahmed et al, 1981;Chiarini et al, 1983;Delli Bovi et al, 1984;Ron & Tal, 1985, 1986Cummings & Rinaldo, 1989;Dermody et al, 1993;Calvez et al, 1995;Chen & Baric, 1996;Mrukowicz et al, 1998;Zhong et al, 2006). In other persistent infections in cell culture, no cell evolution was observed, and persistence was associated with defective interfering particles or with small-plaque and ts viral mutants (Igarashi et al, 1977;Holland et al, 1980Holland et al, , 1982Youngner & Preble, 1980).…”

Section: Discussionmentioning

confidence: 99%

Persistence of foot-and-mouth disease virus in cell culture revisited: implications for contingency in evolution

Herrera

Grande-Pérez

Perales

et al. 2008

Journal of General Virology

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If we could rewind the tape of evolution and play it again, would it turn out to be similar to or different from what we know? Obviously, this key question can only be addressed by fragmentary experimental approaches. Twenty-two years ago, we described the establishment of BHK-21 cells persistently infected with foot-and-mouth disease virus (FMDV), a system that displayed as its major biological feature a coevolution of the cells and the resident virus in the course of persistence. Now we report the establishment of two persistently infected cell lines in parallel, starting with the same clones of FMDV and BHK-21 cells used 22 years ago. We have asked whether the evolution of the two newly established cell lines and of the earlier cell line would be similar or different. The main conclusions of the study are: (i) the basic behaviour characterized by virus-cell coevolution is similar in the three carrier cell lines, despite differences in some genetic alterations of FMDV; (ii) a strikingly parallel behaviour has been observed with the two newly established cell lines passaged in parallel, unveiling a deterministic virus behaviour during persistence; and (iii) selective RT-PCR amplifications have detected imbalances in the proportion of positive-versus negative-strand viral RNA, mediated by both viral and cellular factors. The results confirm coevolution of cells and virus as a major and reproducible feature of FMDV persistence in cell culture, and suggest that rapidly evolving viruses may constitute adequate test systems to probe the influence of historical contingency on evolutionary events.

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“…Alterations of both viral and host cell characteristics may contribute to the establishment of persistent virus infections (Ahmed et al, 1981 ;Hampar & Burroughs, 1969;Ron & Tal, 1985;Cummings & Rinaldo, 1989). Moreover variants of MHV have been isolated from persistent infections initially established in vivo or in vitro with wild-type virus (Baybutt et al, 1984;Jackson et al, 1984;Taguchi et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Mutation of Host Cell Determinants which Discriminate between Lytic and Persistent Mouse Hepatitis Virus Infection Results in a Fusion-resistant Phenotype

Daya

Wong

Cervin

et al. 1989

Journal of General Virology

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SUMMARYThe expression of mouse hepatitis virus (MHV) E2-specific mRNA, the E 2 polypeptide and its associated cell fusing activity was monitored in various cell types inoculated with a recombinant vaccinia virus, designated vMS containing the Ez gene. The results suggest that host cell permissiveness to MHV infection correlates with cellular susceptibility to membrane fusion mediated by the MHV E2 glycoprotein. In addition, we utilized a genetic approach to the analysis of host cell functions involved in determining permissiveness to MHV. By using the chemical mutagen ethyl methanesulphonate, mouse fibroblast cell mutants were generated and selected for their resistance to cell killing by MHV. When challenged with MHV, all five mutants examined gave rise to persistent infections, in contrast to wild-type L-2 cells which were rapidly killed by the virus. The results provide genetic evidence in support of a previous correlation proposed between MHV permissiveness and two host determinants, namely susceptibility to MHV infection and to MHV-mediated cell fusion. Fusion resistance was specific to fusion mediated by the MHV E2 glycoprotein as shown in contact fusion assays between uninfected cells and cells infected either with MHV or with an E2-expressing recombinant vaccinia virus. In contrast, mutant cells were not resistant to fusion after treatment with polyethylene glycol. The observed high rate of generation of these mutants suggests that the conversion of a fully MHVsusceptible cell to a semi-resistant one is a fairly common event, possibly involving a single mutation. In this case, resistance to MHV infection and to E2-mediated membrane fusion may depend on a common host function. This result provides prospects for the precise genetic and biochemical characterization of the steps involved in host cell permissiveness to MHV infection. INTRODUCTIONMouse hepatitis virus (MHV) produces infections ranging from persistent to acute, depending on the host cell type as well as other factors. Despite recent advances in the molecular biology of coronaviruses such as MHV, the mechanisms which determine the outcome of infection remain largely unclear. MHV gives rise to certain cytopathic functions, such as cell fusion and inhibition of host cell protein synthesis, which, if differentially expressed in a cell-specific manner, could determine the severity of MHV infection. In fact, cell differences in susceptibility to MHV-induced fusion have been implicated as host cell factors which, at least in part,

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Coevolution of Virulent Virus and Resistant Cells as a Mechanism of Persistence of Herpes Simplex Virus Type 1 in a Human T Lymphoblastoid Cell Line

Cited by 8 publications

References 22 publications

Transcriptional and translational analyses of the UL2 gene of equine herpesvirus 1: a homolog of UL55 of herpes simplex virus type 1 that is maintained in the genome of defective interfering particles

Transcriptional and translational analyses of the UL2 gene of equine herpesvirus 1: a homolog of UL55 of herpes simplex virus type 1 that is maintained in the genome of defective interfering particles

Persistence of foot-and-mouth disease virus in cell culture revisited: implications for contingency in evolution

Mutation of Host Cell Determinants which Discriminate between Lytic and Persistent Mouse Hepatitis Virus Infection Results in a Fusion-resistant Phenotype

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