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Journal articles on the topic 'Virus replication'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Lee-Chen, G. J., and M. Woodworth-Gutai. "Evolutionarily selected replication origins: functional aspects and structural organization." Molecular and Cellular Biology 6, no. 9 (1986): 3077–85. http://dx.doi.org/10.1128/mcb.6.9.3077-3085.1986.

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A selective replicative pressure occurs during the evolution of simian virus 40 variants. When the replication origin is duplicated as an inverted repeat, there is a dramatic enhancement of replication. Having regulatory sequences located between the inverted repeat of ori magnifies their enhancing effect on replication. A passage 20 variant and a passage 45 variant containing three pairs of an inverted repeat of ori replicated more efficiently than a passage 13 variant containing nine copies of ori arranged in tandem. A 69-base-pair cellular sequence inserted between inverted repeats of ori o

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Lee-Chen, G. J., and M. Woodworth-Gutai. "Evolutionarily selected replication origins: functional aspects and structural organization." Molecular and Cellular Biology 6, no. 9 (1986): 3077–85. http://dx.doi.org/10.1128/mcb.6.9.3077.

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A selective replicative pressure occurs during the evolution of simian virus 40 variants. When the replication origin is duplicated as an inverted repeat, there is a dramatic enhancement of replication. Having regulatory sequences located between the inverted repeat of ori magnifies their enhancing effect on replication. A passage 20 variant and a passage 45 variant containing three pairs of an inverted repeat of ori replicated more efficiently than a passage 13 variant containing nine copies of ori arranged in tandem. A 69-base-pair cellular sequence inserted between inverted repeats of ori o

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3

Targett-Adams, Paul, Steeve Boulant, and John McLauchlan. "Visualization of Double-Stranded RNA in Cells Supporting Hepatitis C Virus RNA Replication." Journal of Virology 82, no. 5 (2007): 2182–95. http://dx.doi.org/10.1128/jvi.01565-07.

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ABSTRACT The mechanisms involved in hepatitis C virus (HCV) RNA replication are unknown, and this aspect of the virus life cycle is not understood. It is thought that virus-encoded nonstructural proteins and RNA genomes interact on rearranged endoplasmic reticulum (ER) membranes to form replication complexes, which are believed to be sites of RNA synthesis. We report that, through the use of an antibody specific for double-stranded RNA (dsRNA), dsRNA is readily detectable in Huh-7 cells that contain replicating HCV JFH-1 genomes but is absent in control cells. Therefore, as that of other RNA v

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Avemann, K., R. Knippers, T. Koller, and J. M. Sogo. "Camptothecin, a specific inhibitor of type I DNA topoisomerase, induces DNA breakage at replication forks." Molecular and Cellular Biology 8, no. 8 (1988): 3026–34. http://dx.doi.org/10.1128/mcb.8.8.3026-3034.1988.

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The structure of replicating simian virus 40 minichromosomes, extracted from camptothecin-treated infected cells, was investigated by biochemical and electron microscopic methods. We found that camptothecin frequently induced breaks at replication forks close to the replicative growth points. Replication branches were disrupted at about equal frequencies at the leading and the lagging strand sides of the fork. Since camptothecin is known to be a specific inhibitor of type I DNA topoisomerase, we suggest that this enzyme is acting very near the replication forks. This conclusion was supported b

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Avemann, K., R. Knippers, T. Koller, and J. M. Sogo. "Camptothecin, a specific inhibitor of type I DNA topoisomerase, induces DNA breakage at replication forks." Molecular and Cellular Biology 8, no. 8 (1988): 3026–34. http://dx.doi.org/10.1128/mcb.8.8.3026.

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The structure of replicating simian virus 40 minichromosomes, extracted from camptothecin-treated infected cells, was investigated by biochemical and electron microscopic methods. We found that camptothecin frequently induced breaks at replication forks close to the replicative growth points. Replication branches were disrupted at about equal frequencies at the leading and the lagging strand sides of the fork. Since camptothecin is known to be a specific inhibitor of type I DNA topoisomerase, we suggest that this enzyme is acting very near the replication forks. This conclusion was supported b

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Peri, Piritta, Veijo Hukkanen, Kristiina Nuutila, Pekka Saukko, Magnus Abrahamson, and Tytti Vuorinen. "The cysteine protease inhibitors cystatins inhibit herpes simplex virus type 1-induced apoptosis and virus yield in HEp-2 cells." Journal of General Virology 88, no. 8 (2007): 2101–5. http://dx.doi.org/10.1099/vir.0.82990-0.

