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Journal articles on the topic 'Early steps of retroviral replication cycle'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Masson, Christel, Stéphanie Bury-Moné, Elvire Guiot, et al. "Ku80 Participates in the Targeting of Retroviral Transgenes to the Chromatin of CHO Cells." Journal of Virology 81, no. 15 (2007): 7924–32. http://dx.doi.org/10.1128/jvi.02015-06.

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ABSTRACT The heterodimer Ku70/80 Ku is the DNA-binding component of the DNA-PK complex required for the nonhomologous end-joining pathway. It participates in numerous nuclear processes, including telomere and chromatin structure maintenance, replication, and transcription. Ku interacts with retroviral preintegration complexes and is thought to interfere with the retroviral replication cycle, in particular the formation of 2-long terminal repeat (LTR) viral DNA circles, viral DNA integration, and transcription. We describe here the effect of Ku80 on both provirus integration and the resulting t

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2

Morcock, David R., James A. Thomas, Tracy D. Gagliardi, et al. "Elimination of Retroviral Infectivity by N-Ethylmaleimide with Preservation of Functional Envelope Glycoproteins." Journal of Virology 79, no. 3 (2005): 1533–42. http://dx.doi.org/10.1128/jvi.79.3.1533-1542.2005.

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ABSTRACT The zinc finger motifs in retroviral nucleocapsid (NC) proteins are essential for viral replication. Disruption of these Cys-X2-Cys-X4-His-X4-Cys zinc-binding structures eliminates infectivity. To determine if N-ethylmaleimide (NEM) can inactivate human immunodeficiency virus type 1 (HIV-1) or simian immunodeficiency virus (SIV) preparations by alkylating cysteines of NC zinc fingers, we treated infectious virus with NEM and evaluated inactivation of infectivity in cell-based assays. Inactivation was rapid and proportional to the NEM concentration. NEM treatment of HIV-1 or SIV result

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3

Kim, Steve S., Xue Juan You, Mary-Elizabeth Harmon, Julie Overbaugh, and Hung Fan. "Use of Helper-Free Replication-Defective Simian Immunodeficiency Virus-Based Vectors To Study Macrophage and T Tropism: Evidence for Distinct Levels of Restriction in Primary Macrophages and a T-Cell Line." Journal of Virology 75, no. 5 (2001): 2288–300. http://dx.doi.org/10.1128/jvi.75.5.2288-2300.2001.

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ABSTRACT Cell tropism of human and simian immunodeficiency viruses (HIV and SIV, respectively) is governed in part by interactions between the viral envelope protein and the cellular receptors. However, there is evidence that envelope-host cell interactions also affect postentry steps in viral replication. We used a helper-free replication-defective SIV macaque (SIVmac)-based retroviral vector carrying the enhanced jellyfish green fluorescent protein inserted into thenef region (V1EGFP) to examine SIV tropism in a single cycle of infection. Vector stocks containing envelope proteins from three

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4

Zhu, Kai, Charles Dobard, and Samson A. Chow. "Requirement for Integrase during Reverse Transcription of Human Immunodeficiency Virus Type 1 and the Effect of Cysteine Mutations of Integrase on Its Interactions with Reverse Transcriptase." Journal of Virology 78, no. 10 (2004): 5045–55. http://dx.doi.org/10.1128/jvi.78.10.5045-5055.2004.

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ABSTRACT Retroviral integrase catalyzes the essential step of integrating a double-stranded DNA copy of the viral genome into a host cell chromosome. Mutational studies have revealed that integrase is involved in additional steps of viral replication, but the mechanism for the pleiotropic effect is not well characterized. Since Cys residues generally play crucial roles in protein structure and function, we introduced Cys-to-Ser substitutions at positions 56, 65, and 130 of human immunodeficiency virus type 1 (HIV-1) integrase to determine their effects on integration activity and viral replica

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5

Griffith, Jacqulyn L., Laura E. Coleman, Adam S. Raymond, et al. "Functional Genomics Reveals Relationships Between the Retrovirus-Like Ty1 Element and Its Host Saccharomyces cerevisiae." Genetics 164, no. 3 (2003): 867–79. http://dx.doi.org/10.1093/genetics/164.3.867.

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Abstract Retroviruses and their relatives, the long terminal repeat (LTR) retrotransposons, carry out complex life cycles within the cells of their hosts. We have exploited a collection of gene deletion mutants developed by the Saccharomyces Genome Deletion Project to perform a functional genomics screen for host factors that influence the retrovirus-like Ty1 element in yeast. A total of 101 genes that presumably influence many different aspects of the Ty1 retrotransposition cycle were identified from our analysis of 4483 homozygous diploid deletion strains. Of the 101 identified mutants, 46 h

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6

Heusinger, Elena, Silvia F. Kluge, Frank Kirchhoff, and Daniel Sauter. "Early Vertebrate Evolution of the Host Restriction Factor Tetherin." Journal of Virology 89, no. 23 (2015): 12154–65. http://dx.doi.org/10.1128/jvi.02149-15.

