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Journal articles on the topic 'Negative strand RNA'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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1

Enami, Masayoshi. "Negative-strand RNA viruses. Reverse genetics of negative-strand RNA viruses." Uirusu 45, no. 2 (1995): 145–57. http://dx.doi.org/10.2222/jsv.45.145.

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2

Baric, Ralph S., and Boyd Yount. "Subgenomic Negative-Strand RNA Function during Mouse Hepatitis Virus Infection." Journal of Virology 74, no. 9 (2000): 4039–46. http://dx.doi.org/10.1128/jvi.74.9.4039-4046.2000.

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ABSTRACT Mouse hepatitis virus (MHV)-infected cells contain full-length and subgenomic-length positive- and negative-strand RNAs. The origin and function of the subgenomic negative-strand RNAs is controversial. In this report we demonstrate that the synthesis and molar ratios of subgenomic negative strands are similar in alternative host cells, suggesting that these RNAs function as important mediators of positive-strand synthesis. Using kinetic labeling experiments, we show that the full-length and subgenomic-length replicative form RNAs rapidly accumulate and then saturate with label, suggesting that the subgenomic-length negative strands are the principal mediators of positive-strand synthesis. Using cycloheximide, which preferentially inhibits negative-strand and to a lesser extent positive-strand synthesis, we demonstrate that cycloheximide treatment equally inhibits full-length and subgenomic-length negative-strand synthesis. Importantly, following treatment, previously transcribed negative strands remain in transcriptionally active complexes even in the absence of new negative-strand synthesis. These findings indicate that the subgenomic-length negative strands are the principal templates of positive-strand synthesis during MHV infection.

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3

Pringle, Craig R., and Andrew J. Easton. "Monopartite Negative Strand RNA Genomes." Seminars in Virology 8, no. 1 (1997): 49–57. http://dx.doi.org/10.1006/smvy.1997.0105.

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4

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

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The replication of tobacco mosaic virus (TMV) RNA involves synthesis of a negative–strand RNA using the genomic positive–strand RNA as a template, followed by the synthesis of positive–strand RNA on the negative–strand RNA templates. Intermediates of replication isolated from infected cells include completely double–stranded RNA (replicative form) and partly double–stranded and partly single–stranded RNA (replicative intermediate), but it is not known whether these structures are double–stranded or largely single–stranded in vivo . The synthesis of negative strands ceases before that of positive strands, and positive and negative strands may be synthesized by two different polymerases. The genomic–length negative strand also serves as a template for the synthesis of subgenomic mRNAs for the virus movement and coat proteins. Both the virus–encoded 126–kDa protein, which has amino–acid sequence motifs typical of methyltransferases and helicases, and the 183–kDa protein, which has additional motifs characteristic of RNA–dependent RNA polymerases, are required for efficient TMV RNA replication. Purified TMV RNA polymerase also contains a host protein serologically related to the RNA–binding subunit of the yeast translational initiation factor, eIF3. Study of Arabidopsis mutants defective in RNA replication indicates that at least two host proteins are needed for TMV RNA replication. The tomato resistance gene Tm–1 may also encode a mutant form of a host protein component of the TMV replicase. TMV replicase complexes are located on the endoplasmic reticulum in close association with the cytoskeleton in cytoplasmic bodies called viroplasms, which mature to produce ‘X bodies’. Viroplasms are sites of both RNA replication and protein synthesis, and may provide compartments in which the various stages of the virus mutiplication cycle (protein synthesis, RNA replication, virus movement, encapsidation) are localized and coordinated. Membranes may also be important for the configuration of the replicase with respect to initiation of RNA synthesis, and synthesis and release of progeny single–stranded RNA.

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5

Shaklee, Patrick N. "Negative-strand RNA replication by Qβ and MS2 positive-strand RNA phage replicases". Virology 178, № 1 (1990): 340–43. http://dx.doi.org/10.1016/0042-6822(90)90417-p.

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6

Luo, Ming, James Ross Terrell, and Shelby Ashlyn Mcmanus. "Nucleocapsid Structure of Negative Strand RNA Virus." Viruses 12, no. 8 (2020): 835. http://dx.doi.org/10.3390/v12080835.

