Relevant bibliographies by topics / Virus replication

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Virus replication'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Virus replication"

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 (September 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 of both passage 40 and 45 variants enhanced simian virus 40 DNA replication. Differences in replication efficiencies became greater as the total number of replicating species was increased in the transfection mixture, under conditions where T antigen is limiting. In a competitive environment, sequences flanking the replication origin may be inhibitory to replication.
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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 (September 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 of both passage 40 and 45 variants enhanced simian virus 40 DNA replication. Differences in replication efficiencies became greater as the total number of replicating species was increased in the transfection mixture, under conditions where T antigen is limiting. In a competitive environment, sequences flanking the replication origin may be inhibitory to replication.
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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 (August 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 by experiments with aphidicolin, a drug that blocks replicative fork movement, but did not prevent the camptothecin-induced breakage of replication forks. The drug teniposide, an inhibitor of type II DNA topoisomerase, had only minor effects on the structure of these replicative intermediates.
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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 (August 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 by experiments with aphidicolin, a drug that blocks replicative fork movement, but did not prevent the camptothecin-induced breakage of replication forks. The drug teniposide, an inhibitor of type II DNA topoisomerase, had only minor effects on the structure of these replicative intermediates.
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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 (December 19, 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 virus genomes, the replication of the HCV genome may involve the generation of a dsRNA replicative intermediate. In Huh-7 cells supporting HCV RNA replication, dsRNA was observed as discrete foci, associated with virus-encoded NS5A and core proteins and identical in morphology and distribution to structures containing HCV RNA visualized by fluorescence-based hybridization methods. Three-dimensional reconstruction of deconvolved z-stack images of virus-infected cells provided detailed insight into the relationship among dsRNA foci, NS5A, the ER, and lipid droplets (LDs). This analysis revealed that dsRNA foci were located on the surface of the ER and often surrounded, partially or wholly, by a network of ER-bound NS5A protein. Additionally, virus-induced dsRNA foci were juxtaposed to LDs, attached to the ER. Thus, we report the visualization of HCV-induced dsRNA foci, the likely sites of virus RNA replication, and propose that HCV genome synthesis occurs at LD-associated sites attached to the ER in virus-infected cells.
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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 (December 15, 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 subgenomic and full-length HCV replication. The increased permissiveness of one of the cured cell lines allowed us to readily detect HCV RNA and antigens early after RNA transfection, eliminating the need for selection of replication-positive cells. We also demonstrate that a single amino acid substitution in NS5A is sufficient for establishing HCV replication in a majority of cured cells and that the major phosphate acceptor site of subtype 1b NS5A is not essential for HCV replication.
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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 (August 1, 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 virus-induced apoptosis. Moreover, cystatin A inhibited R7041-induced apoptosis. These inhibitory effects of cystatins on virus replication and apoptosis are likely to be separate functions. Cystatin D treatment decreased cellular cathepsin B activity in HSV-1 infection, suggesting that cathepsin B is involved in virus-induced apoptosis.
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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 (August 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 involved the HSV DNA polymerase itself or a viral gene product(s) which was expressed following the replication of HSV DNA. Analyses of test plasmids lacking SV40 or HSV DNA sequences showed that, under some conditions, HSV also induced low-level replication of test plasmids containing no known eucaryotic replication origins. Together, these results show that HSV induces a DNA replicative activity which amplifies foreign DNA. The relevance of these findings to the putative transforming potential of HSV is discussed.
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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 (August 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 involved the HSV DNA polymerase itself or a viral gene product(s) which was expressed following the replication of HSV DNA. Analyses of test plasmids lacking SV40 or HSV DNA sequences showed that, under some conditions, HSV also induced low-level replication of test plasmids containing no known eucaryotic replication origins. Together, these results show that HSV induces a DNA replicative activity which amplifies foreign DNA. The relevance of these findings to the putative transforming potential of HSV is discussed.
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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 (May 1, 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 injection. To further determine the effect of RLRs on HBV replication, we cotransfected MDA5 or RIG-I with HBV replicative plasmids into Huh-7 cells and measured HBV replication. The results showed that with similar protein levels of MDA5 and RIG-I, only MDA5, but not RIG-I, significantly inhibited HBV replication. In line with these results, knockdown of MDA5 by siRNA in cells transfected with HBV replicative plasmids increased HBV replication while knockdown of RIG-I did not have any effect on HBV replication. Interestingly, activation of MDA5 by HBV significantly induces IRF3 phosphorylation and NF-κB translocation. This result suggests that HBV-mediated MDA5 activation may be responsible for the IRF3 and NF-κB activation. In summary, our results demonstrate that MDA5, a known cytosolic sensor for RNA virus, contributes to the innate immune response against HBV infection.
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Dissertations / Theses on the topic "Virus replication"

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Thomas, C. M. "Cauliflower mosaic virus DNA replication." Thesis, Bucks New University, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374828.

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Ekström, Jens-Ola. "Ljungan Virus Replication in Cell Culture." Doctoral thesis, Högskolan i Kalmar, Naturvetenskapliga institutionen, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:hik:diva-10.