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ABSTRACTTetherin is an interferon-inducible restriction factor targeting a broad range of enveloped viruses. Its antiviral activity depends on an unusual topology comprising an N-terminal transmembrane domain (TMD) followed by an extracellular coiled-coil region and a C-terminal glycosylphosphatidylinositol (GPI) anchor. One of the two membrane anchors is inserted into assembling virions, while the other remains in the plasma membrane of the infected cell. Thus, tetherin entraps budding viruses by physically bridging viral and cellular membranes. Although tetherin restricts the release of a la

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7

Wainberg, Mark A., Andre Dascal, and Jack Mendelson. "Anti-Retroviral Strategies for AIDS and Related Diseases." Canadian Journal of Infectious Diseases 2, no. 3 (1991): 121–28. http://dx.doi.org/10.1155/1991/487657.

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The replication cycle of human immunodeficiency virus type 1 (HIV-1) and other retroviruses consists of four stages: attachment of the virus to specific receptors on the cell surface; uncoating of the viral nucleic acid and conversion to DNA; production of viral RNA and proteins; and assembly and liberation of progeny virus from the cell. Each of these steps represents a potential target for antiviral chemotherapy. Combinations of drugs which act against different steps in the viral replication cycle might be expected to have synergistic potential. Zidovudine (AZT) is the most widely used drug

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8

Katz, Richard A., James G. Greger, and Anna Marie Skalka. "Effects of cell cycle status on early events in retroviral replication." Journal of Cellular Biochemistry 94, no. 5 (2005): 880–89. http://dx.doi.org/10.1002/jcb.20358.

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9

Sabahi, Ali. "Hepatitis C Virus entry: the early steps in the viral replication cycle." Virology Journal 6, no. 1 (2009): 117. http://dx.doi.org/10.1186/1743-422x-6-117.

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10

Lehmann-Che, Jacqueline, Marie-Lou Giron, Olivier Delelis, et al. "Protease-Dependent Uncoating of a Complex Retrovirus." Journal of Virology 79, no. 14 (2005): 9244–53. http://dx.doi.org/10.1128/jvi.79.14.9244-9253.2005.

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ABSTRACT Although retrovirus egress and budding have been partly unraveled, little is known about early stages of the replication cycle. In particular, retroviral uncoating, a process during which incoming retroviral cores are altered to allow the integration of the viral genome into host chromosomes, is poorly understood. To get insights into these early events of the retroviral cycle, we have used foamy complex retroviruses as a model. In this report, we show that a protease-defective foamy retrovirus is noninfectious, although it is still able to bud and enter target cells efficiently. Simi

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11

Shin, Nam-Hee, Dennis Hartigan-O'Connor, Julie K. Pfeiffer, and Alice Telesnitsky. "Replication of Lengthened Moloney Murine Leukemia Virus Genomes Is Impaired at Multiple Stages." Journal of Virology 74, no. 6 (2000): 2694–702. http://dx.doi.org/10.1128/jvi.74.6.2694-2702.2000.

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ABSTRACT It has been assumed that RNA packaging constraints limit the size of retroviral genomes. This notion of a retroviral “headful” was tested by examining the ability of Moloney murine leukemia virus genomes lengthened by 4, 8, or 11 kb to participate in a single replication cycle. Overall, replication of these lengthened genomes was 5- to 10-fold less efficient than that of native-length genomes. When RNA expression and virion formation, RNA packaging, and early stages of replication were compared, long genomes were found to complete each step less efficiently than did normal-length geno

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12

Siva, Amara C., and Frederic Bushman. "Poly(ADP-Ribose) Polymerase 1 Is Not Strictly Required for Infection of Murine Cells by Retroviruses." Journal of Virology 76, no. 23 (2002): 11904–10. http://dx.doi.org/10.1128/jvi.76.23.11904-11910.2002.

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ABSTRACT The DNA-breaking and -joining steps initiating retroviral integration are well understood, but the later steps, thought to be carried out by cellular DNA repair enzymes, have not been fully characterized. Poly(ADP-ribose) polymerase 1 (PARP-1) has been proposed to play a role late during retroviral integration, because infection by human immunodeficiency virus (HIV)-based vectors was reported to be strongly inhibited in PARP-1-deficient fibroblasts. PARP-1, a nuclear enzyme, binds tightly to nicked DNA and synthesizes poly(ADP-ribose) as an early response to DNA damage. To investigate

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13

Gao, Guangxia, and Stephen P. Goff. "Somatic Cell Mutants Resistant to Retrovirus Replication: Intracellular Blocks during the Early Stages of Infection." Molecular Biology of the Cell 10, no. 6 (1999): 1705–17. http://dx.doi.org/10.1091/mbc.10.6.1705.

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To identify cellular functions involved in the early phase of the retroviral life cycle, somatic cell mutants were isolated after selection for resistance to infection. Rat2 fibroblasts were treated with chemical mutagens, and individual virus-resistant clones were recovered after selection for resistance to infection. Two clones were characterized in detail. Both mutant lines were resistant to infection by both ecotropic and amphotropic murine viruses, as well as by human immunodeficiency virus type 1 pseudotypes. One clone showed a strong block to reverse transcription of the retroviral RNA,

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14

Bruce, James W., Kenneth A. Bradley, Paul Ahlquist, and John A. T. Young. "Isolation of Cell Lines That Show Novel, Murine Leukemia Virus-Specific Blocks to Early Steps of Retroviral Replication." Journal of Virology 79, no. 20 (2005): 12969–78. http://dx.doi.org/10.1128/jvi.79.20.12969-12978.2005.