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Negative strand RNA viruses (NSVs) include many important human pathogens, such as influenza virus, Ebola virus, and rabies virus. One of the unique characteristics that NSVs share is the assembly of the nucleocapsid and its role in viral RNA synthesis. In NSVs, the single strand RNA genome is encapsidated in the linear nucleocapsid throughout the viral replication cycle. Subunits of the nucleocapsid protein are parallelly aligned along the RNA genome that is sandwiched between two domains composed of conserved helix motifs. The viral RNA-dependent-RNA polymerase (vRdRp) must recognize the protein–RNA complex of the nucleocapsid and unveil the protected genomic RNA in order to initiate viral RNA synthesis. In addition, vRdRp must continuously translocate along the protein–RNA complex during elongation in viral RNA synthesis. This unique mechanism of viral RNA synthesis suggests that the nucleocapsid may play a regulatory role during NSV replication.

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7

Curran, Joseph, and Daniel Kolakofsky. "Nonsegmented negative-strand RNA virus RNA synthesis in vivo." Virology 371, no. 2 (2008): 227–30. http://dx.doi.org/10.1016/j.virol.2007.11.022.

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8

Radkowski, Marek, Jeffrey Wilkinson, Marek Nowicki, et al. "Search for Hepatitis C Virus Negative-Strand RNA Sequences and Analysis of Viral Sequences in the Central Nervous System: Evidence of Replication." Journal of Virology 76, no. 2 (2002): 600–608. http://dx.doi.org/10.1128/jvi.76.2.600-608.2002.

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ABSTRACT Patients with chronic hepatitis C are more likely to have significant changes in their physical and mental well-being than patients with liver disease of other etiology, and hepatitis C virus (HCV) has been occasionally implicated in diseases of the central nervous system. We analyzed the presence of the HCV negative-strand RNA sequence, which is the viral replicative intermediary, in autopsy brain tissue samples from six HCV-infected patients. Negative-strand HCV RNA was searched for by a strand-specific Tth-based reverse transcriptase PCR, and viral sequences amplified from brain tissue and serum were compared by single-strand conformational polymorphism analysis and direct sequencing. HCV RNA negative strands were detected in brain tissue in three patients. In two of these patients, serum- and brain-derived viral sequences were different and classified as belonging to different genotypes. In one of the latter patients, HCV RNA negative strands were detected in lymph node and, while being different from serum-derived sequences, were identical to those present in the brain. The results of the present study suggest that HCV can replicate in the central nervous system, probably in cells of the macrophage/monocyte lineage.

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9

Steil, Benjamin P., and David J. Barton. "Conversion of VPg into VPgpUpUOH before and during Poliovirus Negative-Strand RNA Synthesis." Journal of Virology 83, no. 24 (2009): 12660–70. http://dx.doi.org/10.1128/jvi.01676-08.

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ABSTRACT There are two protein primers involved in picornavirus RNA replication, VPg, the viral protein of the genome, and VPgpUpUOH. A cis-acting replication element (CRE) within the open reading frame of poliovirus (PV) RNA allows the viral RNA-dependent RNA polymerase 3DPol to catalyze the conversion of VPg into VPgpUpUOH. In this study, we used preinitiation RNA replication complexes (PIRCs) to determine when CRE-dependent VPg uridylylation occurs relative to the sequential synthesis of negative- and positive-strand RNA. Guanidine HCl (2 mM), a reversible inhibitor of PV 2CATPase, prevented CRE-dependent VPgpUpUOH synthesis and the initiation of negative-strand RNA synthesis. VPgpUpUOH and nascent negative-strand RNA molecules were synthesized coincident in time following the removal of guanidine, consistent with PV RNA functioning simultaneously as a template for CRE-dependent VPgpUpUOH synthesis and negative-strand RNA synthesis. The amounts of [32P]UMP incorporated into VPgpUpUOH and negative-strand RNA products indicated that 100 to 400 VPgpUpUOH molecules were made coincident in time with each negative-strand RNA. 3′-dCTP inhibited the elongation of nascent negative-strand RNAs without affecting CRE-dependent VPg uridylylation. A 3′ nontranslated region mutation which inhibited negative-strand RNA synthesis did not inhibit CRE-dependent VPg uridylylation. Together, the data implicate 2CATPase in the mechanisms whereby PV RNA functions as a template for reiterative CRE-dependent VPg uridylylation before and during negative-strand RNA synthesis.