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Ljungan virus (LV) is a recently identified picornavirus of the genus Parechovirus. LV has been isolated from voles trapped in Sweden and also in the United States. LV infected small rodents may suffer from diabetes type 1 and type 2 like symptoms, myocarditis and encephalitis. LV has been proposed as a human pathogen, with indications of causing diabetes type 1, myocarditis and intrauterine fetal deaths. In this thesis, cell culture adapted LV strains were utilised for development and adaptation of several basic methodological protocols to study the LV biology, e.g. real time PCR, highly specific antibodies and a reverse genetics system. These methods allowed detailed studies of this virus and how it interacts with the host cell. The genomic 5'-end was identified and modelling showed unique secondary structure folding of this region. The LV encodes an aphthovirus-like 2A protein with a DvExNPGP motif. This motif was found to mediate primary cleavage of the LV polyprotein in vitro and is proposed to constitute the carboxy terminus of the structural protein VP1 in LV. Rabbit polyclonal antibodies generated against recombinant structural proteins were used to verify that the LV virion is composed of the structural proteins VP0, VP1 and VP3. Cell culture studies showed that LV replicates to low titer with an absent or delayed cell lysis. LV is proposed to be able to spread by a, for picornaviruses, not previously demonstrated direct cell-to-cell transmission. All results taken together suggest a maintenance strategy of LV including low amounts of the LV genome and persistently infected hosts. Stability studies showed that the LV virion not only maintain activity in acidic and alkaline environments but also exhibit resistance to the commonly used disinfectant Virkon®.The results presented in this thesis show that LV has several unique properties, not previously observed for a picornavirus.
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Ekström, Jens-Ola. "Ljungan virus replication in cell culture /." Kalmar : University of Kalmar, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:hik:diva-10.

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McQuillin, Andrew. "Aspects of cucumber mosaic virus replication." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321682.

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Evans, Elizabeth Van Amburg. "Molecular genetic analysis of a vaccinia virus gene with an essential role in DNA replication /." Access full-text from WCMC, 1989. http://proquest.umi.com/pqdweb?did=744576211&sid=1&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Nayak, Arabinda. "Foot and mouth disease virus RNA replication." Thesis, University of Surrey, 2005. http://epubs.surrey.ac.uk/842873/.

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Infection of susceptible cells with foot and mouth disease virus (FMDV) results in multiplication of the RNA genome and assembly of mature virions. The entire process of genome replication is completed in a few hours and encompasses many intracellular events. Like other picornaviruses, FMDV uses a peptide primed RNA replication mechanism. The factors that are required to uridylylate each of the three FMDV VPg peptides and the role of the FMDV cis-acting replication element (cre) or 3B Uridylylation Site (bus) in VPg uridylylation have been determined. The native N-terminus of the FMDV 3Dpol enzyme is a pre-requisite for VPg uridylylation in vitro and the effects of mutations in the RNA template are consistent with a slide-back mechanism. The role of the poly(A) tail in uridylylating VPg was insignificant using full-length FMDV RNA transcripts suggesting the possibility of an alternative mechanism of VPg incorporation into negative strand RNA. The optimal RNA sequences required for VPg uridylylation were found to be within the 5' non-coding region (NCR). Furthermore, the results also showed evidence for RNA-RNA interactions between distinct structures from within the 5' NCR that influence VPg uridylylation. The polymerase precursor 3CDpro is also a prerequisite for uridylylation of each of the FMDV VPg peptides. However BCpro alone can substitute for 3 CD, but is much less efficient. It also appeared that the overall charge of the VPg peptides determines their recognition by the FMDV 3Dpol. The RNA binding activity of the 3C was found to be required for its stimulatory effects on VPg uridylylation. Unlike the poliovirus cloverleaf, the FMDV S-fragment (at the 5' end of the genome) does not interact with the FMDV 3CD precursor protein; however it binds specifically to a cellular factor p48. The crude replication complexes (CRCs) isolated from FMDV-infected cells were found to synthesize viral RNA very efficiently and an in vitro RNA replication system developed using these CRCs can be used to study the complete RNA replication events of FMDV.
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Szemiel, Agnieszka M. "Replication of Bunyamwera virus in mosquito cells." Thesis, University of St Andrews, 2011. http://hdl.handle.net/10023/2570.

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The Bunyaviridae family is one of the largest among RNA viruses, comprising more than 350 serologically distinct viruses. The family is classified into five genera, Orthobunyavirus, Hantavirus, Nairovirus, Phlebovirus, and Tospovirus. Orthobunyaviruses, nairoviruses and phleboviruses are maintained in nature by a propagative cycle involving blood-feeding arthropods and susceptible vertebrate hosts. Like most arthropod-borne viruses, bunyavirus replication causes little damage to the vector, whereas infection of the mammalian host may lead to death. This situation is mimicked in the laboratory: in cultured mosquito cells no cytopathology is observed and a persistent infection is established, whereas in cultured mammalian cells orthobunyavirus infection is lytic and leads to cell death. Bunyaviruses encode four common structural proteins: an RNA-dependent RNA polymerase, two glycoproteins (Gc and Gn), and a nucleoprotein N. Some viruses also code for nonstructural proteins called NSm and NSs. The NSs protein of the prototype bunyavirus, Bunyamwera virus, seems to be one of the factors responsible for the different outcomes of infection in mammalian and mosquito cell lines. However, only limited information is available on the growth of bunyaviruses in cultured mosquito cell lines other than Aedes albopictus C6/36 cells. Here, I compared the replication of Bunyamwera virus in two additional Aedes albopictus cell clones, C7-10 and U4.4, and two Aedes aegypti cell clones, Ae and A20, and investigated the impact of virus replication on cell function. In addition, whereas the vertebrate innate immune response to arbovirus infection is well studied, relatively little is known about mosquitoes’ reaction to these infections. I investigated the immune responses of the different mosquito cells to Bunyamwera virus infection, in particular antimicrobial signaling pathways (Toll and IMD) and RNA interference (RNAi). The data obtained in U4.4 cells suggest that NSs plays an important role in the infection of mosquitoes. Moreover infection of U4.4 cells more closely resembles infection in Ae and A20 cells and live Aedes aegypti mosquitoes. My data showed that the investigated cell lines have various properties, and therefore they can be used to study different aspects of mosquito-virus interactions.
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Napoli, Andrea. "Glycerophospholipid fluorescence imaging during vaccinia virus replication." Thesis, Sorbonne Paris Cité, 2019. https://theses.md.univ-paris-diderot.fr/NAPOLI_Andrea_1_va_20190415.pdf.