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The role of cystatins in herpes simplex virus (HSV)-induced apoptosis and viral replication has been studied. Human epithelial (HEp-2) cells infected with wild-type HSV-1 (F), with a deletion virus lacking the anti-apoptotic gene Us3 (R7041) or with a deletion virus lacking the anti-apoptotic genes Us3 and ICP4 (d120) were treated with cystatin A, C or D. Cells and culture media were studied at different time points for replicating HSV-1 and for apoptosis. Cystatins C and D inhibited the yield of replicative HSV-1 significantly in HEp-2 cells. In addition, cystatin D inhibited R7041 and d120 v

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7

Blight, Keril J., Jane A. McKeating, and Charles M. Rice. "Highly Permissive Cell Lines for Subgenomic and Genomic Hepatitis C Virus RNA Replication." Journal of Virology 76, no. 24 (2002): 13001–14. http://dx.doi.org/10.1128/jvi.76.24.13001-13014.2002.

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ABSTRACT Hepatitis C virus (HCV) replication appears to be restricted to the human hepatoma cell line Huh-7, indicating that a favorable cellular environment exists within these cells. Although adaptive mutations in the HCV nonstructural proteins typically enhance the replicative capacity of subgenomic replicons in Huh-7 cells, replication can only be detected in a subpopulation of these cells. Here we show that self-replicating subgenomic RNA could be eliminated from Huh-7 clones by prolonged treatment with alpha interferon (IFN-α) and that a higher frequency of cured cells could support both

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Danovich, R. M., and N. Frenkel. "Herpes simplex virus induces the replication of foreign DNA." Molecular and Cellular Biology 8, no. 8 (1988): 3272–81. http://dx.doi.org/10.1128/mcb.8.8.3272-3281.1988.

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Plasmids containing the simian virus 40 (SV40) DNA replication origin and the large T gene are replicated efficiently in Vero monkey cells but not in rabbit skin cells. Efficient replication of the plasmids was observed in rabbit skin cells infected with herpes simplex virus type 1 (HSV-1) and HSV-2. The HSV-induced replication required the large T antigen and the SV40 replication origin. However, it produced concatemeric molecules resembling replicative intermediates of HSV DNA and was sensitive to phosphonoacetate at concentrations known to inhibit the HSV DNA polymerase. Therefore, it invol

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9

Danovich, R. M., and N. Frenkel. "Herpes simplex virus induces the replication of foreign DNA." Molecular and Cellular Biology 8, no. 8 (1988): 3272–81. http://dx.doi.org/10.1128/mcb.8.8.3272.

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Plasmids containing the simian virus 40 (SV40) DNA replication origin and the large T gene are replicated efficiently in Vero monkey cells but not in rabbit skin cells. Efficient replication of the plasmids was observed in rabbit skin cells infected with herpes simplex virus type 1 (HSV-1) and HSV-2. The HSV-induced replication required the large T antigen and the SV40 replication origin. However, it produced concatemeric molecules resembling replicative intermediates of HSV DNA and was sensitive to phosphonoacetate at concentrations known to inhibit the HSV DNA polymerase. Therefore, it invol

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Kong, Ling, Rebekah Karns, Mohamed Tarek M. Shata, et al. "The synthetic opioid fentanyl enhances viral replication in vitro." PLOS ONE 16, no. 4 (2021): e0249581. http://dx.doi.org/10.1371/journal.pone.0249581.

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The US is in the midst of a major drug epidemic fueled in large part by the widespread recreational use of synthetic opioids such as fentanyl. Persons with opioid use disorder are at significant risk for transmission of injection-associated infections such as hepatitis B virus (HBV) and hepatitis C virus (HCV). Commonly abused substances may antagonize immune responses and promote viral replication. However, the impact of synthetic opioids on virus replication has not been well explored. Thus, we evaluated the impact of fentanyl and carfentanil using in vitro systems that replicate infectious

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Handa, Atsushi, and Kevin E. Brown. "GB virus C/hepatitis G virus replicates in human haematopoietic cells and vascular endothelial cells." Journal of General Virology 81, no. 10 (2000): 2461–69. http://dx.doi.org/10.1099/0022-1317-81-10-2461.

