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Results for “Virus Replication”

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At least 703 records · Page 39Linked to original sources

PubMed1985

Effects of temperature on Epstein-Barr virus replication in epithelial/nasopharyngeal carcinoma hybrid cells.

The authors studied the replication of Epstein-Barr virus (EBV) in the epithelial hybrid cells derived from nasopharyngeal carcinoma (NPCKT) caused by the effects of sub-optimal incubation at 34, 32 and 28 degrees C, respectively, using an immunofluorescence technique. The intensity of EBV induction by sub-optimal temperatures was in the order of 32 degrees C----28 degrees C----34 degrees C. In particular, 18-24% positive cells for early antigen and viral capsid antigen were observed at around 10 to 14 days after shift-down of the incubation temperature from 37 to 32 degrees C.

Animals↗

PubMed1978

Type B and type C RNA tumor virus replication in single cells. Electron microscopy with tannic acid.

Simultaneous replication of murine mammary tumor virus (type B) and murine leukemia virus (type C) was demonstrated electron microscopically along continuous stretches of the plasma membrane of single cells in cultures ofthe Mm5mt/c1 cell line. Types B and C virus buds were discriminated in thin sections with the aid of a tannic acid fixative that revealed the type B surface spikes as a homogeneous band of intermediate density and constant width on the surfaces of some buds (type B), whereas others (type C) remained with relatively smooth envelopes. Both types B and C buds may contain morphologically identical horseshoe-shaped nucleoids. Therefore, their identify (type B or C) could be ascertained in thin sections only on the basis of recognition of surface spikes.

Hydrolyzable Tannins↗

PubMed1992

Cellular antioxidant status and human immunodeficiency virus replication.

The factors that stimulate replication of the human immunodeficiency virus (HIV) and determine the period of disease latency are poorly understood. Recent evidence from in vitro cell culture studies of HIV-infected cells suggest that HIV activity is profoundly affected by the presence of antioxidants, such as glutathione and ascorbic acid, in the cell culture medium. These in vitro observations and reports of global glutathione deficiency in nonsymptomatic HIV-seropositive subjects suggest that cellular antioxidant status may be an important factor determining the latency period of HIV infection. The molecular mechanisms underlying HIV activation are beginning to be understood and point to a potentially important role for NK-kappa B, a cellular transcription factor that may be modulated by cellular antioxidant status.

Acetylcysteine↗

PubMed1986

Antiviral effect of ribavirin on Junin virus replication in vitro.

The effect of Ribavirin (1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide) on the replication in vitro of Junin virus, the causative agent of Argentine Hemorrhagic Fever (AHF), was examined. A concentration as low as 3.12 micrograms/ml of the drug inhibited the cytopathic effect observed five days post-infection (pi) on Vero cells. On the other hand, a concentration of 25 micrograms/ml reduced the virus yield and specific antigen formation to undetectable levels. This same concentration of Ribavirin prevented plaque formation under methylcellulose. The high sensitivity of Junin virus to Ribavirin in vitro, the low toxicity of the drug for mammals and the therapeutic effect observed on in vivo infections with other arenaviruses, makes Ribavirin a promising antiviral agent that deserves testing on AHF primate models before clinical trials are undertaken.

Animals↗

PubMed1988

Inhibition of feline infectious peritonitis virus replication by recombinant human leukocyte (alpha) interferon and feline fibroblastic (beta) interferon.