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ABSTRACT In order to identify cellular proteins required for early stages of retroviral replication, a high volume screening with mammalian somatic cells was performed. Ten pools of chemically mutagenized Chinese hamster ovary (CHO-K1) cells were challenged with a murine leukemia virus (MLV) vector pseudotyped with the vesicular stomatitis virus glycoprotein (VSV-G), and cells that failed to be transduced were enriched by cell sorting. Each pool yielded a clonally derived cell line with a 5-fold or greater resistance to virus infection, and five cell lines exhibited a >50-fold resistance. T

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15

Diogo Dias, João, Nazim Sarica, and Christine Neuveut. "Early Steps of Hepatitis B Life Cycle: From Capsid Nuclear Import to cccDNA Formation." Viruses 13, no. 5 (2021): 757. http://dx.doi.org/10.3390/v13050757.

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Hepatitis B virus (HBV) remains a major public health concern, with more than 250 million chronically infected people who are at high risk of developing liver diseases, including cirrhosis and hepatocellular carcinoma. Although antiviral treatments efficiently control virus replication and improve liver function, they cannot cure HBV infection. Viral persistence is due to the maintenance of the viral circular episomal DNA, called covalently closed circular DNA (cccDNA), in the nuclei of infected cells. cccDNA not only resists antiviral therapies, but also escapes innate antiviral surveillance.

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16

Luo, Kun, Tao Wang, Bindong Liu, et al. "Cytidine Deaminases APOBEC3G and APOBEC3F Interact with Human Immunodeficiency Virus Type 1 Integrase and Inhibit Proviral DNA Formation." Journal of Virology 81, no. 13 (2007): 7238–48. http://dx.doi.org/10.1128/jvi.02584-06.

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ABSTRACT APOBEC3G (A3G) is a single-stranded DNA cytidine deaminase that targets retroviral minus-strand DNA and has potent antiviral activity against diverse retroviruses. However, the mechanisms of A3G antiviral functions are incompletely understood. Here we demonstrate that A3G, A3F, and, to a lesser extent, the noncatalytic A3GC291S block human immunodeficiency virus type 1 (HIV-1) replication by interfering with proviral DNA formation. In HIV-1 virions, A3G interacted with HIV-1 integrase and nucleocapsid, key viral factors for reverse transcription and integration. Unlike A3G, the weak a

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17

Gao, Yong, Michael A. Lobritz, Justin Roth, et al. "Targets of Small Interfering RNA Restriction during Human Immunodeficiency Virus Type 1 Replication." Journal of Virology 82, no. 6 (2008): 2938–51. http://dx.doi.org/10.1128/jvi.02126-07.

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ABSTRACT Small interfering RNAs (siRNAs) have been shown to effectively inhibit human immunodeficiency virus type 1 (HIV-1) replication in vitro. The mechanism(s) for this inhibition is poorly understood, as siRNAs may interact with multiple HIV-1 RNA species during different steps of the retroviral life cycle. To define susceptible HIV-1 RNA species, siRNAs were first designed to specifically inhibit two divergent primary HIV-1 isolates via env and gag gene targets. A self-inactivating lentiviral vector harboring these target sequences confirmed that siRNA cannot degrade incoming genomic RNA.

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18

Schneider, Martha, Kerstin Ackermann, Melissa Stuart, et al. "Severe Acute Respiratory Syndrome Coronavirus Replication Is Severely Impaired by MG132 due to Proteasome-Independent Inhibition of M-Calpain." Journal of Virology 86, no. 18 (2012): 10112–22. http://dx.doi.org/10.1128/jvi.01001-12.

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The ubiquitin-proteasome system (UPS) is involved in the replication of a broad range of viruses. Since replication of the murine hepatitis virus (MHV) is impaired upon proteasomal inhibition, the relevance of the UPS for the replication of the severe acute respiratory syndrome coronavirus (SARS-CoV) was investigated in this study. We demonstrate that the proteasomal inhibitor MG132 strongly inhibits SARS-CoV replication by interfering with early steps of the viral life cycle. Surprisingly, other proteasomal inhibitors (e.g., lactacystin and bortezomib) only marginally affected viral replicati

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19

Boso, Guney, and Christine A. Kozak. "Retroviral Restriction Factors and Their Viral Targets: Restriction Strategies and Evolutionary Adaptations." Microorganisms 8, no. 12 (2020): 1965. http://dx.doi.org/10.3390/microorganisms8121965.

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The evolutionary conflict between retroviruses and their vertebrate hosts over millions of years has led to the emergence of cellular innate immune proteins termed restriction factors as well as their viral antagonists. Evidence accumulated in the last two decades has substantially increased our understanding of the elaborate mechanisms utilized by these restriction factors to inhibit retroviral replication, mechanisms that either directly block viral proteins or interfere with the cellular pathways hijacked by the viruses. Analyses of these complex interactions describe patterns of accelerate

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20

Koutsoudakis, George, Artur Kaul, Eike Steinmann, et al. "Characterization of the Early Steps of Hepatitis C Virus Infection by Using Luciferase Reporter Viruses." Journal of Virology 80, no. 11 (2006): 5308–20. http://dx.doi.org/10.1128/jvi.02460-05.