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Le virus de la vaccine (VACV) est l'organisme modèle pour l'étude des Poxviridae. Son cycle de réplication dans le cytoplasme de la cellule hôte a été largement étudié par microscopie optique et microscopie électronique. Grâce à des études génétiques approfondies, le rôle de certaines des 250 protéines du virus a été élucidé. Cependant, les mécanismes d’acquisition de la membrane du virus, notamment le rôle des lipides cellulaires impliqués, restent mal connus. L’étude de la composition des membranes de VACV purifiés par spectrométrie de masse a montré qu’elles présentent un enrichissement en acide phosphatidique (PA) et en dérivés de phosphatidylinositoles (PIPs). De plus, des études in vitro ont permis d’identifier certaines protéines virales capables de se lier aux PIPs in vitro. Le rôle de ces lipides dans le cycle de vie du virus, en particulier, dans la biogenèse de ses membranes n'a pas été identifié. L'objectif de ce projet de thèse est de déterminer l’implication du PA et des PIPs dans la biogenèse des membranes virales. L’expression transitoire de protéines recombinantes contenant des domaines de liaison à ces lipides a permis de déterminer la localisation du PA et des PIPs au cours de la réplication du virus. Afin de compléter ces résultats nous avons également utilisé des anticorps reconnaissant la PI4K et le PI4P. Enfin, l’utilisation d’inhibiteurs des PI3Ks et des PI4Ks a permis d’étudier le rôle de ces kinases durant l’assemblage de la membrane virale. A l'aide de ces outils, j'ai pu montrer que la localisation de ces lipides, à l'exception du PI3P, n'est pas altérée dans les cellules infectées. De plus, aucune co-localisation n’a été observée entre ces lipides et les sites de réplication du virus. Par ailleurs, nous avons observé une co-localisation entre le PI4P et les virus enveloppés ce qui est en accord avec les études précédentes montrant que les membranes du virus mature seraient dérivées de l'appareil de Golgi. Toutefois, des inhibiteurs de la synthèse du PI3P et du PI4P n'ont pas montré d’effets sur la production des membranes virales observables par microscopie optique. En conclusion, ce travail a permis de mieux définir le rôle des lipides durant la réplication de VACV. Ces résultats mettent en lumière un rôle potentiel du PI4P au cours de l’acquisition de l’enveloppe du virus ainsi qu’un rôle PI3P et de protéines reconnaissant spécifiquement le PI3P au cours des phases tardives de la réplication
Vaccinia Virus (VACV) is the model organism for the study of the Poxviridae. Its cytoplasmic life cycle has been studied extensively by light- and electron microscopy. Thanks to a robust genetic system the role of some of its 250 proteins is beginning to be understood. Nevertheless, the acquisition of its membranes is still a matter of debate, in particular the role of cellular lipids. Lipid mass spectrometry of purified VACV previously showed an enrichment of phosphatidic acid (PA) and phosphatidylinositol derivatives (PIPs) in the viral membrane. Although some viral proteins have been shown to bind PIPs in vitro the role of these lipids in the viral life cycle, in particular viral membrane biogenesis, remains elusive.The aim of this work is to determine whether PA and PIPs are relocated in infected cells to the site of viral membrane biogenesis. For both PA and PIPs, I used recombinant proteins containing PA or PIP binding domains fused to eGFP, expressed them by transient transfection to follow their localization during viral replication. In addition, I used antibodies for the recognition of PI4K and PI4P. In order to understand the biochemical role of PIPs, I used pan-PI3K and PI4K inhibitors to study their effect on viral assembly. Using these tools, I could show that the lipids under investigation did not display an altered localization, with the exception of PI3P which showed a different pattern in infected cells. None of the PIPs analyzed co-localized with the sites of primary VACV membrane biogenesis. Consistent with the fact that the mature virus acquires additional membranes derived from the Golgi complex, I could show a co-localization of wrapped virus with PI4P, known to localize to this cellular organelle. However, drugs inhibiting PI3P and PI4P biosynthesis did not show any effect on VACV membrane biogenesis, at least at the light microscopy level. In conclusion, this work sharper defines the role of lipids during VACV replication. In particular, it opens the way to further studies on the putative role of PI4P during wrapping and the fate of PI3P and PI3P binding proteins during late replication
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Lu, Jia. "Norovirus translation and replication." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/278610.