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A novel flavivirus, GB virus C (GBV-C)/hepatitis G virus (HGV), has been detected in chronic liver disease patients. It is known that the viral RNA can be detected in ∼5% of American blood donors. However, the implications for liver disease and the sites of virus replication remain unknown. Possible sites of virus replication were studied by using cell lines and/or primary cells derived from human lymphoid cells, myeloid cells, hepatocytes and endothelial cells. RNA was detected by virus strand-specific RT–PCR and GBV-C/HGV antigen was detected with a rabbit polyclonal anti-E2 (envelope 2) ant

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Lu, Hsin-Lin, and Fang Liao. "MDA5 Inhibits the Replication of Hepatitis B Virus (108.13)." Journal of Immunology 188, no. 1_Supplement (2012): 108.13. http://dx.doi.org/10.4049/jimmunol.188.supp.108.13.

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Abstract Hepatitis B virus (HBV) infection causes a wide spectrum of liver diseases; however, the innate immunity against HBV infection has been rarely studied and remains elusive. Here, we investigated the involvement of pattern recognition receptors, RIG-I like receptors (RLRs), in HBV replication. We demonstrated that the expression of MDA5, but not RIG-I, was increased in Huh-7 cells transfected with HBV replicative plasmids. Consistent with the in vitro finding, the expression of MDA5, but not RIG-I, was also increased in mice receiving HBV replicative plasmids through hydrodynamic inject

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Marriott, Anthony C., Joanne M. Smith, and Andrew J. Easton. "Fidelity of Leader and Trailer Sequence Usage by the Respiratory Syncytial Virus and Avian Pneumovirus Replication Complexes." Journal of Virology 75, no. 14 (2001): 6265–72. http://dx.doi.org/10.1128/jvi.75.14.6265-6272.2001.

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ABSTRACT The specificity of usage of promoters for replication and transcription by the pneumoviruses human respiratory syncytial virus (HRSV) and avian pneumovirus (APV) was studied using minigenomes containing a reporter gene. When infectious HRSV or APV was used as helper virus, replication could occur only if both the leader and trailer regions (containing the replicative and transcriptional promoters) were derived from the helper virus. In contrast, when the HRSV replication complex was supplied from cDNA plasmids, a minigenome containing either the APV leader or trailer was recognized an

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Snapka, R. M., M. A. Powelson, and J. M. Strayer. "Swiveling and decatenation of replicating simian virus 40 genomes in vivo." Molecular and Cellular Biology 8, no. 2 (1988): 515–21. http://dx.doi.org/10.1128/mcb.8.2.515-521.1988.

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We have found that type II topoisomerase inhibitors have two effects on replicating simian virus 40 genomes in vivo: production of catenated dimers and slowed replication of the last 5% of the genome. This suggests that type II topoisomerase simultaneously decatenates and facilitates replication fork movement at this stage of DNA replication. On the basis of this observation, a detailed model is proposed for the roles of topoisomerases I and II in simian virus 40 DNA replication.

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Snapka, R. M., M. A. Powelson, and J. M. Strayer. "Swiveling and decatenation of replicating simian virus 40 genomes in vivo." Molecular and Cellular Biology 8, no. 2 (1988): 515–21. http://dx.doi.org/10.1128/mcb.8.2.515.

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We have found that type II topoisomerase inhibitors have two effects on replicating simian virus 40 genomes in vivo: production of catenated dimers and slowed replication of the last 5% of the genome. This suggests that type II topoisomerase simultaneously decatenates and facilitates replication fork movement at this stage of DNA replication. On the basis of this observation, a detailed model is proposed for the roles of topoisomerases I and II in simian virus 40 DNA replication.

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16

Schultz, Kimberly L. W., and Paul D. Friesen. "Baculovirus DNA Replication-Specific Expression Factors Trigger Apoptosis and Shutoff of Host Protein Synthesis during Infection." Journal of Virology 83, no. 21 (2009): 11123–32. http://dx.doi.org/10.1128/jvi.01199-09.

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ABSTRACT Apoptosis is an important antivirus defense. To define the poorly understood pathways by which invertebrates respond to viruses by inducing apoptosis, we have identified replication events that trigger apoptosis in baculovirus-infected cells. We used RNA silencing to ablate factors required for multiplication of Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV). Transfection with double-stranded RNA (dsRNA) complementary to the AcMNPV late expression factors (lefs) that are designated as replicative lefs (lef-1, lef-2, lef-3, lef-11, p143, dnapol, and ie-1/ie-0) blocked

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Qiao, Zimu, Jin Wang, Kaiyun Huang, et al. "The non-template functions of helper virus RNAs create optimal replication conditions to enhance the proliferation of satellite RNAs." PLOS Pathogens 20, no. 4 (2024): e1012174. http://dx.doi.org/10.1371/journal.ppat.1012174.