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ABSTRACT The lack of an efficient system to produce hepatitis C virus (HCV) particles has impeded the analysis of the HCV life cycle. Recently, we along with others demonstrated that transfection of Huh7 hepatoma cells with a novel HCV isolate (JFH1) yields infectious viruses. To facilitate studies of HCV replication, we generated JFH1-based bicistronic luciferase reporter virus genomes. We found that RNA replication of the reporter construct was only slightly attenuated and that virus titers produced were only three- to fivefold lower compared to the parental virus, making these reporter viru

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21

Pyrc, Krzysztof, Berend Jan Bosch, Ben Berkhout, et al. "Inhibition of Human Coronavirus NL63 Infection at Early Stages of the Replication Cycle." Antimicrobial Agents and Chemotherapy 50, no. 6 (2006): 2000–2008. http://dx.doi.org/10.1128/aac.01598-05.

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ABSTRACT Human coronavirus NL63 (HCoV-NL63), a recently discovered member of the Coronaviridae family, has spread worldwide and is associated with acute respiratory illness in young children and elderly and immunocompromised persons. Further analysis of HCoV-NL63 pathogenicity seems warranted, in particular because the virus uses the same cellular receptor as severe acute respiratory syndrome-associated coronavirus. As there is currently no HCoV-NL63-specific and effective vaccine or drug therapy available, we evaluated several existing antiviral drugs and new synthetic compounds as inhibitors

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22

Guedán, Anabel, Eve R. Caroe, Genevieve C. R. Barr, and Kate N. Bishop. "The Role of Capsid in HIV-1 Nuclear Entry." Viruses 13, no. 8 (2021): 1425. http://dx.doi.org/10.3390/v13081425.

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HIV-1 can infect non-dividing cells. The nuclear envelope therefore represents a barrier that HIV-1 must traverse in order to gain access to the host cell chromatin for integration. Hence, nuclear entry is a critical step in the early stages of HIV-1 replication. Following membrane fusion, the viral capsid (CA) lattice, which forms the outer face of the retroviral core, makes numerous interactions with cellular proteins that orchestrate the progress of HIV-1 through the replication cycle. The ability of CA to interact with nuclear pore proteins and other host factors around the nuclear pore de

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23

Kirchmaier, Ann L., and Jasper Rine. "Cell Cycle Requirements in Assembling Silent Chromatin in Saccharomyces cerevisiae." Molecular and Cellular Biology 26, no. 3 (2006): 852–62. http://dx.doi.org/10.1128/mcb.26.3.852-862.2006.

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ABSTRACT The establishment of silencing at the silent mating-type locus, HMR, in Saccharomyces cerevisiae requires that yeast pass through S phase of the cell cycle, yet requires neither the initiation of DNA replication at the locus destined to become silenced nor the passage of a replication fork through that locus. We tested whether this S-phase requirement reflects a window within the cell cycle permissive for recruitment of Sir proteins to HMR. The S-phase-restricted event necessary for silencing occurred after recruitment of Sir proteins to HMR. Moreover, cells arrested in early S phase

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24

Groschel, Bettina, and Frederic Bushman. "Cell Cycle Arrest in G2/M Promotes Early Steps of Infection by Human Immunodeficiency Virus." Journal of Virology 79, no. 9 (2005): 5695–704. http://dx.doi.org/10.1128/jvi.79.9.5695-5704.2005.

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ABSTRACT We have identified four small molecules that boost transduction of cells by human immunodeficiency virus (HIV) and investigated their mechanism of action. These molecules include etoposide and camptothecin, which induce DNA damage by inhibiting religation of cleaved topoisomerase-DNA complexes, taxol, which interferes with the function of microtubules, and aphidicolin, which inhibits DNA polymerases. All four compounds arrest the cell cycle at G2/M, though in addition high concentrations of aphidicolin arrest in G1. We find that early events of HIV replication, including synthesis of

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Kim, Soo Jin, and Paul K. Y. Wong. "ROS upregulation during the early phase of retroviral infection plays an important role in viral establishment in the host cell." Journal of General Virology 94, no. 10 (2013): 2309–17. http://dx.doi.org/10.1099/vir.0.055228-0.

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Recent studies suggest that low levels of reactive oxygen species (ROS) often modulate normal intracellular signalling pathways, determine cell fates and control cell proliferation. We found that infection of astrocytes with the neuropathogenic retrovirus ts1, a mutant of Moloney murine leukemia retrovirus, upregulated ROS at low levels during the early phase of infection. This upregulation of intracellular ROS with downregulation of NADPH levels during the early phase of ts1 infection was a separate event from the upregulation of ROS during the late phase while ts1-mediated cell death occurre

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26

McKnight, Áine, David J. Griffiths, Matthias Dittmar, Paul Clapham, and Elaine Thomas. "Characterization of a Late Entry Event in the Replication Cycle of Human Immunodeficiency Virus Type 2." Journal of Virology 75, no. 15 (2001): 6914–22. http://dx.doi.org/10.1128/jvi.75.15.6914-6922.2001.

