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PubMed2004

Effects of cell cycle on telomerase activity and on hepatitis B virus replication in HepG2 2.2.15 cells.

BACKGROUND: It has been shown that telomerase activity and hepatitis B virus (HBV) replication are closely associated with cell cycle. This study aimed to further investigate the effects of cell cycle on telomerase activity and on HBV replication. METHODS: Human hepatoma cells transfected with HBV DNA (HepG2 2.2.15 cell line) were treated respectively with serum deprivation, all-trans retinoic acid (RA), dimethyl sulfoxide (DMSO), or sodium butyrate. The cell cycle of HepG2 2.2.15 cells was analyzed by flow cytometry. The telomerase activities of the cells were detected by TRAP-PCR-ELISA. HBV DNA in culture medium was assayed by a fluorescent quantitative PCR assay and a semiquantitative dot blot hybridization technique. HBsAg and HBeAg in culture media were quantitatively examined by an ELISA assay. RESULTS: Treatments with serum deprivation, RA, DMSO, or sodium butyrate inhibited the proliferation of HepG2 2.2.15 cells and led to cell arrest in the G0/G1 phase of cell cycle. The percentage of the G0/G1 phase in the groups of sodium butyrate, DMSO, RA and serum-free was 85.2%, 71.9%, 68.3% and 65.2%, respectively, but in the control group, 43.1% (P<0.01). The activities of telomerase of the cells were also significantly inhibited by 82.8%, 74.6%, 76.1% and 69.4% respectively. In addition, HBV replication of the HepG2 2.2.15 cells remarkably increased as shown by the contents of HBV DNA, HBsAg and HBeAg in the culture media of the cells treated with sodium butyrate, DMSO, RA or serum deprivation (P<0.01). The amounts of HBV DNA in the groups of sodium butyrate, DMSO, RA, serum deprivation and control were 6.7X10(6), 4.8X10(6), 4.4X10(6), 5.1X10(6) and 1.2X10(6) copies/ml, respectively (P<0.01). Telomerase was expressed mainly in the cells in S phase. HBV replication increased in quiescent cells (G0/G1 phase), and decreased in proliferating phase (S phase). CONCLUSION: The current data approve that HBV replication is associated with the cellular proliferative activity.

Carcinoma, Hepatocellular↗
PubMedDate not supplied

Mutagenic virus replication in human tumor cells.

Herpes simplex virus was grown in different lines of human tumor and normal cells. The progeny virus was assayed for resistance to iododeoxycytidine, an indicator of a forward mutation in the virus genome. Virus grown in cells from 4 of 5 tumor lines demonstrated greater fractions mutated to iododeoxycytidine resistance than did virus grown in 7 normal human skin cell lines. The data indicate that some lines of human tumor cells modify the herpesvirus replication process, making it more mutagenic. In 2 cases of osteosarcoma patients, normal skin fibroblasts of the patients yielded normal levels of mutagenesis, while their tumor cells gave enhanced mutagenesis.

Animals↗
PubMed2000

Investigation into the mode of action of R-91650, an arylpiperazinyl fluoroquinolone, on feline immunodeficiency virus replication inhibitory activity.

The mode of action of R-91650, an arylpiperazinyl fluoroquinolone, on feline immunodeficiency virus (FIV) replication inhibitory activity was investigated. R-91650 inhibited replication of FIV at non-cytotoxic concentration levels in both acutely infected peripheral blood mononuclear cells and chronically infected P-CrFK cells. The compound reduced the intracellular p24 concentration levels in P-CrFK cells in a dose-dependent manner. Northern blot analysis revealed that R-91650 selectively prevented the accumulation of FIV mRNA in P-CrFK cells. However, the compound did not inhibit FIV-long terminal repeat (LTR) promoter activity in the reporter gene expression analysis. These data suggest that R-91650 is a novel inhibitor of FIV replication that inhibits a certain step or steps following transcription initiation of the FIV-LTR promoter.

Animals↗
PubMed1997

Vaccine effect using a live attenuated nef-deficient simian immunodeficiency virus of African green monkeys in the absence of detectable vaccine virus replication in vivo.