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As a type of parasitic agent, satellite RNAs (satRNAs) rely on cognate helper viruses to achieve their replication and transmission. During the infection of satRNAs, helper virus RNAs serve as templates for synthesizing viral proteins, including the replication proteins essential for satRNA replication. However, the role of non-template functions of helper virus RNAs in satRNA replication remains unexploited. Here we employed the well-studied model that is composed of cucumber mosaic virus (CMV) and its associated satRNA. In the experiments employing the CMV trans-replication system, we observ

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Boehmer, Paul, and Amitabh Nimonkar. "Herpes Virus Replication." IUBMB Life (International Union of Biochemistry and Molecular Biology: Life) 55, no. 1 (2003): 13–22. http://dx.doi.org/10.1080/1521654031000070645.

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19

Nagy, Peter D., and Wenwu Lin. "Taking over Cellular Energy-Metabolism for TBSV Replication: The High ATP Requirement of an RNA Virus within the Viral Replication Organelle." Viruses 12, no. 1 (2020): 56. http://dx.doi.org/10.3390/v12010056.

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Recent discoveries on virus-driven hijacking and compartmentalization of the cellular glycolytic and fermentation pathways to support robust virus replication put the spotlight on the energy requirement of viral processes. The active recruitment of glycolytic enzymes in combination with fermentation enzymes by the viral replication proteins emphasizes the advantages of producing ATP locally within viral replication structures. This leads to a paradigm shift in our understanding of how viruses take over host metabolism to support the virus’s energy needs during the replication process. This rev

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Reifenberg, Kurt, Petra Nusser, Jürgen Löhler, et al. "Virus replication and virion export in X-deficient hepatitis B virus transgenic mice." Journal of General Virology 83, no. 5 (2002): 991–96. http://dx.doi.org/10.1099/0022-1317-83-5-991.

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The function of the X protein (pX) in the replication cycle of mammalian hepadnaviruses is enigmatic. Using tissue culture experiments it has been shown that the X gene product is not central to hepatitis B virus (HBV) replication and virion export. However, at present it is still unclear whether this also applies to the in vivo situation. Using a terminally redundant X-deficient HBV DNA construct, transgenic mice were established that exhibited high-level expression of the viral core protein in liver and kidneys. Importantly, replicative DNA intermediates and mature viral genomes could be det

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Dutta, Pinky, Andres Lõhmus, Tero Ahola, and Kristiina Mäkinen. "The Replicase Protein of Potato Virus X Is Able to Recognize and Trans-Replicate Its RNA Component." Viruses 16, no. 10 (2024): 1611. http://dx.doi.org/10.3390/v16101611.

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The trans-replication system explores the concept of separating the viral RNA involved in the translation of the replicase protein from the replication of the viral genome and has been successfully used to study the replication mechanisms of alphaviruses. We tested the feasibility of this system with potato virus X (PVX), an alpha-like virus, in planta. A viral RNA template was designed which does not produce the replicase and prevents virion formation but remains recognizable by the replicase. The replicase construct encodes for the replicase protein, while lacking other virus-specific recogn

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Buck, Kenneth W. "Replication of tobacco mosaic virus RNA." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1383 (1999): 613–27. http://dx.doi.org/10.1098/rstb.1999.0413.

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The replication of tobacco mosaic virus (TMV) RNA involves synthesis of a negative–strand RNA using the genomic positive–strand RNA as a template, followed by the synthesis of positive–strand RNA on the negative–strand RNA templates. Intermediates of replication isolated from infected cells include completely double–stranded RNA (replicative form) and partly double–stranded and partly single–stranded RNA (replicative intermediate), but it is not known whether these structures are double–stranded or largely single–stranded in vivo . The synthesis of negative strands ceases before that of positi

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Prakash, Om, Bhawana Jain, and Amita Jain. "Designing of putative siRNA to inhibit dengue virus replication." International Journal of Research and Development in Pharmacy & Life Sciences 7, no. 5 (2018): 3115–18. http://dx.doi.org/10.21276/ijrdpl.2278-0238.2018.7(5).3115-3118.

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Ball-Goodrich, Lisa J., Elizabeth Johnson, and Robert Jacoby. "Divergent replication kinetics of two phenotypically different parvoviruses of rats." Journal of General Virology 82, no. 3 (2001): 537–46. http://dx.doi.org/10.1099/0022-1317-82-3-537.