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ABSTRACT Certain human cell lines and primary macrophage cultures are restricted to infection by some primary isolates of human immunodeficiency virus type 2 (HIV-2), although early steps of the viral life cycle such as fusion at the plasma membrane and reverse transcription are fully supported. The late postintegration events, transcription, translation, assembly, budding, and maturation into infectious virions are functional in restrictive cells. Apart from primary macrophages, the restrictive cell types are actively dividing, and nuclear import of preintegration complexes (PICs) is not requ

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Haberichter, Jarod, Scott Roberts, Imran Abbasi, Phonphanh Dedthanou, Prajakta Pradhan, and Marie L. Nguyen. "The Telomerase Inhibitor MST-312 Interferes with Multiple Steps in the Herpes Simplex Virus Life Cycle." Journal of Virology 89, no. 19 (2015): 9804–16. http://dx.doi.org/10.1128/jvi.01006-15.

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ABSTRACTThe life cycle of herpes simplex virus (HSV) has the potential to be further manipulated to yield novel, more effective therapeutic treatments. Recent research has demonstrated that HSV-1 can increase telomerase activity and that expression of the catalytic component of telomerase, telomerase reverse transcriptase (TERT), alters sensitivity to HSV-dependent apoptosis. Telomerase is a cellular enzyme that synthesizes nucleotide repeats at the ends of chromosomes (telomeres), which prevents shortening of the 3′ ends of DNA with each cell division. Once telomeres reach a critical length,

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28

Hendrix, Jelle, Viola Baumgärtel, Waldemar Schrimpf, et al. "Live-cell observation of cytosolic HIV-1 assembly onset reveals RNA-interacting Gag oligomers." Journal of Cell Biology 210, no. 4 (2015): 629–46. http://dx.doi.org/10.1083/jcb.201504006.

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Assembly of the Gag polyprotein into new viral particles in infected cells is a crucial step in the retroviral replication cycle. Currently, little is known about the onset of assembly in the cytosol. In this paper, we analyzed the cytosolic HIV-1 Gag fraction in real time in live cells using advanced fluctuation imaging methods and thereby provide detailed insights into the complex relationship between cytosolic Gag mobility, stoichiometry, and interactions. We show that Gag diffuses as a monomer on the subsecond timescale with severely reduced mobility. Reduction of mobility is associated wi

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29

AlBurtamani, Nawal, Alwin Paul, and Ariberto Fassati. "The Role of Capsid in the Early Steps of HIV-1 Infection: New Insights into the Core of the Matter." Viruses 13, no. 6 (2021): 1161. http://dx.doi.org/10.3390/v13061161.

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In recent years, major advances in research and experimental approaches have significantly increased our knowledge on the role of the HIV-1 capsid in the virus life cycle, from reverse transcription to integration and gene expression. This makes the capsid protein a good pharmacological target to inhibit HIV-1 replication. This review covers our current understanding of the role of the viral capsid in the HIV-1 life cycle and its interaction with different host factors that enable reverse transcription, trafficking towards the nucleus, nuclear import and integration into host chromosomes. It a

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Moser, Lindsey A., and Stacey Schultz-Cherry. "Suppression of Astrovirus Replication by an ERK1/2 Inhibitor." Journal of Virology 82, no. 15 (2008): 7475–82. http://dx.doi.org/10.1128/jvi.02193-07.

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ABSTRACT Human astroviruses are nonenveloped, positive-sense single-strand RNA viruses associated with self-limiting diarrhea. Although they are recognized as a leading cause of disease in young children, the cellular factors involved in astrovirus replication are not well defined. The extracellular signal-regulated kinase (ERK) pathway has been shown to regulate many viral infections, but its role during astrovirus infection is unknown. In this report, we show that astrovirus activates ERK1/2 early in infection independently of replication. Inhibition of ERK activation with U0126, a specific

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Schilling, Eva-Maria, Myriam Scherer, and Thomas Stamminger. "Intrinsic Immune Mechanisms Restricting Human Cytomegalovirus Replication." Viruses 13, no. 2 (2021): 179. http://dx.doi.org/10.3390/v13020179.

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Cellular restriction factors (RFs) act as important constitutive innate immune barriers against viruses. In 2006, the promyelocytic leukemia protein was described as the first RF against human cytomegalovirus (HCMV) infection which is antagonized by the viral immediate early protein IE1. Since then, at least 15 additional RFs against HCMV have been identified, including the chromatin regulatory protein SPOC1, the cytidine deaminase APOBEC3A and the dNTP triphosphohydrolase SAMHD1. These RFs affect distinct steps of the viral replication cycle such as viral entry, gene expression, the synthesis

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Petit, Caroline, Olivier Schwartz, and Fabrizio Mammano. "Oligomerization within Virions and Subcellular Localization of Human Immunodeficiency Virus Type 1 Integrase." Journal of Virology 73, no. 6 (1999): 5079–88. http://dx.doi.org/10.1128/jvi.73.6.5079-5088.1999.

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ABSTRACT Previous biochemical and genetic evidence indicated that the functional form of retroviral integrase protein (IN) is a multimer. A direct demonstration of IN oligomerization during the infectious cycle was, however, missing, due to the absence of a sensitive detection method. We describe here the generation of infectious human immunodeficiency virus type 1 (HIV-1) viral clones carrying IN protein tagged with highly antigenic epitopes. In this setting, we could readily visualize IN both in producer cells and in viral particles. More interestingly, we detected IN oligomers, the formatio

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Holmes, Allyson M., Atanas Kaykov, and Benoit Arcangioli. "Molecular and Cellular Dissection of Mating-Type Switching Steps in Schizosaccharomyces pombe." Molecular and Cellular Biology 25, no. 1 (2005): 303–11. http://dx.doi.org/10.1128/mcb.25.1.303-311.2005.

