Herpes simplex virus type 1 that exhibits herpes simplex virus type 2 sensitivity to (E)-5-(2-bromovinyl)-2'-deoxyuridine.
Animals; Antibodies; Antiviral Agents/*pharmacology; Bromodeoxyuridine/*analogs & derivatives/pharmacology; DNA; Drug Resistance; Female; Fluorescent Antibody Technique; Humans; Microbial; Monoclonal; Simplexvirus/*drug effects/enzymology/genetics; Thymidine Kinase/analysis/genetics; Viral/analysis/biosynthesis; Virus Replication/drug effects
A clinical isolate, designated 145, of herpes simplex virus (HSV) had type 1 characteristics as determined by monoclonal antibody immunofluorescence, heat stability of viral thymidine kinase (TK), BamHI restriction endonuclease pattern, and absence of the HSV-2-specific 38-kD protein. However, instead of being sensitive to E-5-(2-bromovinyl)-2'-deoxyuridine (BVDU) like HSV-1, isolate 145 displayed a resistance pattern like HSV-2 to the drug as determined by viral replication and viral DNA synthesis. Because BVDU is activated by viral TK phosphorylation, we cloned the TK-containing DNA region from isolate 145 and compared it by restriction mapping using several endonucleases to similar regions of HSV-1 and HSV-2. In each instance, the patterns for HSV-1 and isolate 145 were identical to each other, but distinct from the patterns for the corresponding region of HSV-2, suggesting that the genome TK region of isolate 145 was
Docherty J J; Dobson A T; Trimble J J; Jennings B A
Intervirology
1991
1991
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1159/000150213" target="_blank" rel="noreferrer noopener">10.1159/000150213</a>
Antiviral activity of magnesium and magnesium/poly r(A-U) combinations against two RNA viruses.
Antiviral Agents/*pharmacology; HIV-1/*drug effects; Humans; Magnesium/*pharmacology; Microbial Sensitivity Tests; Poly A-U/*pharmacology; Vesicular stomatitis Indiana virus/*drug effects
Magnesium (Mg2+) potentiated the anti-vesicular stomatitis virus (VSV) activity of poly r(A-U) or poly r(G-C) and the anti-HIV-1 activity of poly r(A-U). Mg2+ did not affect the anti-VSV activity of poly (rI).poly (rC), poly (dA-dT).poly (dA-dT) or poly (dG-dC).poly (dG-dC). Modulation of one or more nuclear (nucleolar) processes of the host cell may be responsible for the synergistic antiviral activity.
Jamison J; Gilloteaux J; Nassiri M R; Tsai C C; Summers J
Nucleosides & nucleotides
1999
1999-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1080/07328319908044668" target="_blank" rel="noreferrer noopener">10.1080/07328319908044668</a>
Enhanced antiviral activity and altered subcellular distribution of magnesium/poly r(A-U) combinations.
Antiviral Agents/*pharmacology; Cells; Chromatin/drug effects; Cultured; Ethidium/*pharmacology; Humans; Magnesium/metabolism/*pharmacology; Nucleolus Organizer Region/*drug effects; Poly A-U/*pharmacology; Vesicular stomatitis Indiana virus/drug effects
When Mg2+ or ethidium bromide (EB) were combined with poly r(A-U) at a ligand/ribonucleotide ratio of 1/4, the antiviral activity of the Mg2+ and EB increased 136-fold and 154-fold. Eriochrome Blue SE was employed to visualize the subcellular distribution of Mg2+ following co-incubation of Human Foreskin Fibroblasts (HSF) with Mg2+ alone or with the Mg2+/poly r(A-U) combination. Phase contrast micrographs of these Mg(2+)-treated HSF cells as well as phase contrast and fluorescence micrographs of EB-treated or EB/poly r(A-U)-treated HSF cells illustrated that the Mg2+ (or EB)/poly r(A-U) combinations display altered subcellular distribution with the Mg2+ and EB being localized in the nucleoli and chromatin of the HSF cells. These results suggest that modulation of nuclear processes may be responsible for the enhanced antiviral activity.
Krabill K; Jamison J M; Gilloteaux J; Summers J L
Cell biology international reports
1992
1992-10
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/s0309-1651(06)80050-0" target="_blank" rel="noreferrer noopener">10.1016/s0309-1651(06)80050-0</a>
Inhibition of human papillomavirus type 16 gene expression by nordihydroguaiaretic acid plant lignan derivatives.
Antiviral Agents/*pharmacology; Cultured; Female; Gene Expression Regulation; Genetic/drug effects; HIV Long Terminal Repeat/drug effects; Humans; Lignans/chemistry/pharmacology; Masoprocol/*analogs & derivatives/*pharmacology; Papillomaviridae/*genetics; Promoter Regions; Simian virus 40/genetics; Tumor Cells; Viral/*drug effects
Several methylated derivatives of a plant lignan, nordihydroguaiaretic acid (NDGA) were found to be potent anti-viral agents by suppressing Sp1 regulated transcription within the sexually transmitted viruses human immunodeficiency virus (HIV) and herpes simplex virus (HSV). A prominent Sp1 DNA binding site within many human papillomavirus (HPV) promoters has been noted to play an active role in HPV gene expression. In this report it is shown that the three NDGA derivatives, Mal.4, M(4)N, and tetra-acetyl NDGA can also inhibit gene expression from the early promoter P(97) of HPV16. The drug activity on gene expression was measured after DNA transfection of recombinant vector constructs linking the viral promoter and enhancer elements to the luciferase reporter gene. Using the specific luciferase activity as the indicator of gene expression, Mal.4 and M(4)N were found to be active in a dose dependent manner that is in the same range of concentrations reported for the promoters of HIV, HSV, and simian virus 40 (SV40) while tetra-acetyl NDGA was much more active in suppression of the HPV P(97) promoter activity than Mal.4 and M(4)N. The drugs showed limited to no effect on gene expression driven by the adenovirus major late promoter and the cytomegalovirus (CMV) promoter. Hence, such drug derivatives may be significant in the therapy of papillomavirus infections and their associated induced human cancers.