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Human norovirus (HuNoV) is the leading cause of gastroenteritis worldwide. Despite the significant disease and economic burden, currently there are no licensed vaccines or antivirals. The understanding of norovirus biology has been hampered by the inability to cultivate HuNoV in cell culture. To establish a tissue culture system, infectious HuNoVs were purified from clinical stool samples. HuNoV replication was tested in different cell types. The B-cell and intestinal organoids culture systems were validated. In addition, using organoids culture a DNA-based reverse genetic system was shown to recover infectious HuNoV. Due to the challenges associated with cultivating HuNoV, murine norovirus (MNV) was used as a surrogate system to understand the role of eIF4E phosphorylation in norovirus pathogenesis, and VP1-RdRp interaction in regulating viral genome replication. MNV infection results in the phosphorylation of the translation initiation factor eIF4E, re-programming host-cell translation during infection. Inhibiting eIF4E phosphorylation reduces MNV replication in cell culture suggesting a role in viral replication. A mouse model with eIF4E S209A, a phosphor-ablative mutation, was established to understand the role of eIF4E phosphorylation in MNV pathogenesis. In vitro and in vivo characterisations demonstrated that eIF4E phosphorylation may have multiple roles in norovirus-host interactions, but overall has little impact on MNV pathogenesis. The shell domain (SD) of norovirus major capsid protein VP1 interacts with viral RNA-dependent RNA polymerase (RdRp) in a genogroup-specific manner to enhance de novo initiation of RdRp, and to promote negative-strand RNA synthesis. To understand how VP1 regulates norovirus genome replication, chimeric MNVs with genogroup-specific residues mutagenised were characterised in vitro and in vivo. A single amino acid mutation was shown to destabilise viral capsid. SDs with reduced VP1-RdRp interaction showed less capacity to stimulate RdRp, resulting in delayed virus replication. In vivo, the replication of an MNV-3 with homologous mutations was abolished, highlighting the crucial role of this interaction.
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Xing, Xuekun. "DNA replication and telomere resolution in vaccinia virus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23557.pdf.

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Books on the topic "Virus replication"

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Alan, Cann, ed. DNA virus replication. Oxford: Oxford University Press, 2000.

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Hartley, Christopher Edward. Mechanism of inhibition of virus replication by lithium. Birmingham: University of Birmingham, 1991.

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Neal, Isaacs Stuart, ed. Vaccinia virus and poxvirology: Methods and protocols. Totowa, N.J: Humana Press, 2004.

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Rohll, Jonathan Bayard. Aspects of the replication and encapsidation of cowpea mosaic virus. Norwich: University of EastAnglia, 1991.

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Huisman, Maria Johanna. Replication of alfalfa mosaic virus temperature-sensitive mutants in protoplasts. Leiden: M.J. Huisman, 1987.

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NATO Advanced Study Institute Summer School on the Molecular Basis of Viral Replication (1986 Maratea, Italy). The molecular basis of viral replication. New York: Plenum Press, 1987.

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Amarilis Paula Alberti de Varennes e. Mendonca. Some aspects of the host involvement in cowpea mosaic virus replication. Norwich: University of East Anglia, 1985.

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Holland, Cheng R., and Miyamura Tatsuo, eds. Structure-based study of viral replication: With CD-ROM. New Jersey: World Scientific, 2008.

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L, DePamphilis Melvin, ed. DNA replication in eukaryotic cells. [Plainview, New York]: Cold Spring Harbor Laboratory Press, 1996.

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W, Compans Richard, Helenius Ari, and Oldstone Michael B. A, eds. Cell biology of virus entry, replication, and pathogenesis: Proceedings of a Glaxo-UCLA Symposium held at Taos, New Mexico, February 28-March 5, 1988. New York: A.R. Liss, 1989.

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Book chapters on the topic "Virus replication"

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Ferrer-Orta, Cristina, and Nuria Verdaguer. "RNA Virus Polymerases." In Viral Genome Replication, 383–401. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/b135974_18.

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Chazal, Nathalie, and Laurence Briant. "Chikungunya Virus Entry and Replication." In Chikungunya Virus, 127–48. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42958-8_8.

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Wendeler, Michaela, Jennifer T. Miller, and Stuart F. J. Le Grice. "Human Immunodeficiency Virus Reverse Transcriptase." In Viral Genome Replication, 403–27. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/b135974_19.

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Lindenbach, Brett D., and Timothy L. Tellinghuisen. "Hepatitis C Virus Genome Replication." In Viral Genome Replication, 61–88. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/b135974_4.

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Su, Wen-Chi, Keigo Machida, and Michael M. C. Lai. "Extrahepatic Replication of HCV." In Hepatitis C Virus II, 165–84. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56101-9_6.

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Suzuki, Tetsuro. "Hepatitis C Virus Replication." In Advances in Experimental Medicine and Biology, 199–209. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4567-7_15.

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Lostroh, Phoebe. "The Virus Replication Cycle." In Molecular and Cellular Biology of Viruses, 21–34. 2nd ed. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003463115-2.

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Peeples, Mark E. "Newcastle Disease Virus Replication." In Newcastle Disease, 45–78. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1759-3_4.

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Yi, Guanghui, and C. Cheng Kao. "Brome Mosaic Virus RNA Replication and Transcription." In Viral Genome Replication, 89–108. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/b135974_5.

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Tabler, Martin, and Mina Tsagris. "Viroid Replication Mechanisms." In Recognition and Response in Plant-Virus Interactions, 185–205. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74164-7_10.

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Conference papers on the topic "Virus replication"

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Morales, Jose Andre, Peter J. Clarke, and Yi Deng. "Characterizing and Detecting Virus Replication." In 2008 3rd International Conference on Systems (ICONS '08). IEEE, 2008. http://dx.doi.org/10.1109/icons.2008.37.

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Zabrodskaya, Y. A., N. V. Gavrilova, M. A. Plotnikova, and A. A. Lozhkov. "THE INFLUENCE OF EXOSOMES SECRETED BY BOTH INFLUENZA VIRUS-INFECTED AND NON-INFECTED CELLS ON VIRUS REPLICATION." In OpenBio-2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-247.