Immunization of adult macaques with live attenuated simian immunodeficiency viruses (SIVs) lacking the nef genes has been shown to protect against challenge with full-length pathogenic SIV. To test live attenuated virus vaccines for the first time in a natural host we have constructed a mutant SIV from African green monkeys (SIVagm) with a deletion of 125 bp in the nef gene (SIVagm3 delta nef). This mutant showed moderately delayed in vitro replication in the T cell line MOLT-4/8 and in primary peripheral blood mononuclear cells from African green monkeys (Cercopithecus aetiops) and pig-tailed macaques (Macaca nemestrina) compared with cloned wild-type SIVagm3. In contrast, in vivo replication of SIVagm3 delta nef in African green monkeys was severely impaired or undetectable and did not induce seroconversion. After challenge with wild-type SIVagm3 the SIVagm3 delta nef preinoculated African green monkeys showed a memory antibody response that declined after week 2. In three of four African green monkeys the cell-associated virus load and in two of four African green monkeys the plasma virus load was dramatically decreased after the challenge compared with naive control animals. The remaining animal showed no evidence of productive challenge virus replication. This study demonstrates that a strong vaccine effect or protection in the SIVagm/African green monkey system is possible using a live attenuated vaccine in the absence of a productive infection and corresponding humoral immune response.

Animals↗
PubMed2003

Disruption of gammaherpesvirus 68 gene 50 demonstrates that Rta is essential for virus replication.

Gammaherpesvirus pathogenesis is dependent on the ability of these viruses to establish a lifelong latent infection and the ability to reactivate from latency. Immediate-early genes of theses viruses are thought to be critical regulators of lytic replication and reactivation from latency. The gene 50-encoded Rta is the only immediate-early gene product that appears to be conserved among all characterized gammaherpesviruses. Previous studies have demonstrated that, in Epstein-Barr virus (EBV), Kaposi's sarcoma-associated virus, and gammaherpesvirus 68 (gamma HV68, also referred to as murine gammaherpesvirus 68), ectopic expression of Rta in latently infected cell lines can lead to induction of the viral cycle. Recently, studies employing null mutants of EBV have provided a formal demonstration that both Rta and the BZLF1 gene product, Zta, the two EBV immediate-early gene products, are essential for EBV replication. Here we generate and characterize a gene 50-null mutant gamma HV68 and demonstrate that the gene 50 product Rta is essential for virus replication. Providing gamma HV68 Rta in trans was sufficient to restore replication of the gene 50-null virus. Notably, Rta expressed from the spliced form of the gene 50 transcript was sufficient to complement growth of the gene 50-null virus. In addition, we provide evidence that loss of Rta expression leads to a complete defect in viral DNA replication and a significant defect in late antigen expression. This work lays the foundation for characterizing the role of Rta in gamma HV68 chronic infection of mice.

Animals↗
PubMed2004

The core 2 beta-1,6-N-acetylglucosaminyltransferase-M encoded by bovine herpesvirus 4 is not essential for virus replication despite contributing to post-translational modifications of structural proteins.

The Bo17 gene of bovine herpesvirus 4 (BoHV-4) is the only virus gene known to date that encodes a homologue of the cellular core 2 beta-1,6-N-acetylglucosaminyltransferase-mucine type (C2GnT-M). Recently, our phylogenetic study revealed that the Bo17 gene has been acquired from an ancestor of the African buffalo around 1.5 million years ago. Despite this recent origin, the Bo17 sequence has spread to fixation in the virus population possibly by natural selection. Supporting the latter hypothesis, it has been shown by our group for the V. test strain that Bo17 is expressed during BoHV-4 replication in vitro, and that Bo17 expression product (pBo17) has all three enzymic activities exhibited by cellular C2GnT-M, i.e. core 2, core 4 and I branching activities. In the present study, firstly it was investigated whether encoding a functional C2GnT-M is a general property of BoHV-4 strains. Analysis of nine representative strains of the BoHV-4 species revealed that all of them express the Bo17 gene and the associated core 2 branching activity during virus replication in vitro. Secondly, in order to investigate the roles of Bo17, its kinetic class of expression was analysed and a deleted recombinant strain was produced. These experiments revealed that Bo17 is expressed as an early gene which is not essential for virus replication in vitro. However, comparison of the structural proteins, produced by the wild-type, the revertant and the deleted viruses, by 2D gels demonstrated that pBo17 contributes to the post-translational modifications of structural proteins. Possible roles of Bo17 in vivo are discussed.