Craigo J; Callahan M; Huang R C; DeLucia A L
Antiviral research
2000
2000-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/s0166-3542(00)00089-9" target="_blank" rel="noreferrer noopener">10.1016/s0166-3542(00)00089-9</a>
Resveratrol inhibition of varicella-zoster virus replication in vitro.
Antiviral Agents/*pharmacology; Blotting; Cell Line; Dose-Response Relationship; Drug; Fibroblasts/virology; Herpesvirus 3; Human/*drug effects/physiology; Humans; Immediate-Early Proteins/biosynthesis; Messenger/biosynthesis; Resveratrol; Reverse Transcriptase Polymerase Chain Reaction; RNA; Stilbenes/*pharmacology; Trans-Activators/biosynthesis; Viral Envelope Proteins/biosynthesis; Viral Plaque Assay; Viral/biosynthesis; Virus Attachment/drug effects; Virus Inactivation/drug effects; Virus Replication/*drug effects; Western
Resveratrol was found to inhibit varicella-zoster virus (VZV) replication in a dose-dependent and reversible manner. This decrease in virus production in the presence of resveratrol was not caused by direct inactivation of VZV or inhibition of virus attachment to MRC-5 cells. The drug effectively limited VZV replication if added during the first 30 h of infection. Western blot analysis and real-time RT-PCR studies demonstrated that protein and mRNA levels of IE62, an essential immediate early viral protein, were reduced when compared to controls. These results demonstrate that VZV replication is adversely affected by resveratrol which is negatively impacting IE62 synthesis.
Docherty John J; Sweet Thomas J; Bailey Erin; Faith Seth A; Booth Tristan
Antiviral research
2006
2006-12
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.antiviral.2006.07.004" target="_blank" rel="noreferrer noopener">10.1016/j.antiviral.2006.07.004</a>
Resveratrol suppresses nuclear factor-kappaB in herpes simplex virus infected cells.
Animals; Antiviral Agents/*pharmacology; Cell Nucleus/chemistry; Cercopithecus aethiops; Cytoplasm/chemistry; DNA; Electrophoretic Mobility Shift Assay; Fluorescence; Herpesvirus 1; Herpesvirus 2; Human/drug effects/genetics/*growth & development; Human/drug effects/genetics/*physiology; I-kappa B Proteins/metabolism; Messenger/biosynthesis; Microscopy; NF-kappa B/*metabolism; NF-KappaB Inhibitor alpha; Polymerase Chain Reaction; Resveratrol; Reverse Transcriptase Polymerase Chain Reaction; RNA; Stilbenes/*pharmacology; Transcription Factor RelA/metabolism; Vero Cells; Viral/biosynthesis; Virus Replication/*drug effects
Resveratrol inhibits herpes simplex virus (HSV) replication by an unknown mechanism. Previously it was suggested that this inhibition may be mediated through a cellular factor essential for HSV replication [Docherty, J.J., Fu, M.M., Stiffler, B.S., Limperos, R.J., Pokabla, C.M., DeLucia, A.L., 1999. Resveratrol inhibition of herpes simplex virus replication. Antivir. Res. 43,
Faith Seth A; Sweet Thomas J; Bailey Erin; Booth Tristan; Docherty John J
Antiviral research
2006
2006-12
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.antiviral.2006.06.011" target="_blank" rel="noreferrer noopener">10.1016/j.antiviral.2006.06.011</a>
Subcellular localization and antiviral activity of carminic acid/poly r(A-U) combinations.
Antiviral Agents/*pharmacology; Carmine/*analogs & derivatives/pharmacokinetics/pharmacology; Cell Nucleolus/metabolism; Cells; Chromatin/metabolism; Cultured; Doxorubicin/pharmacology; Drug Combinations; Drug Synergism; Fluorescence; Humans; Interferon-beta/biosynthesis/physiology; Microscopy; Phase-Contrast; Poly A-U/*pharmacokinetics/*pharmacology; Vesicular stomatitis Indiana virus/drug effects/growth & development; Viral Plaque Assay
Carminic acid (CAR) enhances the antiviral activity of poly r(A-U) twelve-fold without increasing interferon induction, inactivating the vesicular stomatitis virus or inducing host cell cytotoxicity. Phase contrast photomicrographs of human foreskin fibroblasts (HSF) incubated with CAR alone, poly r(A-U) alone or with a CAR/poly r(A-U) combination illustrate that the CAR/poly r(A-U) combinations display altered subcellular distribution with the CAR being localized in the nucleoli and chromatin. Phase contrast and fluorescence photomicrographs of adriamycin (ADR)-treated and ADR/poly r(A-U)-treated HSF cells corroborate these findings. These results suggest that modulation of one or more nucleolar processes may be responsible for the enhanced antiviral activity.
Krabill K; Jamison J M; Gilloteaux J; Summers J L
Cell biology international
1993
1993-10
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1006/cbir.1993.1014" target="_blank" rel="noreferrer noopener">10.1006/cbir.1993.1014</a>