Herpes simplex virus‐induced amplification of SV40 sequences in transformed Chinese hamster embryo cells

Schlehofer, Jörg R.; Gissmann, Lutz; Matz, Bertfried; Hausen, Harald zur

doi:10.1002/ijc.2910320116

Cited by 80 publications

(42 citation statements)

References 19 publications

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“…AAV-2, propagated in HeLa cells by infection with adenovirus type 2 (Ad-2) as described (Botquin et al, 1994 ;Yakobson et al, 1987), was purified and titrated as described previously (Botquin et al, 1994 ;Schlehofer et al, 1983 b). Viral plasmid constructs and hybridization probes.…”

Section: Methodsmentioning

confidence: 99%

Interaction of human papillomavirus type 16 and adeno-associated virus type 2 co-infecting human cervical epithelium.

Walz

Deprez

Dupressoir³

et al. 1997

Journal of General Virology

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Recently, we hypothesized that the tumour-suppressive, human helper-virus-dependent, adenoassociated parvoviruses (AAV) may interfere with transforming functions of human papillomaviruses (HPV) in the development of cervical carcinoma. Here, we demonstrate that in cervical epithelium containing papillomavirus DNA, AAV DNA can be detected in a replication-competent form and that AAV proteins are expressed. In cultured cells con-

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Section: Methodsmentioning

confidence: 99%

Interaction of human papillomavirus type 16 and adeno-associated virus type 2 co-infecting human cervical epithelium.

Walz

Deprez

Dupressoir³

et al. 1997

Journal of General Virology

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“…A high percentage of squamous cell carcinomas of the skin contains the same HPV types (Shamanin et al, 1996;Astori et al, 1998; although their copy number is far below one copy per tumor cell. This would be (Schlehofer et al, 1983;Schmitt et al, 1989;Heilbronn and zur Hausen, 1989). Similarly, human cytomegalovirus (CMV) e ectively promotes the replication of the human polyomavirus JC in human ®broblasts, although these cells are non-permissive for JC in the absence of CMV (Heilbronn et al, 1993).…”

Section: Mechanisms By Which Viruses Contribute To Cancermentioning

confidence: 99%

Oncogenic DNA viruses

Hausen

2001

Oncogene

111

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“…Chromosome analyses with HSV-infected cells revealed various areas of damage and reorganization compatible with amplification of genetic material of the host cell (Nachtigal et al, 1975;Pratt et al, 1984;Chenet-Monte et al, 1986/87). A typical example of aberrant DNA replication caused by HSV is the fact that SV40 DNA integrated into the genome of transformed cells can be extensively amplified (Schlehofer et al, 1983(Schlehofer et al, , 1986Matz et al, 1985). This is not simply due to induction of papovavirus replication.…”

Section: Amplification Of Plasmids In Bhk Cells Infected With Hsvmentioning

confidence: 99%

“…It is, therefore, surprising that in several simian virus 40 (SV40)-transformed cell lines, SV40 DNA sequences are over-replicated upon HSV infection (Schlehofer et al, 1983(Schlehofer et al, , 1986Matz et al, 1984Matz et al, , 1985. This specific DNA amplification has been shown to depend on the herpesviral DNA polymerase (Matz et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

Herpes Simplex Virus Causes Amplification of Recombinant Plasmids Containing Simian Virus 40 Sequences

Matz

1989

Journal of General Virology

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SUMMARYSimian virus 40 (SV40) DNA, inserted into a plasmid vector, does not replicate when transfected into baby hamster kidney cells. However, when the recipient cells are superinfected with herpes simplex virus type 1 (HSV-1), extensive amplification of the introduced plasmid occurs. Deletion of the late SV40 region or part of the coding sequences of the small tumour (t) antigen has no effect on the efficiency of amplification, whereas manipulations affecting either the SV40 origin of replication or the integrity of large tumour (T) antigen substantially decrease HSV-induced amplification. Phosphonoacetic acid, an inhibitor of HSV DNA polymerase, strongly inhibits plasmid replication. Also, an HSV-1 mutant with a temperature-sensitive defect in the DNA polymerase gene (tsH) is unable to carry out amplification of test plasmids at the non-permissive temperature. On the other hand, a further mutant (tsS) causes SV40-plasmid amplification independent of the temperature, but this mutant fails to amplify a plasmid with an HSV origin at the non-permissive temperature. Thus, HSV-induced amplification of heterologous DNA is possible in the absence of HSV DNA replication. Since tsS putatively has a defect in the gene coding for an HSV origin-binding protein (UL9), this observation appears plausible. The implications for interaction between herpesviral replication functions and heterologous (possibly cellular) DNA sequences are discussed. INTRODUCTIONInfection with herpes simplex virus (HSV) turns off the DNA replication of the host cell (Fenwick & Walker, 1978). It is, therefore, surprising that in several simian virus 40 (SV40)-transformed cell lines, SV40 DNA sequences are over-replicated upon HSV infection (Schlehofer et al., 1983(Schlehofer et al., , 1986Matz et al., 1984Matz et al., , 1985. This specific DNA amplification has been shown to depend on the herpesviral DNA polymerase (Matz et al., 1984). The structure of amplified SV40 DNA in the Syrian hamster cell line Elona has been analysed and found to consist of large concatemeric molecules (Matz, 1987). The structural similarity of the amplified DNA species with herpesviral DNA from defective interfering particles (Frenkel, 1981) supported the assumption that this illegitimate over-replication occurs under the direction of herpesviral DNA replication functions. Analysis of the amplified SV40 DNA revealed minor differences from standard SV40 DNA and failed to identify any sequence element that resembled a herpesvirus-specific origin of replication (Matz, 1987). In this report the question was addressed as to whether amplified DNA, isolated from the HSV-infected Elona cell line, or simply standard SV40 DNA can substitute for a herpesviral origin of replication in a functional assay previously designed for the identification of HSV replication origins (Stow, 1982).

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Herpes simplex virus‐induced amplification of SV40 sequences in transformed Chinese hamster embryo cells

Cited by 80 publications

References 19 publications

Interaction of human papillomavirus type 16 and adeno-associated virus type 2 co-infecting human cervical epithelium.

Interaction of human papillomavirus type 16 and adeno-associated virus type 2 co-infecting human cervical epithelium.

Oncogenic DNA viruses

Herpes Simplex Virus Causes Amplification of Recombinant Plasmids Containing Simian Virus 40 Sequences

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