Enzyme Induction↗
PubMed1998

Retinoid-induced repression of human immunodeficiency virus type 1 core promoter activity inhibits virus replication.

The rates of mother-to-child transmission of human immunodeficiency virus type 1 (HIV-1), progression to AIDS following HIV-1 infection, and AIDS-associated mortality are all inversely correlated with serum vitamin A levels (R. D. Semba, W. T. Caiaffa, N. M. H. Graham, S. Cohn, and D. Vlahov, J. Infect. Dis. 171:1196-1202, 1995; R. D. Semba, N. M. H. Graham, W. T. Caiaffa, J. B. Margolik, L. Clement, and D. Vlahov, Arch. Intern. Med. 153:2149-2154, 1993; R. D. Semba, P. G. Miotti, J. D. Chiphangwi, A. J. Saah, J. K. Canner, G. A. Dallabetta, and D. R. Hoover, Lancet 343:1593-1596, 1994). Here we show that physiological concentrations of vitamin A, as retinol or as its metabolite, all-trans retinoic acid, repressed HIV-1Ba-L replication in monocyte-derived macrophages (MDMs). Repression required retinoid treatment of peripheral monocytes during their in vitro differentiation into MDMs. Retinoids had no repressive effect if they were added after virus infection. Retinol, as well as all-trans retinoic acid and 9-cis retinoic acid, also repressed HIV-1 long terminal repeat (LTR)-directed expression up to 200-fold in transfected THP-1 monocytes. Analysis of HIV-1 LTR deletion mutants demonstrated that retinoids were able to repress activation of HIV-1 expression by both NF-kappaB and Tat. A cis-acting sequence required for retinoid-mediated repression of HIV-1 transcription was localized between nucleotides -51 and +12 of the HIV-1 LTR within the core promoter. Protein-DNA cross-linking experiments identified four proteins specific to retinoid-treated cells that bound to the core promoter. We conclude that retinoids render macrophages resistant to virus replication by modulating the interaction of cellular transcription factors with the viral core promoter.

Cell Differentiation↗
PubMed2004

Human cytomegalovirus proteins encoded by UL37 exon 1 protect infected fibroblasts against virus-induced apoptosis and are required for efficient virus replication.

Human cytomegalovirus (HCMV) strain AD169 mutants carrying transposon insertions or large deletions in UL37 exon 1 (UL37x1) were recovered from modified bacterial artificial chromosomes by reconstitution in human fibroblasts expressing the adenovirus anti-apoptotic protein E1B19K. UL37x1 mutant growth was severely compromised in normal fibroblasts, with minimal release of infectious progeny. Growth in E1B19K-expressing cells was restored, but did not reach wild-type levels. Normal fibroblasts infected by UL37x1 mutants underwent apoptosis spontaneously between 48 and 96 h after infection. Apoptosis was inhibited by treatment of cells with the broad-spectrum caspase inhibitor z-Val-Ala-Asp(OMe)-fluoromethylketone, resulting in substantially increased release of virus. Inhibition of viral DNA replication by phosphonoformate or ganciclovir also inhibited apoptosis, implying that death was triggered by late viral functions or by replication and packaging of the viral genome. Immunofluorescent staining showed that although viral proteins accumulated normally during delayed-early phase and viral DNA replication compartments formed, viral late proteins were detected only rarely, suggesting that spontaneous apoptosis occurs early in late phase. These results demonstrate that anti-apoptotic proteins encoded by HCMV UL37x1 [pUL37x1 (vMIA), gpUL37 and gpUL37(M)] prevent apoptosis that would otherwise be initiated by the replication programme of the virus and are required for efficient and sustainable virus replication.

