DNA polymerases of normal and neoplastic mammalian cells

Sarngadharan, M. G.

doi:10.1016/0304-419x(78)90019-7

Cited by 52 publications

(40 citation statements)

References 322 publications

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“…The enzyme originated from highly purified HTLV-IIIB-infected Jurkat cells (Wendler et al, 1987). To test for contamination with cellular enzymes poly(rA), oligo(dT) and poly(dA).oligo(dT) were also used as the primer-template (Sarngadharan et al, 1972(Sarngadharan et al, , 1978Poiesz et al, 1980). According to these tests, the amount of contaminating cellular polymerases was less than 10~o of the total polymerase activity.…”

Section: Chemical Modification Of Suramin Results In More Potent Hiv-mentioning

confidence: 99%

Inhibition of Human Immunodeficiency Virus Type I Reverse Transcriptase by Suramin-related Compounds

Jentsch

Hunsmann

Hartmann

et al. 1987

Journal of General Virology

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SUMMARYNinety analogues of suramin have been examined for their ability to inhibit the exogenous reverse transcriptase (RT) of human immunodeficiency virus type I (HIV-I). Of these compounds, 57 inhibited the poly(rC)-oligo(dG)-dependent RT activity. Three classes of dose-response curves could be discriminated. Allocation of a compound to one class did not correspond with obvious structural features. Twentyfour substances were superior to suramin in our RT inhibition assay. The RTinhibitory activity of these compounds did not correlate with their effect against filariae or trypanosomes. Preliminary antiviral evaluation in susceptible human T cells inoculated with HIV-I demonstrated in vitro therapeutic efficacy for some compounds with lower drug-related cellular toxicity than suramin. Certain structural features relevant for the RT-inhibitory effect of these compounds were recognized. Predictions are made for the design of more effective RT inhibitors. Such compounds will help to understand the molecular mechanism of reverse transcription and might be useful in the therapy of retroviral infections.

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Section: Chemical Modification Of Suramin Results In More Potent Hiv-mentioning

confidence: 99%

Inhibition of Human Immunodeficiency Virus Type I Reverse Transcriptase by Suramin-related Compounds

Jentsch

Hunsmann

Hartmann

et al. 1987

Journal of General Virology

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“…Moreover, the use of methylated cytosine template [poly(C)m] in the RT assay greatly limited the nonspecific RT-like activity of cellular DNA polymerase gamma and of HSV-1 polymerase. Poly(C)m is known to be an inefficient template for DNA-directed DNA polymerases (Sarngadharan et al, 1978;Verma, 1977) and LM7 virus RT activity is best detected with it (Perron et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Herpes simplex virus ICP0 and ICP4 immediate early proteins strongly enhance expression of a retrovirus harboured by a leptomeningeal cell line from a patient with multiple sclerosis

Perron¹,

Suh²,

Lalande³

et al. 1993

Journal of General Virology

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A leptomeningeal cell line (LM7) harbouring an unknown retrovirus was recently isolated from the cerebrospinal fluid of a patient with multiple sclerosis. However, spontaneous expression of the LM7 retrovirus in this primary culture is quite low. We present results showing that in vitro infection of LM7 cells with herpes simplex virus type 1 (HSV-1), but not that of control cells, results in (i) potent stimulation of the specific reverse transcriptase (RT) activity detected in the culture supernatant and (ii) co-expression of both typical HSV-1 virions and abundant retrovirus-like particles. Transfection of LM7 cells with plasmids expressing HSV-1 immediate early (IE) ICP0 and ICP4 proteins produced a similar enhancement of RT activity in culture supernatants with retrovirus-like particles being identifiable by electron microscopy. These effects were not observed with a plasmid expressing ICP27 or with the parental plasmid in LM7 cells, nor with any of these four plasmids in control cells. These results show that HSV IE trans-activating proteins strongly enhance the expression of the latent retrovirus present in LM7 cells. The possible role in vivo of herpesviruses as 'triggering' cofactors in the retrovirus hypothesis for multiple sclerosis aetiology is also discussed.

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“…There are several viral functions that can (3,4); in addition, a DNase (5) and a nucleoside phosphotransferase (6) are induced in cells upon infection with HSV. These virus-induced enzymes are significantly different from their cellular counterparts in many of their properties (7)(8)(9). For example, the HSV-induced DNA polymerase differs from the host cellular DNA polymerases a, /3, and 'y in elution profile on ion-exchange columns, molecular weight, primer template preference, effect of monovalent and divalent cations, and other requirements for maximal activity.…”

mentioning

confidence: 99%

On the mechanism of selective inhibition of herpesvirus replication by (E)-5-(2-bromovinyl)-2'-deoxyuridine.

Allaudeen¹,

Kozarich²,

Bertino³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

119

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Bromovinyldeoxyuridine (BVdUrd) is a potent antiherpesvirus compound with low cytotoxicity. To gain an insight into its selectivity and mechanism of inhibition, we chemically synthesized the 5'-triphosphate of BVdUrd, BVdUTP, and (3, 4); in addition, a DNase (5) and a nucleoside phosphotransferase (6) are induced in cells upon infection with HSV. These virus-induced enzymes are significantly different from their cellular counterparts in many of their properties (7-9). For example, the HSV-induced DNA polymerase differs from the host cellular DNA polymerases a,

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DNA polymerases of normal and neoplastic mammalian cells

Cited by 52 publications

References 322 publications

Inhibition of Human Immunodeficiency Virus Type I Reverse Transcriptase by Suramin-related Compounds

Inhibition of Human Immunodeficiency Virus Type I Reverse Transcriptase by Suramin-related Compounds

Herpes simplex virus ICP0 and ICP4 immediate early proteins strongly enhance expression of a retrovirus harboured by a leptomeningeal cell line from a patient with multiple sclerosis

On the mechanism of selective inhibition of herpesvirus replication by (E)-5-(2-bromovinyl)-2'-deoxyuridine.

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