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Rat virus (RV) is an important infectious agent of laboratory rats because of its high prevalence and capacity to disrupt research. Additionally, RV infection serves as a model for characterizing virus–host interactions during acute, persistent and prenatal infection. Our research has examined the pathogenesis of two RV strains, RV-UMass and RV-Y. RV-UMass is more pathogenic, causes a higher level of persistent infection and transmits to the foetus after oronasal inoculation of the pregnant dam. To determine in vitro distinctions between the strains that may account for these differences and t

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Zhang, Zhensheng, Ulrike Protzer, Zongyi Hu, James Jacob, and T. Jake Liang. "Inhibition of Cellular Proteasome Activities Enhances Hepadnavirus Replication in an HBX-Dependent Manner." Journal of Virology 78, no. 9 (2004): 4566–72. http://dx.doi.org/10.1128/jvi.78.9.4566-4572.2004.

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ABSTRACT The X protein (HBX) of the hepatitis B virus (HBV) is not essential for the HBV life cycle in vitro but is important for productive infection in vivo. Our previous study suggests that interaction of HBX with the proteasome complex may underlie the pleiotropic functions of HBX. With the woodchuck model, we demonstrated that the X-deficient mutants of woodchuck hepatitis virus (WHV) are not completely replication defective, possibly behaving like attenuated viruses. In the present study, we analyzed the effects of the proteasome inhibitors on the replication of wild-type and X-negative

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Matano, Tetsuro, Masahiro Kobayashi, Hiroko Igarashi, et al. "Cytotoxic T Lymphocyte–based Control of Simian Immunodeficiency Virus Replication in a Preclinical AIDS Vaccine Trial." Journal of Experimental Medicine 199, no. 12 (2004): 1709–18. http://dx.doi.org/10.1084/jem.20040432.

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Recently, encouraging AIDS vaccine trials in macaques have implicated cytotoxic T lymphocytes (CTLs) in the control of the simian human immunodeficiency virus SHIV89.6P that induces acute CD4+ T cell depletion. However, none of these vaccine regimens have been successful in the containment of replication of the pathogenic simian immunodeficiency viruses (SIVs) that induce chronic disease progression. Indeed, it has remained unclear if vaccine-induced CTL can control SIV replication. Here, we show evidence suggesting that vaccine-induced CTLs control SIVmac239 replication in rhesus macaques. Ei

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Bocharov, Gennady, Burkhard Ludewig, Antonio Bertoletti, et al. "Underwhelming the Immune Response: Effect of Slow Virus Growth on CD8+-T-Lymphocyte Responses." Journal of Virology 78, no. 5 (2004): 2247–54. http://dx.doi.org/10.1128/jvi.78.5.2247-2254.2004.

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ABSTRACT The speed of virus replication has typically been seen as an advantage for a virus in overcoming the ability of the immune system to control its population growth. Under some circumstances, the converse may also be true: more slowly replicating viruses may evoke weaker cellular immune responses and therefore enhance their likelihood of persistence. Using the model of lymphocytic choriomeningitis virus (LCMV) infection in mice, we provide evidence that slowly replicating strains induce weaker cytotoxic-T-lymphocyte (CTL) responses than a more rapidly replicating strain. Conceptually, w

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DiNapoli, Sarah R., Vanessa M. Hirsch, and Jason M. Brenchley. "Macrophages in Progressive Human Immunodeficiency Virus/Simian Immunodeficiency Virus Infections." Journal of Virology 90, no. 17 (2016): 7596–606. http://dx.doi.org/10.1128/jvi.00672-16.

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The cells that are targeted by primate lentiviruses (HIV and simian immunodeficiency virus [SIV]) are of intense interest given the renewed effort to identify potential cures for HIV. These viruses have been reported to infect multiple cell lineages of hematopoietic origin, including all phenotypic and functional CD4 T cell subsets. The two most commonly reported cell types that become infectedin vivoare memory CD4 T cells and tissue-resident macrophages. Though viral infection of CD4 T cells is routinely detected in both HIV-infected humans and SIV-infected Asian macaques, significant viral i

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Yao, Feng, Nao Murakami, Oliver Bleiziffer, et al. "Development of a Regulatable Oncolytic Herpes Simplex Virus Type 1 Recombinant Virus for Tumor Therapy." Journal of Virology 84, no. 16 (2010): 8163–71. http://dx.doi.org/10.1128/jvi.00059-10.