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ABSTRACT A strand-specific imprint (break) controls mating-type switching in fission yeast. By introducing a thiamine repressible promoter upstream of the mat1 locus, we can force transcription through the imprinted region, erasing the imprint and inhibiting further mating-type switching, in a reversible manner. Starting from a synchronized, virgin M-cell population, we show that the site- and strand-specific break is formed when DNA replication intermediates appear at mat1 during the first S phase. The formation of the break is concomitant with a replication fork pause and binding of the Swi1

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Valerdi, Karl M., Adam Hage, Sarah van Tol, Ricardo Rajsbaum, and Maria I. Giraldo. "The Role of the Host Ubiquitin System in Promoting Replication of Emergent Viruses." Viruses 13, no. 3 (2021): 369. http://dx.doi.org/10.3390/v13030369.

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Ubiquitination of proteins is a post-translational modification process with many different cellular functions, including protein stability, immune signaling, antiviral functions and virus replication. While ubiquitination of viral proteins can be used by the host as a defense mechanism by destroying the incoming pathogen, viruses have adapted to take advantage of this cellular process. The ubiquitin system can be hijacked by viruses to enhance various steps of the replication cycle and increase pathogenesis. Emerging viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV

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35

Carey, Brooke L., Maryam Ahmed, Shelby Puckett, and Douglas S. Lyles. "Early Steps of the Virus Replication Cycle Are Inhibited in Prostate Cancer Cells Resistant to Oncolytic Vesicular Stomatitis Virus." Journal of Virology 82, no. 24 (2008): 12104–15. http://dx.doi.org/10.1128/jvi.01508-08.

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ABSTRACT Vesicular stomatitis virus (VSV) is currently being studied as a candidate oncolytic virus for tumor therapies due to its potent tumoricidal activity. Previous studies have demonstrated that VSV selectively infects tumor cells due to defects in their antiviral pathways. These defects make them more susceptible to VSV-induced killing than normal cells. However, some cancer cells display differential sensitivity to VSV. Specifically, LNCaP prostate cancer cells are sensitive to infection with VSV, while PC3 prostate cancer cells are relatively resistant to VSV. This suggests that tumor

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Yu, Julie H., and David V. Schaffer. "High-Throughput, Library-Based Selection of a Murine Leukemia Virus Variant To Infect Nondividing Cells." Journal of Virology 80, no. 18 (2006): 8981–88. http://dx.doi.org/10.1128/jvi.00615-06.

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ABSTRACT Gammaretroviruses, such as murine leukemia virus (MLV), are functionally distinguished from lentiviruses, such as human immunodeficiency virus, by their inability to infect nondividing cells. Attempts to engineer this property into MLV have been hindered by an incomplete understanding of early events in the viral life cycle. We utilized a transposon-based method to generate saturated peptide insertion libraries of MLV gag-pol variants with nuclear localization signals randomly incorporated throughout these overlapping genes. High-throughput selection of the libraries via iterative ret

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Mallardo, Massimo, Edward Leithe, Sibylle Schleich, Norbert Roos, Laura Doglio, and Jacomine Krijnse Locker. "Relationship between Vaccinia Virus Intracellular Cores, Early mRNAs, and DNA Replication Sites." Journal of Virology 76, no. 10 (2002): 5167–83. http://dx.doi.org/10.1128/jvi.76.10.5167-5183.2002.

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ABSTRACT Virus assembly, a late event in the life cycle of vaccinia virus (VV), is preceded by a number of steps that all occur in the cytoplasm of the infected host cell: virion entry, delivery of the viral core into the cytoplasm, and transcription from these cores of early mRNAs, followed by the process of DNA replication. In the present study the quantitative and structural relationships between these distinct steps of VV morphogenesis were investigated. We show that viral RNA and DNA synthesis increases linearly with increasing amounts of incoming cores. Moreover, at multiplicities of inf

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Bona, Roberta, Mauro Andreotti, Viviana Buffa, et al. "Development of a Human Immunodeficiency Virus Vector-Based, Single-Cycle Assay for Evaluation of Anti-Integrase Compounds." Antimicrobial Agents and Chemotherapy 50, no. 10 (2006): 3407–17. http://dx.doi.org/10.1128/aac.00517-06.

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ABSTRACT Therapeutic strategies aimed at inhibiting human immunodeficiency virus type 1 (HIV-1) replication employ a combination of drugs targeted to two viral enzymes (reverse transcriptase and protease) and to the viral entry/fusion step. However, the high propensity of HIV-1 to develop resistance makes the development of novel compounds targeting different steps of the HIV-1 life cycle essential. Among these, integrase (IN) inhibitors have successfully passed the early phases of clinical development. By preventing integration, IN inhibitors preclude viral replication while allowing producti

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García, Mayra, Xiao-Fang Yu, Diane E. Griffin, and William J. Moss. "Measles virus inhibits human immunodeficiency virus type 1 reverse transcription and replication by blocking cell-cycle progression of CD4+ T lymphocytes." Journal of General Virology 89, no. 4 (2008): 984–93. http://dx.doi.org/10.1099/vir.0.83601-0.