Replication of feline infectious peritonitis virus (FIPV) in feline cell cultures was inhibited after incubation of cells with either human recombinant leukocyte (alpha) interferon (IFN) or feline fibroblastic (beta) IFN for 18 to 24 hours before viral challenge exposure. Compared with virus control cultures, FIPV yields were reduced by ranges of 0.1 to 2.7 log10 or 2 to 5.2 log10 TCID50 in cultures treated with human alpha- or feline beta-IFN, respectively; yield reductions were IFN dose dependent. Sensitivity to the antiviral activities of IFN varied with cell type; feline embryo cells had greater FIPV yield reductions than did similarly treated feline kidney or feline lung cells. Comparison of the virus growth curves in IFN-treated and virus control cultures indicated marked reduction in intracellular and extracellular FIPV in IFN-treated cultures. Compared with virus control cultures, intracellular and extracellular infectivity in IFN-treated cultures was delayed in onset by 12 and 30 hours, respectively, and FIPV titers subsequently were reduced by 3 to 3.5 and 5 log10 TCID50, respectively. Frequently, immunofluorescent and electron microscopy of IFN-treated cells or cell culture fluids did not reveal virus; however, even in cultures without viral cytopathic changes, small amounts of virus occasionally persisted in cells.

Animals↗

PubMed1975

Virus replication and cell modifications in organ cultures of tumor tissue from chickens with Marek's disease.

Organ cultures of lymphomas from chickens infected with Marek's disease (MD) virus were examined by electron microscopy at various periods after explantation. Non-enveloped herpes-type virions were observed in explants 18 days after the culture was initiated. Cytolytic virus was replicated often in lymphoblastoid cells and occasionally in other cell types (permissive and nonpermissive transformed). The permissive cells were numerous, but nonpermissive transformed cells were also present as indicated by the longevity of some cultures. The presence of both permissive and transformed cell types in the organ cultures and reasons for their sequential appearance were discussed. The results unequivocally demonstrated that lymphoid cells of tumors induced by MD virus were sites of virus replication under proper culture conditions.

Animals↗

PubMed2004

The role of inducer cells in mediating in vitro suppression of feline immunodeficiency virus replication.

CD8+ T-cell-mediated suppression of feline immunodeficiency virus (FIV) replication has been described by several groups, although the mechanisms of activation and conditions for viral suppression vary with the methodologies. We have previously reported that CD8+ T-cell-mediated suppression of FIV replication required inducer cell stimulation of the effector cells. The focus of the present study was to examine the essential role of inducer cells required for the induction of this soluble anti-FIV activity. Both FIV-PPR-infected T cells and feline skin fibroblasts (FSF) infected with an alphavirus vector expressing FIV capsid or the irrelevant antigen lacZ, stimulated autologous or heterologous effector cells to produce supernatants that suppressed FIV replication. Thus, induction of this suppression of FIV replication did not strictly require autologous inducer cells and did not require the presence of FIV antigen. Anti-viral activity correlated with the presence of CD8+ T cells. Suppression was maximal when the inducer cells and the effector cells were in contact with each other, because separation of the inducer and effector cells by a 0.45-microm membrane reduced FIV suppression by approximately 50%. These findings emphasize the importance for membrane antigen interactions and cytokines in the optimal induction of effector cell synthesis of the soluble anti-FIV activity.

Animals↗

PubMed1999

Resveratrol inhibition of herpes simplex virus replication.

Resveratrol, a phytoalexin, was found to inhibit herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) replication in a dose-dependent, reversible manner. The observed reduction in virus yield was not caused by the direct inactivation of HSV by resveratrol nor inhibition of virus attachment to the cell. The chemical did, however, target an early event in the virus replication cycle since it was most effective when added within 1 h of cell infection, less effective if addition was delayed until 6 h post-infection and not effective if added 9 h post-infection. Resveratrol was also found to delay the cell cycle at S-G2-M interphase, inhibit reactivation of virus from latently-infected neurons and reduce the amount of ICP-4, a major immediate early viral regulatory protein, that is produced when compared to controls. These results suggest that a critical early event in the viral replication cycle, that has a compensatory cellular counterpart, is being adversely affected.

Animals↗

PubMed1996

Role of interferon-stimulated gene ISG-15 in the interferon-omega-mediated inhibition of human immunodeficiency virus replication.