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ABSTRACT Oncolytic viruses are genetically modified viruses that preferentially replicate in host cancer cells, leading to the production of new viruses and, ultimately, cell death. Currently, no oncolytic viruses that are able to kill only tumor cells while leaving normal cells intact are available. Using T-REx (Invitrogen, Carlsbad, CA) gene switch technology and a self-cleaving ribozyme, we have constructed a novel oncolytic HSV-1 recombinant, KTR27, whose replication can be tightly controlled and regulated by tetracycline in a dose-dependent manner. Infection of normal replicating cells as

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Arthos, James, Andrea Rubbert, Ronald L. Rabin, et al. "CCR5 Signal Transduction in Macrophages by Human Immunodeficiency Virus and Simian Immunodeficiency Virus Envelopes." Journal of Virology 74, no. 14 (2000): 6418–24. http://dx.doi.org/10.1128/jvi.74.14.6418-6424.2000.

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ABSTRACT The capacity of human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) envelopes to transduce signals through chemokine coreceptors on macrophages was examined by measuring the ability of recombinant envelope proteins to mobilize intracellular calcium stores. Both HIV and SIV envelopes mobilized calcium via interactions with CCR5. The kinetics of these responses were similar to those observed when macrophages were treated with MIP-1β. Distinct differences in the capacity of envelopes to mediate calcium mobilization were observed. Envelopes derived from viruses capa

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Rubino, Luisa, Vitantonio Pantaleo, Beatriz Navarro, and Marcello Russo. "Expression of tombusvirus open reading frames 1 and 2 is sufficient for the replication of defective interfering, but not satellite, RNA." Journal of General Virology 85, no. 10 (2004): 3115–22. http://dx.doi.org/10.1099/vir.0.80296-0.

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Yeast cells co-expressing the replication proteins p36 and p95 of Carnation Italian ringspot virus (CIRV) support the RNA-dependent replication of several defective interfering (DI) RNAs derived from either the genome of CIRV or the related Cymbidium ringspot virus (CymRSV), but not the replication of a satellite RNA (sat RNA) originally associated with CymRSV. DI, but not sat RNA, was replicated in yeast cells co-expressing both DI and sat RNA. Using transgenic Nicotiana benthamiana plants constitutively expressing CymRSV replicase proteins (p33 and p92), or transiently expressing either thes

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Grant, Ashley, Alexey Seregin, Cheng Huang, et al. "Junín Virus Pathogenesis and Virus Replication." Viruses 4, no. 10 (2012): 2317–39. http://dx.doi.org/10.3390/v4102317.

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Wang, Linya, and Jing-hsiung James Ou. "Hepatitis C virus and autophagy." Biological Chemistry 396, no. 11 (2015): 1215–22. http://dx.doi.org/10.1515/hsz-2015-0172.

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Abstract Autophagy is a catabolic process by which cells remove protein aggregates and damaged organelles for recycling. It can also be used by cells to remove intracellular microbial pathogens, including viruses, in a process known as xenophagy. However, many viruses have developed mechanisms to subvert this intracellular antiviral response and even use this pathway to support their own replications. Hepatitis C virus (HCV) is one such virus and is an important human pathogen that can cause severe liver diseases. Recent studies indicated that HCV could activate the autophagic pathway to suppo

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Zheng, Min, Pui Wang, Wenjun Song, et al. "An A14U Substitution in the 3′ Noncoding Region of the M Segment of Viral RNA Supports Replication of Influenza Virus with an NS1 Deletion by Modulating Alternative Splicing of M Segment mRNAs." Journal of Virology 89, no. 20 (2015): 10273–85. http://dx.doi.org/10.1128/jvi.00919-15.

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ABSTRACTThe NS1 protein of influenza virus has multiple functions and is a determinant of virulence. Influenza viruses with NS1 deletions (DelNS1 influenza viruses) are a useful tool for studying virus replication and can serve as effective live attenuated vaccines, but deletion of NS1 severely diminishes virus replication, hampering functional studies and vaccine production. We found that WSN-DelNS1 viruses passaged in cells consistently adapted to gain an A14U substitution in the 3′ noncoding region of the M segment of viral RNA (vRNA) which restored replicative ability. DelNS1-M-A14U viruse

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Dunn, Ewan F., Rachel Fearns, and John H. Connor. "Akt Inhibitor Akt-IV Blocks Virus Replication through an Akt-Independent Mechanism." Journal of Virology 83, no. 22 (2009): 11665–72. http://dx.doi.org/10.1128/jvi.01092-09.