Apoptosis↗
PubMed1981

Varicella-zoster virus infection of diploid and chemically transformed guinea-pig embryo cells: factors influencing virus replication.

Factors influencing the replication of varicella-zoster virus (VZV) in guinea-pig embryo cells were evaluated using both diploid cells (GPEC) and a chemically transformed cell line (GPT). Wild-type and vaccine strains of VZV were successfully isolated and serially propagated in GPEC prepared from early gestation whole embryos (less than 2 cm in length). Low passage GPEC (less than or equal to 5 subcultivations) were more susceptible to VZV infection than high passage GPEC (greater than 5 subcultivations), and guinea-pig cells were consistently less permissive than human diploid cells. Cell-free virus was produced from VZV-infected GPEC cultures by sonication and peak yields of 10(3) p.f.u./ml were obtained. In addition, we report the isolation and propagation of VZV, as well as production of cell-free virus, in GPT. Both GPEC and GPT cells were less susceptible to VZV infection than human cells. However, viral replication was enhanced by incubation of VZV-infected GPT cultures at 32 degree C rather than 36 degree C.

Animals↗
PubMedDate not supplied

Duck plague virus replication in muscovy duck fibroblast cells.

Duck embryo fibroblast cell cultures from seven species of ducks were compared for virus yield, plaque quality, and sensitivity to infection by the duck plague herpesvirus (duck virus enteritis). Muscovy duck and wood duck cells gave the best results for virus yield and plaque quality, but muscovies were considered superior because they are more available than wood ducks. Pintails and lesser scaup gave the poorest results, and pekin duck, black duck, and redhead duck were intermediate. A growth curve for the virus, determined in muscovy cells, had a latent period of six hours and a maximum new virus titer reached at 36 hours. Because of their superior plaque production and ability to replicate the virus, muscovy embryo fibroblasts (MCE) are recommended for diagnostic and research work.

Animals↗
PubMed1991

Epstein-Barr virus infection in oral hairy leukoplakia: virus replication in the absence of a detectable latent phase.

Epstein-Barr virus (EBV) infects both B lymphocytes and oropharyngeal epithelium, and it has been argued that the true reservoir of virus persistence in vivo is the self-renewing basal epithelial compartment. The identification of oral hairy leukoplakia (HL) of AIDS patients as a clinically apparent focus of EBV replication in lingual epithelium therefore provides a means of studying the EBV-epithelial cell interaction in situ. Replicative EBV DNA and productive cycle antigens are restricted to the upper, more differentiated epithelial layers in HL, and here we have applied highly sensitive in situ hybridization and immunohistological methods to examine the lower basal/suprabasal layers for evidence of latent EBV infection. We could not detect EBV DNA in these layers using an in situ DNA hybridization protocol which, on reference B cell lines, detected 1 viral genome/cell. Likewise, using sensitive in situ RNA hybridization for both the small non-polyadenylated EBER RNAs (abundant transcripts seen in all known forms of EBV latency) and the latent membrane protein (LMP) mRNA (the most abundant viral mRNA in B lymphoblastoid cell lines), the basal/suprabasal cells in HL were consistently negative; immunohistological staining with specific monoclonal antibodies also gave no evidence of latently infected LMP-positive cells. When the biopsy extracts were analysed by immunoblotting with selected human antisera, in addition to abundant productive cycle antigens, a band of constant size (66K) was observed which also reacted with immunopurified antibodies monospecific for one of the latency-associated nuclear antigens, EBNA 1; the cellular origin of this EBNA 1 could not be ascertained, but it is possible that in HL the protein is expressed during the productive cycle. The absence of demonstrable EBV latency in the basal/suprabasal cells of HL suggests that this is purely a virus replicative lesion which is sustained by continual re-infection of the maturing epithelium, not by the maturation of latently infected cells from the basal compartment.

Antigens, Viral↗
PubMed1999

Liver and peripheral blood mononuclear cells are not major sites for GB virus-C/hepatitis G virus replication.