Interferon-alpha (IFN-alpha) inhibits human immunodeficiency virus (HIV) replication in vivo and in vitro. In this study, we show that IFN-omega (IFN-omega) is also a potent inhibitor of HIV replication in vitro and that both laboratory and primary isolates of HIV-1 are more sensitive to IFN-omega than to IFN-alpha 2. Like IFN-alpha 2, IFN-omega inhibited proviral synthesis in acutely infected cells, but in contrast to IFN-alpha 2, IFN-omega did not alter the levels of HIV-1 unspliced messages. Yet, inhibition of HIV protein synthesis was greater in IFN-omega-treated than in IFN-alpha 2-treated cells. Whereas expression of IFN-stimulated genes was transient in IFN-alpha 2-treated cells, their expression was sustained in IFN-omega-treated cells. Expression of ISG-15 in particular was higher on treatment with IFN-omega than with IFN-alpha 2. Overexpression of ISG-15 in IFN-alpha 2-treated cells mimicked the effects of IFN-omega. In untreated cells, it resulted in the trapping of HIV unspliced RNA in the nucleus and a decrease in cytoplasmic HIV transcripts and HIV protein synthesis. These findings suggest that the sustained induction of IFN-stimulated genes by IFN-omega and that of ISG-15 in particular may confer a higher therapeutic index to IFN-omega in controlling HIV infection.

Antiviral Agents↗

PubMed2004

Structural and virological studies of the stages of virus replication that are affected by antirhinovirus compounds.

Pleconaril is a broad-spectrum antirhinovirus and antienterovirus compound that binds into a hydrophobic pocket within viral protein 1, stabilizing the capsid and resulting in the inhibition of cell attachment and RNA uncoating. When crystals of human rhinovirus 16 (HRV16) and HRV14 are incubated with pleconaril, drug occupancy in the binding pocket is lower than when pleconaril is introduced during assembly prior to crystallization. This effect is far more marked in HRV16 than in HRV14 and is more marked with pleconaril than with other compounds. These observations are consistent with virus yield inhibition studies and radiolabeled drug binding studies showing that the antiviral effect of pleconaril against HRV16 is greater on the infectivity of progeny virions than the parent input viruses. These data suggest that drug integration into the binding pocket during assembly, or at some other late stage in virus replication, may contribute to the antiviral activity of capsid binding compounds.

Antiviral Agents↗

PubMed1985

Human cytomegalovirus completely helps adeno-associated virus replication.

Coinfection of adeno-associated virus (AAV) with human cytomegalovirus (HCMV) strain Towne in human embryonic fibroblasts resulted in accumulation of AAV capsid antigen and production of infectious AAV with a lag of 24 hr compared to AAV replication in AAV-adenovirus coinfections. In contrast to previous observation, these findings demonstrated that HCMV is a competent helper virus for the complete replication of AAV. In addition, HCMV and AAV were synergistic in their cytopathic effects on cells, suggesting the possibility that AAV may play a role in the pathogenicity of HCMV infections.

Antigens, Viral↗

PubMed2003

Transcription factor USF, expressed during the entire phase of varicella-zoster virus infection, interacts physically with the major viral transactivator IE62 and plays a significant role in virus replication.

The expression of the genes of varicella-zoster virus (VZV) is regulated by self-encoded viral as well as cellular transcription factors. A potential candidate with an ability to influence the transcription of VZV genes is USF (upstream stimulatory factor), which recognizes the consensus E-box motif. Quantitative RT-PCR and immunoblot assays indicate stable expression of both USF1 and USF2 throughout infection. It was also found that USF binds to a variety of E-boxes (consensus and closely related motifs) within the promoters of ORF 8/9 (two elements), ORF 22 and ORF 67. Co-immunoprecipitation experiments and His-tag protein affinity pull-down assays indicate that a direct physical interaction occurs between USF and the major virus transactivator IE62. To study the general effects of USF in the replication of VZV, a cell line expressing a dominant-negative form of USF (A-USF), which inhibits binding of USF to its recognition sites, was created. A significant decrease in virus replication was detected when this cell line was infected with cell-free virus, indicating that USF is an important cellular factor that regulates the transcription of VZV genes.