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Acute measles virus (MV) infection results in a decrease in plasma human immunodeficiency virus type 1 (HIV-1) RNA levels in co-infected children. An in vitro peripheral blood mononuclear cell (PBMC) culture system was used to assess the mechanisms by which MV blocks HIV-1 replication. MV inhibited proliferation of CD4+ T lymphocytes, the target cell for HIV-1 replication. In the presence of MV, cells did not progress to G1b and S phases, steps critical for the completion of HIV-1 reverse transcription and productive replication. This block in cell-cycle progression was characterized by an inc

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Sirikanchana, Kwanrawee, Joanna L. Shisler, and Benito J. Mariñas. "Effect of Exposure to UV-C Irradiation and Monochloramine on Adenovirus Serotype 2 Early Protein Expression and DNA Replication." Applied and Environmental Microbiology 74, no. 12 (2008): 3774–82. http://dx.doi.org/10.1128/aem.02049-07.

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ABSTRACT The mechanisms of adenovirus serotype 2 inactivation with either UV light (with a narrow emission spectrum centered at 254 nm) or monochloramine were investigated by assessing the potential inhibition of two key steps of the adenovirus life cycle, namely, E1A protein synthesis and viral genomic replication. E1A early protein synthesis was assayed by using immunoblotting, while the replication of viral DNA was analyzed by using slot blotting. Disinfection experiments were performed in phosphate buffer solutions at pH 8 and room temperature (UV) or 20°C (monochloramine). Experimental re

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Carroll, S. M., J. Trotter, and G. M. Wahl. "Replication timing control can be maintained in extrachromosomally amplified genes." Molecular and Cellular Biology 11, no. 9 (1991): 4779–85. http://dx.doi.org/10.1128/mcb.11.9.4779.

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Extrachromosomal elements are common early intermediates of gene amplification in vivo and in cell culture. The time at which several extrachromosomal elements replicate was compared with that of the corresponding amplified or unamplified chromosomal sequences. The replication timing analysis employed a retroactive synchrony method in which fluorescence-activated cell sorting was used to obtain cells at different stages of the cell cycle. Extrachromosomally amplified Syrian hamster CAD genes (CAD is an acronym for the single gene which encodes the trifunctional protein which catalyzes the firs

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Carroll, S. M., J. Trotter, and G. M. Wahl. "Replication timing control can be maintained in extrachromosomally amplified genes." Molecular and Cellular Biology 11, no. 9 (1991): 4779–85. http://dx.doi.org/10.1128/mcb.11.9.4779-4785.1991.

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Extrachromosomal elements are common early intermediates of gene amplification in vivo and in cell culture. The time at which several extrachromosomal elements replicate was compared with that of the corresponding amplified or unamplified chromosomal sequences. The replication timing analysis employed a retroactive synchrony method in which fluorescence-activated cell sorting was used to obtain cells at different stages of the cell cycle. Extrachromosomally amplified Syrian hamster CAD genes (CAD is an acronym for the single gene which encodes the trifunctional protein which catalyzes the firs

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O'Connor, Christopher, Thomas Pertel, Seth Gray та ін. "p62/Sequestosome-1 Associates with and Sustains the Expression of Retroviral Restriction Factor TRIM5α". Journal of Virology 84, № 12 (2010): 5997–6006. http://dx.doi.org/10.1128/jvi.02412-09.

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ABSTRACT TRIM5 proteins mediate a potent block to the cross-species transmission of retroviruses, the most well known being the TRIM5α protein from rhesus macaques, which potently inhibits human immunodeficiency virus type 1 (HIV-1) infection. This restriction occurs at an early stage in the replication cycle and is mediated by the binding of TRIM5 proteins to determinants present in the retroviral capsid. TRIM5α, as well as other TRIM family proteins, has been shown to be regulated by interferons (IFN). Here we show that TRIM5α associates with another IFN-induced gene, sequestosome-1/p62 (p62

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Pannecouque, Christophe, Beata Szafarowicz, Natalia Volkova, et al. "Inhibition of HIV-1 Replication by a Bis-Thiadiazolbenzene-1,2-Diamine That Chelates Zinc Ions from Retroviral Nucleocapsid Zinc Fingers." Antimicrobial Agents and Chemotherapy 54, no. 4 (2010): 1461–68. http://dx.doi.org/10.1128/aac.01671-09.

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ABSTRACT The human immunodeficiency virus type 1 (HIV-1) nucleocapsid p7 (NCp7) protein holds two highly conserved “CCHC” zinc finger domains that are required for several phases of viral replication. Basic residues flank the zinc fingers, and both determinants are required for high-affinity binding to RNA. Several compounds were previously found to target NCp7 by reacting with the sulfhydryl group of cysteine residues from the zinc fingers. Here, we have identified an N,N′-bis(1,2,3-thiadiazol-5-yl)benzene-1,2-diamine (NV038) that efficiently blocks the replication of a wide spectrum of HIV-1

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Wolny, Elzbieta, Alexander Betekhtin, Magdalena Rojek, Agnieszka Braszewska-Zalewska, Joanna Lusinska, and Robert Hasterok. "Germination and the Early Stages of Seedling Development in Brachypodium distachyon." International Journal of Molecular Sciences 19, no. 10 (2018): 2916. http://dx.doi.org/10.3390/ijms19102916.