The pathogenesis and replication sites of GB virus-C/hepatitis G virus (GBV-C/HGV) in humans remain unclear. The presence of GBV-C/HGV and hepatitis C virus (HCV) RNA sequences in matched serum, peripheral blood mononuclear cells (PBMC) and liver samples in 10 patients with GBV-C/HGV infection, 8 of whom were coinfected with HCV was explored. Positive- and negative-strand GBV-C/HGV and HCV RNA were detected by strand-specific reverse-transcription polymerase chain reaction (RT-PCR), and virus titers were quantified by competitive PCRs. Positive-strand GBV-C/HGV RNA was detected in 7 of 10 PBMC samples of the patients with serum GBV-C/HGV RNA, but negative-strand GBV-C/HGV RNA was not found in these cells. Positive-strand GBV-C/HGV RNA was found in 9 liver samples, and 2 (22%) of them also had negative strand. In contrast, negative-strand HCV RNA was frequently found in PBMC and liver samples. A positive correlation between the titer of viral RNA in liver tissue and that in serum sample was demonstrated in HCV infection, but not in GBV-C/HGV infection. These findings suggest that liver and PBMC are not the major replication sites for GBV-C/HGV and that GBV-C/HGV is not a primary hepatotropic virus.

Adult↗
PubMed1975

Sindbis virus replication in vertebrate and mosquito cells: an interpretation.

This paper summarizes recent comparative studies of Sindbis virus (SV) replication in cultured Aedes albopictus (A. albo) or (A. aegypti (A. aeg) and BHK21 or chick embryo (CEF) cells. 1. Viral growth kinetics and yields are similar in A. albo cells at 28 degress C and in vertebrate cells at 37 degrees C. A. albo exhibit no CPE and yield persistenetly infected cultures. 2. SV grown in A. albo cells lacks sialic acid but is antigenically and in terms of particle/PFU or particle/HAU ratios equivalent to SV derived from vertebrate cells. The contrast to VSV in the latter respect is discussed. 3. SV from persistently infected A. albo or A. aeg cells is temperature-sensitive, thermolabile, and produces small plaques. Partial characterization of these mutants, of RNA associated with their replication, and their high reversion rate to ts+ upon serial undiluted passage in GHK21 cells are presented. 4. Hostdependent differences in the generation of defective-interfering (DI) SV particles and of low molecular weight viral RNA species have been observed upon undiluted serial passages in BHK21 and CEF. In contrast, serial passage in A. albo cells appears not to produce DI particles or small RNA species nor do these cells "recognize" as such DI particles from BHK21 cells. 5. Possible implications of these observations fro the natural life cycle of arthropod-borne togaviruses are discussed.

Aedes↗
PubMed1986

Modification of Epstein-Barr virus replication by tunicamycin.

The effect of tunicamycin, which inhibits N-linked glycosylation, on the replication of Epstein-Barr virus was examined. Tunicamycin markedly reduced the yield of virus from producing cells. At concentrations of 1 to 2 micrograms of tunicamycin per ml, there was a buildup of intracellular virus in P3HR1-Cl13 cells but not in MCUV5 cells; at a concentration of 5 micrograms of tunicamycin per ml in P3HR1-Cl13 cells, viral DNA synthesis was inhibited as well. Viral glycoproteins lacking N-linked sugars were apparently inserted into the cell membrane, and the small amount of virus made in the presence of drug was able to bind specifically to its receptor on B cells. However, the ability of the virus to induce immunoglobulin secretion by fresh human lymphocytes was impaired. This implies a role for viral glycoproteins in the penetration as well as the attachment of virus.

Animals↗
PubMed2005

Hepatitis C virus replicates in peripheral blood mononuclear cells of patients with occult hepatitis C virus infection.