Animals↗

PubMed2001

Structure-activity of inhibition of HIV-1 integrase and virus replication by G-quartet oligonucleotides.

As novel anti-HIV agents, the G-tetrad-forming oligonucleotides have been explored for their structure-activity relations with regard to inhibition of integrase (IN) (N. Jing, Expert Opin. Investig. Drugs (2000) 9, 1777-1785). We have now developed two families of G-quartet oligonucleotides: T40217-T40222, with potential formation of a tail-to-tail G-quartet dimer, and T40224-T40227, with phosphorothioate (PT) linkages in the guanine loops. The results obtained from biophysical measurements and the assays of the inhibition of HIV-1 IN and virus replication demonstrated that an increase in the length of the G-quartet structure from a monomer (15A) to a tail-to-tail dimer (47A) does not distinctly disrupt the inhibition of HIV-1 IN activity or the inhibition of HIV-1 replication in cell cultures. G-quartet oligonucleotides were observed to induce molecular aggregation of HIV-1 IN and interrupt the binding of viral DNA to HIV-1 IN. Also, PT substitutions did not confer any advantages compared with the regular phosphodiesters for the inhibition of HIV-1 replication by intramolecular G-quartets. The G-quartet motif is the primary requirement for the remarkable nuclease resistance and pronounced biological efficacy of these oligonucleotides.

Cell Line↗

PubMed2003

The latency-associated nuclear antigen homolog of herpesvirus saimiri inhibits lytic virus replication.

Herpesvirus saimiri (HVS), a T-lymphotropic tumor virus of neotropical primates, and the Kaposi's sarcoma-associated human herpesvirus 8 (KSHV) belong to the gamma-(2)-herpesvirus (Rhadinovirus) subfamily and share numerous features of genome structure and organization. The KSHV latency-associated nuclear antigen (LANA) protein appears to be relevant for viral persistence, latency, and transformation. It binds to DNA, colocalizes with viral episomal DNA, and presumably mediates efficient persistence of viral genomes. LANA further represses the transcriptional and proapoptotic activities of the p53 tumor suppressor protein. Here we report on the ORF73 gene of HVS strain C488, which is the positional and structural homolog of KSHV LANA. The ORF73 gene in OMK cells can encode a 62-kDa protein that localizes to the nucleus in a pattern similar to that of LANA. We show that the ORF73 gene product can regulate viral gene expression by acting as a transcriptional modulator of latent and lytic viral promoters. To define the HVS ORF73 function in the background of a replication-competent virus, we constructed a viral mutant that expresses ORF73 under the transcriptional control of a mifepristone (RU-486)-inducible promoter. The HVS ORF73 gene product efficiently suppresses lytic viral replication in permissive cells, indicating that it defines a critical control point between viral persistence and lytic replication.

Animals↗

PubMed2006

Formation of nsP3-specific protein complexes during Sindbis virus replication.

Alphaviruses are arthropod-borne viruses (arboviruses) that include a number of important human and animal pathogens. Their replication proceeds in the cytoplasm of infected cells and does not directly depend on nuclei. Alphaviruses encode only four nonstructural proteins that are required for the replication of viral genome and transcription of the subgenomic RNA. However, the replicative enzyme complexes (RCs) appear to include cellular proteins and assemble on cellular organelles. We have developed a set of recombinant Sindbis (SIN) viruses with green fluorescent protein (GFP) insertions in one of the nonstructural proteins, nsP3, to further understand the RCs' genesis and structure. We studied the assembly of nsP3/GFP-containing protein complexes at different stages of infection and isolated a combination of cellular proteins that are associated with SIN nsP3. We demonstrated the following. (i) SIN nsP3 can tolerate the insertion of GFP into different fragments of the coding sequence; the designed recombinant viruses are viable, and their replication leads to the assembly of nsP3/GFP chimeric proteins into gradually developing, higher-order structures differently organized at early and late times postinfection. (ii) At late times postinfection, nsP3 is assembled into complexes of similar sizes, which appear to be bound to cytoskeleton filaments and can aggregate into larger structures. (iii) Protein complexes that are associated with nsP3/GFP contain a high concentration of cytoskeleton proteins, chaperones, elongation factor 1A, heterogeneous nuclear ribonucleoproteins, 14-3-3 proteins, and some of the ribosomal proteins. These proteins are proposed to be essential for SIN RC formation and/or functioning.