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ABSTRACT Many viruses activate the phosphatidylinositol 3′-kinase (PI3k)/Akt intracellular signaling pathway to promote viral replication. We have analyzed whether a rapidly replicating rhabdovirus, vesicular stomatitis virus (VSV), requires the PI3k/Akt signaling pathway for its replication. Through the use of chemical inhibitors of PI3k and Akt, we show that VSV replication and cytopathic effects do not require activation of these kinases. Inhibitors that block the activating phosphorylations of Akt at threonine 308 (Thr308) and serine 473 (Ser473) did not inhibit VSV protein expression or t

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Ali, Naushad, Keith D. Tardif, and Aleem Siddiqui. "Cell-Free Replication of the Hepatitis C Virus Subgenomic Replicon." Journal of Virology 76, no. 23 (2002): 12001–7. http://dx.doi.org/10.1128/jvi.76.23.12001-12007.2002.

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ABSTRACT The hepatitis C virus (HCV) contains a plus-strand RNA genome. The 5′ noncoding region (NCR) of the viral genome functions as an internal ribosome entry site, and its unique 3′ NCR is required for the assembly of the replication complex during initiation of HCV RNA replication. Lohmann et al. (V. Lohmann, F. Korner, J.-O. Koch, U. Herian, L. Theilman, and R. Batenschlager, Science 285:110-113, 1999) developed a subgenomic HCV replicon system, which represents an important tool in studying HCV replication in cultured cells. In this study, we describe a cell-free replication system that

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Weerasooriya, Savithri, Katherine A. DiScipio, Anthar S. Darwish, Ping Bai, and Sandra K. Weller. "Herpes simplex virus 1 ICP8 mutant lacking annealing activity is deficient for viral DNA replication." Proceedings of the National Academy of Sciences 116, no. 3 (2018): 1033–42. http://dx.doi.org/10.1073/pnas.1817642116.

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Most DNA viruses that use recombination-dependent mechanisms to replicate their DNA encode a single-strand annealing protein (SSAP). The herpes simplex virus (HSV) single-strand DNA binding protein (SSB), ICP8, is the central player in all stages of DNA replication. ICP8 is a classical replicative SSB and interacts physically and/or functionally with the other viral replication proteins. Additionally, ICP8 can promote efficient annealing of complementary ssDNA and is thus considered to be a member of the SSAP family. The role of annealing during HSV infection has been difficult to assess in pa

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Bose, Purabi Deka, Bhudev Chandra Das, Rajib Kishore Hazam, Ashok Kumar, Subhash Medhi, and Premashis Kar. "Evidence of extrahepatic replication of hepatitis E virus in human placenta." Journal of General Virology 95, no. 6 (2014): 1266–71. http://dx.doi.org/10.1099/vir.0.063602-0.

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The incidence and severity of hepatitis E virus (HEV) infection in pregnant women is high in developing countries. Transplacental transmission of HEV in the third trimester of pregnancy has been found to be associated with high fetal mortality. Based on this evidence and in the absence of reports on HEV replication in extrahepatic sites, this study was carried out to investigate if HEV replication occurs in the placenta of infected mothers. The study included 68 acute viral hepatitis (AVH) and 22 acute liver failure (ALF) pregnant patients. Viral RNA was extracted from blood and placenta. HEV

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Das, Atze T., Chris E. Baldwin, Monique Vink, and Ben Berkhout. "Improving the Safety of a Conditional-Live Human Immunodeficiency Virus Type 1 Vaccine by Controlling both Gene Expression and Cell Entry." Journal of Virology 79, no. 6 (2005): 3855–58. http://dx.doi.org/10.1128/jvi.79.6.3855-3858.2005.

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ABSTRACT Live attenuated human immunodeficiency virus type 1 (HIV-1) vaccines are considered unsafe because faster-replicating pathogenic virus variants may evolve after vaccination. We previously presented a conditional-live HIV-1 variant of which replication can be switched off as an alternative vaccination strategy. To improve the safety of such a vaccine, we constructed a new HIV-1 variant that depends not only on doxycycline for gene expression but also on the T20 peptide for cell entry. Replication of this virus can be limited to the level required to induce the immune system by transien

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Daikoku, Tohru, Ayumi Kudoh, Masatoshi Fujita, et al. "Architecture of Replication Compartments Formed during Epstein-Barr Virus Lytic Replication." Journal of Virology 79, no. 6 (2005): 3409–18. http://dx.doi.org/10.1128/jvi.79.6.3409-3418.2005.