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Exosomes secreted by both influenza virus infected (EV) and non-infected (E) cells were isolated. It was demonstrated that EVs could suppress the immune response of cells. When cells were infected with the influenza virus in the presence of either E or EV, it was observed that E had a protective effect, reducing virus replication. Conversely, EV had a proviral effect, meaning it enhanced virus replication.
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Ejima, Miho, Keiko Haraguchi, Tadashi Yamamoto, and Ayae Honda. "Effect of PB1c45 on Influenza Virus Replication." In 2006 IEEE International Symposium on MicroNanoMechanical and Human Science. IEEE, 2006. http://dx.doi.org/10.1109/mhs.2006.320241.

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Elbashir, Israa, Heba Al Khatib, and Hadi Yassine. "Replication Dynamics, Pathogenicity, and Evolution of Influenza Viruses in Intestinal Caco-2 Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0166.

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Background: Influenza virus is a major cause of respiratory infections worldwide. Besides the common respiratory symptoms, namouras cases with gastrointestinal symptoms have been reported. Moreover, influenza virus has been detected in feces of up to 20.6 % of influenza-infected patients. Therefore, direct infection of intestinal cells with influenza virus is suspected; however, the mechanism of this infection has not been explored. AIM: To investigate influenza virus replication, cellular responses to infection, and virus evolution following serial infection in human Caucasian colon adenocarcinoma cells (Caco-2 cells). Method: Two influenza A subtypes (A/H3N2 and A/H1N1pdm 09) and one influenza B virus (B/Yamagata) were serially passaged in Caco-2. Quantitative PCR was used to study hormones and cytokines expression following infection. Deep sequencing analysis of viral genome was used to assess the virus evolution. Results: The replication capacity of the three viruses was maintained throughout 12 passages, with H3N2 virus being the fastest in adaptation. The expression of hormone and cytokines in Caco-2 cells was considerably different between the viruses and among the passages, however, a pattern of induction was observed at the late phase of infection. Deep sequencing analysis revealed a few amino acid substitutions in the HA protein of H3N2 and H1N1 viruses, mostly in the antigenic site. Moreover, virus evolution at the quasispecies level based on HA protein revealed that H3N2 and H1N1 harbored more diverse virus populations when compared to IBV, indicating their higher evolution within Caco-2 cells. Conclusion: The findings of this study indicate the possibility of influenza virus replication in intestinal cells. To further explain the gastrointestinal complications of influenza infections in-vivo experiments with different influenza viruses are needed.
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Twu, WI, K. Tabata, D. Paul, and R. Bartenschlager. "Role of autophagy in hepatitis C virus replication." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677294.

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Jung, Mi-Yeon, Matthew K. Ennis, Chetan P. Offord, and David Dingli. "Abstract 4947: Quantitativein vivoimaging of oncolytic virus replication." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4947.

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Guedes, Duschinka Ribeiro Duarte. "Dynamics of Zika virus replication inAedes aegyptiandCulex quinquefasciatus." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.111722.

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Maruoka, Shuichiro, Sotaro Shikano, Yasuhiro Gon, Kazumichi Kuroda, Kaori Soda, Eriko Tsuboi, Ikuko Takeshita, Kazufumi Shimizu, and Shu Hashimoto. "Carbocisteine attenuates influenza virus A replication in the bronchoalveolar lavage fluids of virus-infected mice." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa489.

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Fonseca, Angela, Naomi Scott, Deborah Strickland, and Mark Everard. "Persistence of respiratory syncytial virus replication in lung dendritic cells." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3624.

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Hartmann, Evelyn, Beate Kümmerer, Anja Wieland, Janos Ludwig, Thomas Zillinger, and Gunther Hartmann. "RIG-I-mediated protection from SARS-CoV-2 virus replication." In 100 JAHRE DGHNO-KHC: WO KOMMEN WIR HER? WO STEHEN WIR? WO GEHEN WIR HIN? Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727763.

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Reports on the topic "Virus replication"

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Wang, X. F., and M. Schuldiner. Systems biology approaches to dissect virus-host interactions to develop crops with broad-spectrum virus resistance. Israel: United States-Israel Binational Agricultural Research and Development Fund, 2020. http://dx.doi.org/10.32747/2020.8134163.bard.