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Successful germination and seedling development are crucial steps in the growth of a new plant. In this study, we investigated the course of the cell cycle during germination in relation to grain hydration in the model grass Brachypodium distachyon (Brachypodium) for the first time. Flow cytometry was performed to monitor the cell cycle progression during germination and to estimate DNA content in embryo tissues. The analyses of whole zygotic embryos revealed that the relative DNA content was 2C, 4C, 8C, and 16C. Endoreplicated nuclei were detected in the scutellum and coleorhiza cells, wherea

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Lee, Chyan-Jang, Hui-Ru Lin, Ching-Len Liao, and Yi-Ling Lin. "Cholesterol Effectively Blocks Entry of Flavivirus." Journal of Virology 82, no. 13 (2008): 6470–80. http://dx.doi.org/10.1128/jvi.00117-08.

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ABSTRACT Japanese encephalitis virus (JEV) and dengue virus serotype 2 (DEN-2) are enveloped flaviviruses that enter cells through receptor-mediated endocytosis and low pH-triggered membrane fusion and then replicate in intracellular membrane structures. Lipid rafts, cholesterol-enriched lipid-ordered membrane domains, are platforms for a variety of cellular functions. In this study, we found that disruption of lipid raft formation by cholesterol depletion with methyl-β-cyclodextrin or cholesterol chelation with filipin III reduces JEV and DEN-2 infection, mainly at the intracellular replicati

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Vial, Thomas, Wei-Lian Tan, Eric Deharo, Dorothée Missé, Guillaume Marti, and Julien Pompon. "Mosquito metabolomics reveal that dengue virus replication requires phospholipid reconfiguration via the remodeling cycle." Proceedings of the National Academy of Sciences 117, no. 44 (2020): 27627–36. http://dx.doi.org/10.1073/pnas.2015095117.

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Dengue virus (DENV) subdues cell membranes for its cellular cycle by reconfiguring phospholipids in humans and mosquitoes. Here, we determined how and why DENV reconfigures phospholipids in the mosquito vector. By inhibiting and activating the de novo phospholipid biosynthesis, we demonstrated the antiviral impact of de novo–produced phospholipids. In line with the virus hijacking lipids for its benefit, metabolomics analyses indicated that DENV actively inhibited the de novo phospholipid pathway and instead triggered phospholipid remodeling. We demonstrated the early induction of remodeling d

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He, Ran, Kyoungsook Park, Hongyi Cai, et al. "Artemisinin-Derived Dimer Diphenyl Phosphate Is an Irreversible Inhibitor of Human Cytomegalovirus Replication." Antimicrobial Agents and Chemotherapy 56, no. 7 (2012): 3508–15. http://dx.doi.org/10.1128/aac.00519-12.

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ABSTRACTWe previously reported that among a series of artemisinin-derived monomers and dimers, dimer diphenyl phosphate (838) was the most potent inhibitor of human cytomegalovirus (CMV) replication. Our continued investigation of a prototypic artemisinin monomer (artesunate [AS]) and dimer (838) now reveals that both compounds have specific activity against CMV but do not inhibit lytic replication of human herpesvirus 1 or 2 or Epstein-Barr virus. AS and 838 inhibited CMV replication during the first 24 h of the virus replication cycle, earlier than the time of ganciclovir (GCV) activities an

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Butler, Scott L., Erik P. Johnson, and Frederic D. Bushman. "Human Immunodeficiency Virus cDNA Metabolism: Notable Stability of Two-Long Terminal Repeat Circles." Journal of Virology 76, no. 8 (2002): 3739–47. http://dx.doi.org/10.1128/jvi.76.8.3739-3747.2002.

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ABSTRACT Early steps of retroviral replication involve reverse transcription of the viral RNA to yield a linear double-stranded cDNA copy and then integration of the viral cDNA into a chromosome of the host cell. A portion of the viral cDNA can also follow nonproductive pathways in which it becomes circularized. In one pathway, the ends of the linear cDNA become joined together by the cellular nonhomologous DNA end-joining system to form two-long terminal repeat (2-LTR) circles. It has been argued that 2-LTR circles are quickly degraded in human immunodeficiency virus (HIV)-infected cells, all

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Guimerà Busquets, Marc, Gillian D. Pullinger, Karin E. Darpel, et al. "An Early Block in the Replication of the Atypical Bluetongue Virus Serotype 26 in Culicoides Cells Is Determined by Its Capsid Proteins." Viruses 13, no. 5 (2021): 919. http://dx.doi.org/10.3390/v13050919.

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Arboviruses such as bluetongue virus (BTV) replicate in arthropod vectors involved in their transmission between susceptible vertebrate-hosts. The “classical” BTV strains infect and replicate effectively in cells of their insect-vectors (Culicoides biting-midges), as well as in those of their mammalian-hosts (ruminants). However, in the last decade, some “atypical” BTV strains, belonging to additional serotypes (e.g., BTV-26), have been found to replicate efficiently only in mammalian cells, while their replication is severely restricted in Culicoides cells. Importantly, there is evidence that

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