BACKGROUND: Occult hepatitis C virus (HCV) infection is characterised by the presence of HCV-RNA in the liver in the absence of anti-HCV, and serum viral RNA. Up to 70% of these patients also have HCV-RNA in peripheral blood mononuclear cells (PBMC) but it is not known if HCV is replicating in these cells. AIM: We studied possible HCV replication in PBMC of 18 patients with an occult HCV infection who were selected on the basis of HCV-RNA positivity in PBMC. METHODS: Detection of HCV-RNA positive and negative strands in PBMC was done by strand specific reverse transcriptase-polymerase chain reaction (RT-PCR) and by in situ hybridisation. RESULTS: The presence of HCV-RNA positive strand in PBMC was confirmed in all patients by strand specific RT-PCR and by in situ hybridisation. Mean percentage of PBMC which had the HCV-RNA positive strand was 3.3% (95% confidence interval (CI) 2.1-4.4) The HCV-RNA negative strand was found in the PBMC of 11/18 (61%) patients by strand specific RT-PCR and confirmed by in situ hybridisation, and the percentage of PBMC harbouring the HCV-RNA negative strand was 3.1% (95% CI 0.8-5.5). There was a significant correlation (p = 0.001, r = 0.84) between the percentage of PBMC with the HCV-RNA positive strand and that of PBMC with the HCV-RNA negative strand. CONCLUSION: HCV replicates in the PBMC of patients with occult HCV infection and thus, although these patients do not have serum HCV-RNA, they could be potentially infectious.

Adult↗
PubMed1998

Detection of hepatitis C virus replication in peripheral blood mononuclear cells after orthotopic liver transplantation.

BACKGROUND: The presence of hepatitis C virus (HCV) replication in peripheral blood mononuclear cells (PBMCs) remains controversial. We determined the presence of the negative HCV RNA strand in PBMCs from a group of HCV-positive patients before and after liver transplantation. METHODS: Nine patients receiving orthotopic liver transplantation for end-stage HCV-related liver disease were studied. PBMCs were collected on the day of transplantation and 1 month later. The negative HCV RNA strand was detected by highly strand-specific Tth-based reverse transcriptase polymerase chain reaction. RESULTS: All nine patients were positive for the presence of the HCV RNA-positive strand in serum and PBMCs both before and after transplantation. The presence of the negative HCV RNA strand was documented in three PBMC samples after transplantation but in none of the samples collected before transplantation. CONCLUSION: Our results suggest that under circumstances of impaired immunity associated with pharmacological immunosuppression, HCV may be lymphotropic in vivo.

Hepacivirus↗
PubMed1986

Theiler's virus replication in isolated Schwann cell cultures.

Theiler's murine encephalomyelitis viruses causing both fatal encephalitis (GDVII virus) and chronic demyelinating disease (WW virus) are capable of replicating in isolated Schwann cell cultures. Light microscopy combined with immunohistochemical staining of viral antigens revealed that large numbers of Schwann cells infected with the two viruses show cytopathic effect (rounding) and contain viral antigens. Electron microscopy of virus-infected Schwann cells shows that the morphological alterations that the cells undergo following infection by the two virus isolates are different. In the early stages of GDVII and WW virus infection, different inclusion bodies are formed in the cells cytoplasm. At late stages of the infection GDVII virions are found in all infected cells and are arranged in crystalline arrays around inclusion bodies. In contrast, in WW virus-infected Schwann cells only in few cells virions were observed and they appeared aligned between two membrane units.

Animals↗
PubMed1980

Replication of human cytomegalovirus at supra-optimal temperatures is dependent on the virus strain, multiplicity of infection and phase of virus replication.

The kinetics of replication of five strains of human cytomegalovirus (CMV) were studied to determine the influence of (i) temperature, (ii) virus strain, (iii) m.o.i. and (iv) cell type. Relative to growth at 37 degrees C (m.o.i. = 3 to 9) eclipse periods were extended from 24 to 48 h at 33 degrees C and to 72 h at 40.5 degrees C. Yields were reduced at 33 degrees C and almost eliminated at 40.5 degrees C. No replication occurred in most instances at 40.5 degrees C and with 0.05 p.f.u./cell. Temperature shift studies (40.5 to 37 degrees C) indicated that the block to replication at 40.5 degrees occurred about 12 to 16 h p.i. resulting in little synthesis of CMV DNA or late antigens. The degree of inhibition of late functions at 40.5 degrees C is virus strain and m.o.i. dependent, but is not dependent on the type of fibroblastic cell used. These data suggest that persistent CMV infections are favoured at 40.5 degrees C.

Antigens, Viral↗