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More than 60% of plant viruses are positive-strand RNA viruses that cause billion-dollar losses annually and pose a major threat to stable agricultural production, including cucumber mosaic virus (CMV) that infects numerous vegetables and ornamental trees. A highly conserved feature among these viruses is that they form viral replication complexes (VRCs) to multiply their genomes by hijacking host proteins and remodeling host intracellular membranes. As a conserved and indispensable process, VRC assembly also represents an excellent target for the development of antiviral strategies that can be used to control a wide-range of viruses. Using CMV and a model virus, brome mosaic virus (BMV), and relying on genomic tools and tailor-made large-scale resources specific for the project, our original objectives were to: 1) Identify host proteins that are required for viral replication complex assembly. 2) Dissect host requirements that determine viral host range. 3) Provide proof-of-concept evidence of a viral control strategy by blocking the viral replication complex-localized phospholipid synthesis. We expect to provide new ways and new concepts to control multiple viruses by targeting a conserved feature among positive-strand RNA viruses based on our results. Our work is going according to the expected timeline and we are progressing well on all aims. For Objective 1, among ~6,000 yeast genes, we have identified 96 hits that were possibly play critical roles in viral replication. These hits are involved in cellular pathways of 1) Phospholipid synthesis; 2) Membrane-shaping; 3) Sterol synthesis and transport; 4) Protein transport; 5) Protein modification, among many others. We are pursuing several genes involved in lipid metabolism and transport because cellular membranes are primarily composed of lipids and lipid compositional changes affect VRC formation and functions. For Objective 2, we have found that CPR5 proteins from monocotyledon plants promoted BMV replication while those from dicotyledon plants inhibited it, providing direct evidence that CPR5 protein determines the host range of BMV. We are currently examining the mechanisms by which dicot CPR5 genes inhibit BMV replication and expressing the dicot CPR5 genes in monocot plants to control BMV infection. For Objective 3, we have demonstrated that substitutions in a host gene involved in lipid synthesis, CHO2, prevented the VRC formation by directing BMV replication protein 1a (BMV 1a), which remodels the nuclear membrane to form VRCs, away from the nuclear membrane, and thus, no VRCs were formed. This has been reported in Journal of Biological Chemistry. Based on the results from Objective 3, we have extended our plan to demonstrate that an amphipathic alpha-helix in BMV 1a is necessary and sufficient to target BMV 1a to the nuclear membrane. We further found that the counterparts of the BMV 1a helix from a group of viruses in the alphavirus-like superfamily, such as CMV, hepatitis E virus, and Rubella virus, are sufficient to target VRCs to the designated membranes, revealing a conserved feature among the superfamily. A joint manuscript describing these exciting results and authored by the two labs will be submitted shortly. We have also successfully set up systems in tomato plants: 1) to efficiently knock down gene expression via virus-induced gene silencing so we could test effects of lacking a host gene(s) on CMV replication; 2) to overexpress any gene transiently from a mild virus (potato virus X) so we could test effects of the overexpressed gene(s) on CMV replication. In summary, we have made promising progress in all three Objectives. We have identified multiple new host proteins that are involved in VRC formation and may serve as good targets to develop antiviral strategies; have confirmed that CPR5 from dicot plants inhibited viral infection and are generating BMV-resistance rice and wheat crops by overexpressing dicot CPR5 genes; have demonstrated to block viral replication by preventing viral replication protein from targeting to the designated organelle membranes for the VRC formation and this concept can be further employed for virus control. We are grateful to BARD funding and are excited to carry on this project in collaboration.
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Garcia-Sastre, Adolfo. Diversity, Replication, Pathogenicity and Cell Biology of Crimean Congo Hemorrhagic Fever Virus. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada446914.

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Garcia-Sastre, Adolfo. Diversity, Replication, Pathogenicity and Cell Biology of Crimean Congo Hemorrhagic Fever Virus. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada475156.

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Loebenstein, Gad, M. Chessin, and Abed Gera. Resistance Mechanisms to Viruses in Plants Associated with Antiviral Substances (Inhibitors of Virus Replication). United States Department of Agriculture, March 1987. http://dx.doi.org/10.32747/1987.7695597.bard.

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Kotler, Moshe, Larry Hanson, and Shane Burgess. Replication Defective Cyprinid Herpes Virus-3 (CyHV-3) as a Combined Prophylactic Vaccine in Carps. United States Department of Agriculture, December 2010. http://dx.doi.org/10.32747/2010.7697104.bard.

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Aquacultured koi and common carp fish (Cyprinus carpio) are intensively bred as ornamental and food fish in many countries worldwide. Hatcheries of carp and koi have recently suffered massive financial damages due to two viral diseases caused by the Cyprinid herpesvirus-3 (CyHV-3), previously designated as Carp Interstitial Nephritis and Gill Necrosis Virus (CNGV) and Koi herpesvirus (KHV), and by the Spring Viremia of Carp Virus (SVCV). CyHV-3 is a large dsDNA virus, which is infectious mostly to koi and common carp, while SVCV is a rhabdovirus with a relatively broad host range. Both viruses induce contagious disease with mortality rate up to 90%. Strategies for the control of viral infection in fish are of limited use. While efforts to prevent introduction of infectious agents into culture facilities are desirable, such exclusion strategies are far from fail-safe. Extensive vaccination methods that are useful for use in aquaculture facilities produce weak immunity, when used with proteins or inactivated viruses. Methods to overcome this obstacle are to vaccinate the fish with large amounts of antigen and/or use adjuvant and immune modulators over a long period. These techniques usually require individual handling of the fish. On the other hand, live attenuated virus is efficient and economical when used as an immersionvaccine. However, this technique poses certain environmental risks and thus may be difficult to license and scale up. Another option is a vaccine based on the replication defective virus (RDV) (pseudovirus), which can infect cells, but is unable to produce infectious particles. This vaccine may circumvent many of the problems related to attenuated-live vaccine (e.g., inadvertent infection and reversion to the virulent strain).
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Bar-Joseph, Moshe, William O. Dawson, and Munir Mawassi. Role of Defective RNAs in Citrus Tristeza Virus Diseases. United States Department of Agriculture, September 2000. http://dx.doi.org/10.32747/2000.7575279.bard.