Animals↗

PubMed2004

Bacillus alcalophilus peptidoglycan induces IFN-alpha-mediated inhibition of vaccinia virus replication.

Bacterial products such as cell walls (CW) and peptidoglycan (PGN) are known to activate macrophages and NK cells during microbial infections. In this report, we demonstrated that whole CW and PGN of four Gram-positive bacteria are capable of enhancing the anti-poxviral activity of murine macrophage RAW 264.7 cells. Among the major Bacillus alcalophilus CW components, PGN contributes the most to antiviral activity and induces remarkably higher levels of IFN-alpha. Anti-IFN-alpha/beta antibody, but not anti-IFN-gamma, anti-IFN-gamma receptor, or anti-IL-12, reversed the PGN-induced inhibition of vaccinia virus replication and reduced nitric oxide (NO) production. Our data thus suggest that PGN induce antiviral activity through IFN-alpha and to a lesser extent, through NO production.

Animals↗

PubMed1987

Suppression of human immunodeficiency virus replication by 3'-azido-3'-deoxythymidine in various human hematopoietic cell lines in vitro: augmentation of the effect by lentinan.

The effect of 3'-azido-3'-deoxythymidine (AZT) on replication of human immunodeficiency virus (HIV) in various hematopoietic cell lines was investigated. The concentration of AZT required to block HIV replication varied depending on the cell line used. U-937 cells required as little as 0.01 microM AZT to block HIV replication, a concentration almost 100 times lower than that required for MT-4 or MOLT-4 cells. However, 467 and TALL-1 cells required concentrations of AZT higher than 5 microM. It was clear that AZT was ineffective once the viral gene was integrated into chromosomal DNA; removal of AZT from culture fluids at that stage allowed the full expression of HIV. The effect of the potent immunostimulator lentinan was also examined, and it was shown that lentinan enhanced the effect of AZT.

Cell Line↗

PubMed1999

Status of long-term asymptomatic HIV-1 infection correlates with viral load but not with virus replication properties and cell tropism. French ALT Study Group.

Qualitative and quantitative virological parameters were investigated in 68 long-term nonprogressor (LTNP) HIV-1-infected patients and 9 slow-progressor controls. LTNP status was defined as an asymptomatic HIV infection for at least 8 years, a stability of CD4+ cell counts > or =600 cells/mm3 and no antiretroviral therapy. LTNP subjects exhibited a lower median plasma RNA load than controls (6,000 vs. 40,000 RNA copies/ ml) despite a wide range of values in both groups. When compared to the control group, LTNP subjects also exhibited a lower virus isolation rate (65% vs. 100%) and cell-associated viremia (0.75 vs. 56.8 number of infectious unit/ million cells) when CD8-depleted CD4+ cells were tested. By contrast, no major differences in virus replication properties or cell tropism were observed. After 1 year of follow-up, no major overall changes in the virological parameters was observed in the 50 LTNP subjects evaluated at this time. However, nine patients had started antiretroviral therapy, and six others had increased viral loads. Despite the progression observed during the first year of follow-up, the hypothesis that there is a specific subgroup of LTNP patients who will not develop disease cannot be ruled out as yet.

CD4-Positive T-Lymphocytes↗