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ABSTRACT Epstein-Barr virus (EBV) productive DNA replication occurs at discrete sites, called replication compartments, in nuclei. In this study we performed comprehensive analyses of the architecture of the replication compartments. The BZLF1 oriLyt binding proteins showed a fine, diffuse pattern of distribution throughout the nuclei at immediate-early stages of induction and then became associated with the replicating EBV genome in the replication compartments during lytic infection. The BMRF1 polymerase (Pol) processivity factor showed a homogenous, not dot-like, distribution in the replica

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Marriott, Ian, Vinita S. Chauhan, David G. Sterka, and Valery Z. Grdzelishvili. "Vesicular stomatitis virus infects primary murine microglia and astocytes and induces replication-dependent inflammatory cytokine production (133.47)." Journal of Immunology 182, no. 1_Supplement (2009): 133.47. http://dx.doi.org/10.4049/jimmunol.182.supp.133.47.

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Abstract Vesicular stomatitis virus (VSV) is a rhabdovirus that closely resembles its deadly cousin, rabies virus. Intranasal inoculation of mice with VSV leads to infection of the central nervous system (CNS) and an acute encephalitis that results in a high rate of mortality similar to that observed during human rabies infections. Importantly, this encephalitis is accompanied by the rapid activation and proliferation of resident brain cells including microglia and astrocytes, suggesting a role for such cells in the initiation and/or progression of CNS inflammation. Our recent study showed tha

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El Kalamouni, Chaker, Etienne Frumence, Sandra Bos, et al. "Subversion of the Heme Oxygenase-1 Antiviral Activity by Zika Virus." Viruses 11, no. 1 (2018): 2. http://dx.doi.org/10.3390/v11010002.

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Heme oxygenase-1 (HO-1), a rate-limiting enzyme involved in the degradation of heme, is induced in response to a wide range of stress conditions. HO-1 exerts antiviral activity against a broad range of viruses, including the Hepatitis C virus, the human immunodeficiency virus, and the dengue virus by inhibiting viral growth. It has been reported that HO-1 displays antiviral activity against the Zika virus (ZIKV) but the mechanisms of viral inhibition remain largely unknown. Using a ZIKV RNA replicon with the Green Fluorescent Protein (GFP) as a reporter protein, we were able to show that HO-1

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Beck, Juergen. "Hepatitis B virus replication." World Journal of Gastroenterology 13, no. 1 (2007): 48. http://dx.doi.org/10.3748/wjg.v13.i1.48.

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LeDesma, Robert, Ila Nimgaonkar, and Alexander Ploss. "Hepatitis E Virus Replication." Viruses 11, no. 8 (2019): 719. http://dx.doi.org/10.3390/v11080719.

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Hepatitis E virus (HEV) is a small quasi-enveloped, (+)-sense, single-stranded RNA virus belonging to the Hepeviridae family. There are at least 20 million HEV infections annually and 60,000 HEV-related deaths worldwide. HEV can cause up to 30% mortality in pregnant women and progress to liver cirrhosis in immunocompromised individuals and is, therefore, a greatly underestimated public health concern. Although a prophylactic vaccine for HEV has been developed, it is only licensed in China, and there is currently no effective, non-teratogenic treatment. HEV encodes three open reading frames (OR

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Challberg, M. D., and T. J. Kelly. "Animal Virus DNA Replication." Annual Review of Biochemistry 58, no. 1 (1989): 671–713. http://dx.doi.org/10.1146/annurev.bi.58.070189.003323.

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Tao, Yizhi Jane, and Qiaozhen Ye. "RNA Virus Replication Complexes." PLoS Pathogens 6, no. 7 (2010): e1000943. http://dx.doi.org/10.1371/journal.ppat.1000943.

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Taylor, John M. "Hepatitis D Virus Replication." Cold Spring Harbor Perspectives in Medicine 5, no. 11 (2015): a021568. http://dx.doi.org/10.1101/cshperspect.a021568.

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Tabata, Keisuke, Christopher J. Neufeldt, and Ralf Bartenschlager. "Hepatitis C Virus Replication." Cold Spring Harbor Perspectives in Medicine 10, no. 3 (2019): a037093. http://dx.doi.org/10.1101/cshperspect.a037093.

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Schmid, M., T. Speiseder, T. Dobner, and R. A. Gonzalez. "DNA Virus Replication Compartments." Journal of Virology 88, no. 3 (2013): 1404–20. http://dx.doi.org/10.1128/jvi.02046-13.

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McKay, David. "Influenza virus replication blocked." Trends in Biotechnology 19, no. 5 (2001): 163. http://dx.doi.org/10.1016/s0167-7799(01)01655-9.

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