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This program focused on citrus tristeza virus (CTV), the largest and one of the most complex RNA-plant-viruses. The economic importance of this virus to the US and Israeli citrus industries, its uniqueness among RNA viruses and the possibility to tame the virus and eventually turn it into a useful tool for the protection and genetic improvement of citrus trees justify these continued efforts. Although the overall goal of this project was to study the role(s) of CTV associated defective (d)-RNAs in CTV-induced diseases, considerable research efforts had to be devoted to the engineering of the helper virus which provides the machinery to allow dRNA replication. Considerable progress was made through three main lines of complementary studies. For the first time, the generation of an engineered CTV genetic system that is capable of infecting citrus plants with in vitro modified virus was achieved. Considering that this RNA virus consists of a 20 kb genome, much larger than any other previously developed similar genetic system, completing this goal was an extremely difficult task that was accomplished by the effective collaboration and complementarity of both partners. Other full-length genomic CTV isolates were sequenced and populations examined, resulting in a new level of understanding of population complexities and dynamics in the US and Israel. In addition, this project has now considerably advanced our understanding and ability to manipulate dRNAs, a new class of genetic elements of closteroviruses, which were first found in the Israeli VT isolate and later shown to be omnipresent in CTV populations. We have characterized additional natural dRNAs and have shown that production of subgenomic mRNAs can be involved in the generation of dRNAs. We have molecularly cloned natural dRNAs and directly inoculated citrus plants with 35S-cDNA constructs and have shown that specific dRNAs are correlated with specific disease symptoms. Systems to examine dRNA replication in protoplasts were developed and the requirements for dRNA replication were defined. Several artificial dRNAs that replicate efficiently with a helper virus were created from infectious full-genomic cDNAs. Elements that allow the specific replication of dRNAs by heterologous helper viruses also were defined. The T36-derived dRNAs were replicated efficiently by a range of different wild CTV isolates and hybrid dRNAs with heterologous termini are efficiently replicated with T36 as helper. In addition we found: 1) All CTV genes except of the p6 gene product from the conserved signature block of the Closteroviridae are obligate for assembly, infectivity, and serial protoplast passage; 2) The p20 protein is a major component of the amorphous inclusion bodies of infected cells; and 3) Novel 5'-Co-terminal RNAs in CTV infected cells were characterized. These results have considerably advanced our basic understanding of the molecular biology of CTV and CTV-dRNAs and form the platform for the future manipulation of this complicated virus. As a result of these developments, the way is now open to turn constructs of this viral plant pathogen into new tools for protecting citrus against severe CTV terms and development of virus-based expression vectors for other citrus improvement needs. In conclusion, this research program has accomplished two main interconnected missions, the collection of basic information on the molecular and biological characteristics of the virus and its associated dRNAs toward development of management strategies against severe diseases caused by the virus and building of novel research tools to improve citrus varieties. Reaching these goals will allow us to advance this project to a new phase of turning the virus from a pathogen to an ally.
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Chejanovsky, Nor, and Bruce A. Webb. Potentiation of pest control by insect immunosuppression. United States Department of Agriculture, July 2004. http://dx.doi.org/10.32747/2004.7587236.bard.

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Our original aims were to elucidate the mechanisms through which the immunosuppressive insect virus, the Campoletis sonorensis polydnavirus (CsV) promotes replication of a well-characterized pathogenic virus, the Autographa californica multiple nucleopolyhedrovirus (AcMNPV) in hosts that are mildly or non-permissive to virus replication. According to the BARD panels criticism we modified our short-term goals (see below). Thus, in this feasibility study (one-year funding) we aimed to show that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen (a baculovirus) to infect the pest. 3. S. littoralis cells constitute an efficient tool to study some aspects of the anti- viral immune response. We achieved the above objectives by: 1. Finding melanized viral foci upon following the baculoviral infection in S . littoralis larvae infected with a polyhedra - positive AcMNPV recombinant that expressed the GFP gene under the control of the Drosophila heat shock promoter. 2. Studying the effect of AcMNPV-infection in S . littoralis immunosuppressed by parasitation with the Braconidae wasp Chelonus inanitus that bears the CiV polydna virus, that resulted in higher susceptibility of S. littoralis to AcMNPV- infection. 3. Proving that S. littoralis hemocytes resist AcMNPV -infection. 4. Defining SL2 as a granulocyte-like cell line and demonstrating that as littoralis hemocytic cell line undergoes apoptosis upon AcMNPV -infection. 5. Showing that some of the recombinant AcMNPV expressing the immuno-suppressive polydna virus CsV- vankyrin genes inhibit baculoviral-induced lysis of SL2 cells. This information paves the way to elucidate the mechanisms through which the immuno- suppressive polydna insect viruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication by: - Assessing the extent to which and the mechanisms whereby the immunosuppressive viruses, CiV and CsV or their genes enhance AcMNPV replication in polydnavirus- immunosuppressed H. zea and S. littoralis insects and S. littoralis cells. - Identifying CiV and CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). This study will provide insight to the molecular mechanisms of viral pathogenesis and improve our understanding of insect immunity. This knowledge is of fundamental importance to controlling insect vectored diseases of humans, animals and plants and essential to developing novel means for pest control (including baculoviruses) that strategically weaken insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence.
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Morris, T. J., and A. O. Jackson. Tomato bushy stunt virus and DI RNAs as a model for studying mechanisms of RNA virus replication, pathogenicity and recombination. Final technical report for 1994--1997. Office of Scientific and Technical Information (OSTI), December 1997. http://dx.doi.org/10.2172/353366.

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Loebenstein, Gad, William Dawson, and Abed Gera. Association of the IVR Gene with Virus Localization and Resistance. United States Department of Agriculture, August 1995. http://dx.doi.org/10.32747/1995.7604922.bard.

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We have reported that localization of TMV in tobacco cultivars with the N gene, is associated with a 23 K protein (IVR) that inhibited replication of several plant viruses. This protein was also found in induced resistant tissue of Nicotiana glutinosa x Nicotiana debneyi. During the present grant we found that TMV production is enhanced in protoplasts and plants of local lesion responding tobacco cultivars exposed to 35oC, parallel to an almost complete suppression of the production of IVR. We also found that IVR is associated with resistance mechanisms in pepper cultivars. We succeeded to clone the IVR gene. In the first attempt we isolated a clone - "101" which had a specific insert of 372 bp (the full length gene for the IVR protein of 23 kD should be around 700 bp). However, attempts to isolate the full length gene did not give clear cut results, and we decided not to continue with this clone. The amino acid sequence of the N-terminus of IVR was determined and an antiserum was prepared against a synthetic peptide representing amino acids residues 1-20 of IVR. Using this antiserum as well as our polyclonal antiserum to IVR a new clone NC-330 was isolated using lamba-ZAP library. This NC-330 clone has an insert of about 1 kB with an open reading frame of 596 bp. This clone had 86.6% homology with the first 15 amino acids of the N-terminal part of IVR and 61.6% homology with the first 23 amino acids of IVR. In the QIA expression system and western blotting of the expressed protein, a clear band of about 21 kD was obtained with IVR antiserum. This clone was used for transformation of Samsun tobacco plants and we have presently plantlets which were rooted on medium containing kanamycin. Hybridization with this clone was also obtained with RNA from induced resistant tissue of Samsun NN but not with RNA from healthy control tissue of Samsun NN, or infected or healthy tissue of Samsun. This further strengthens the previous data that the NC 330 clone codes for IVR. In the U.S. it was shown that IVR is induced in plants containing the N' gene when infected with mutants of TMV that elicit the HR. This is a defined system in which the elicitor is known to be due to permutations of the coat protein which can vary in elicitor strength. The objective was to understand how IVR synthesis is induced after recognition of elicitor coat protein in the signal transduction pathway that leads to HR. We developed systems to manipulate induction of IVR by modifying the elicitor and are using these elicitor molecules to isolate the corresponding plant receptor molecules. A "far-western" procedure was developed that found a protein from N' plants that specifically bind to elicitor coat proteins. This protein is being purified and sequenced. This objective has not been completed and is still in progress. We have reported that localization of TMV in tobacco cultivars with the N gene, is associated with a 23 K protein (IVR) that inhibited replication of several plant viruses. This protein was also found in induced resistant tissue of Nicotiana glutinosa x Nicotiana debneyi.
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Chejanovsky, Nor, and Suzanne M. Thiem. Isolation of Baculoviruses with Expanded Spectrum of Action against Lepidopteran Pests. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7586457.bard.

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Our long-term goal is to learn to control (expand and restrict) the host range of baculoviruses. In this project our aim was to expand the host range of the prototype baculovirus Autographa cali/arnica nuclear polyhedrosis virus (AcMNPV) towards American and Israeli pests. To achieve this objective we studied AcMNPV infection in the non-permissive hosts L. dispar and s. littoralis (Ld652Y and SL2 cells, respectively) as a model system and the major barriers to viral replication. We isolated recombinant baculoviruses with expanded infectivity towards L. dispar and S. littoralis and tested their infectivity towards other Lepidopteran pests. The restricted host range displayed by baculoviruses constitutes an obstacle to their further implementation in the control of diverse Lepidopteran pests, increasing the development costs. Our work points out that cellular defenses are major role blocks to AcMNPV replication in non- and semi-permissive hosts. Therefore a major determinant ofbaculovirus host range is the ability of the virus to effectively counter cellular defenses of host cells. This is exemplified by our findings showing tliat expressing the viral gene Ldhrf-l overcomes global translation arrest in AcMNPV -infected Ld652Y cells. Our data suggests that Ld652Y cells have two anti-viral defense pathways, because they are subject to global translation arrest when infected with AcMNPV carrying a baculovirus apoptotic suppressor (e.g., wild type AcMNPV carryingp35, or recombinant AcMNPV carrying Opiap, Cpiap. or p49 genes) but apoptose when infected with AcMNPV-Iacking a functional apoptotic suppressor. We have yet to elucidate how hrf-l precludes the translation arrest mechanism(s) in AcMNPV-infected Ld652Y cells. Ribosomal profiles of AcMNPV infected Ld652Y cells suggested that translation initiation is a major control point, but we were unable to rule-out a contribution from a block in translation elongation. Phosphorylation of eIF-2a did not appear to playa role in AcMNPV -induced translation arrest. Mutagenesis studies ofhrf-l suggest that a highly acidic domain plays a role in precluding translation arrest. Our findings indicate that translation arrest may be linked to apoptosis either through common sensors of virus infection or as a consequence of late events in the virus life-cycle that occur only if apoptosis is suppressed. ~ AcMNPV replicates poorly in SL2 cells and induces apoptosis. Our studies in AcMNPV - infected SL2ceils led us to conclude that the steady-state levels of lEI (product of the iel gene, major AcMNPV -transactivator and multifunctional protein) relative to those of the immediate early viral protein lEO, playa critical role in regulating the viral infection. By increasing the IEl\IEO ratio we achieved AcMNPV replication in S. littoralis and we were able to isolate recombinant AcMNPV s that replicated efficiently in S. lifforalis cells and larvae. Our data that indicated that AcMNPV - infection may be regulated by an interaction between IE 1 and lED (of previously unknown function). Indeed, we showed that IE 1 associates with lED by using protein "pull down" and immunoprecipitation approaches High steady state levels of "functional" IE 1 resulted in increased expression of the apoptosis suppressor p35 facilitating AcMNPV -replication in SL2 cells. Finally, we determined that lED accelerates the viral infection in AcMNPV -permissive cells. Our results show that expressing viral genes that are able to overcome the insect-pest defense system enable to expand baculovirus host range. Scientifically, this project highlights the need to further study the anti-viral defenses of invertebrates not only to maximi~e the possibilities for manipulating baculovirus genomes, but to better understand the evolutionary underpinnings of the immune systems of vertebrates towards virus infection.
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