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10

Olsthoorn, R. C. L., A. Bruyere, A. Dzianott, and J. J. Bujarski. "RNA Recombination in Brome Mosaic Virus: Effects of Strand-Specific Stem-Loop Inserts." Journal of Virology 76, no. 24 (2002): 12654–62. http://dx.doi.org/10.1128/jvi.76.24.12654-12662.2002.

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ABSTRACT A model system of a single-stranded trisegment Brome mosaic bromovirus (BMV) was used to analyze the mechanism of homologous RNA recombination. Elements capable of forming strand-specific stem-loop structures were inserted at the modified 3′ noncoding regions of BMV RNA3 and RNA2 in either positive or negative orientations, and various combinations of parental RNAs were tested for patterns of the accumulating recombinant RNA3 components. The structured negative-strand stem-loops that were inserted in both RNA3 and RNA2 reduced the accumulation of RNA3-RNA2 recombinants to a much higher extent than those in positive strands or the unstructured stem-loop inserts in either positive or negative strands. The use of only one parental RNA carrying the stem-loop insert reduced the accumulation of RNA3-RNA2 recombinants even further, but only when the stem-loops were in negative strands of RNA2. We assume that the presence of a stable stem-loop downstream of the landing site on the acceptor strand (negative RNA2) hampers the reattachment and reinitiation processes. Besides RNA3-RNA2 recombinants, the accumulation of nontargeted RNA3-RNA1 and RNA3-RNA3 recombinants were observed. Our results provide experimental evidence that homologous recombination between BMV RNAs more likely occurs during positive- rather than negative-strand synthesis.

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11

Enami, Masayoshi. "Genetic engineering of negative strand RNA viruses." Uirusu 42, no. 1 (1992): 59–65. http://dx.doi.org/10.2222/jsv.42.59.

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12

Garcı́a-Sastre, Adolfo. "Negative-strand RNA viruses: applications to biotechnology." Trends in Biotechnology 16, no. 5 (1998): 230–35. http://dx.doi.org/10.1016/s0167-7799(98)01192-5.

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13

Reguera, Juan, Stephen Cusack, and Daniel Kolakofsky. "Segmented negative strand RNA virus nucleoprotein structure." Current Opinion in Virology 5 (April 2014): 7–15. http://dx.doi.org/10.1016/j.coviro.2014.01.003.

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14

SUGITA, Yukihiko. "Structural studies on negative-strand RNA virus." Uirusu 70, no. 1 (2020): 91–100. http://dx.doi.org/10.2222/jsv.70.91.

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15

Barton, David J., B. Joan Morasco, and James B. Flanegan. "Translating Ribosomes Inhibit Poliovirus Negative-Strand RNA Synthesis." Journal of Virology 73, no. 12 (1999): 10104–12. http://dx.doi.org/10.1128/jvi.73.12.10104-10112.1999.

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ABSTRACT Poliovirus has a single-stranded RNA genome of positive polarity that serves two essential functions at the start of the viral replication cycle in infected cells. First, it is translated to synthesize viral proteins and, second, it is copied by the viral polymerase to synthesize negative-strand RNA. We investigated these two reactions by using HeLa S10 in vitro translation-RNA replication reactions. Preinitiation RNA replication complexes were isolated from these reactions and then used to measure the sequential synthesis of negative- and positive-strand RNAs in the presence of different protein synthesis inhibitors. Puromycin was found to stimulate RNA replication overall. In contrast, RNA replication was inhibited by diphtheria toxin, cycloheximide, anisomycin, and ricin A chain. Dose-response experiments showed that precisely the same concentration of a specific drug was required to inhibit protein synthesis and to either stimulate or inhibit RNA replication. This suggested that the ability of these drugs to affect RNA replication was linked to their ability to alter the normal clearance of translating ribosomes from the input viral RNA. Consistent with this idea was the finding that the protein synthesis inhibitors had no measurable effect on positive-strand synthesis in normal RNA replication complexes. In marked contrast, negative-strand synthesis was stimulated by puromycin and was inhibited by cycloheximide. Puromycin causes polypeptide chain termination and induces the dissociation of polyribosomes from mRNA. Cycloheximide and other inhibitors of polypeptide chain elongation “freeze” ribosomes on mRNA and prevent the normal clearance of ribosomes from viral RNA templates. Therefore, it appears that the poliovirus polymerase was not able to dislodge translating ribosomes from viral RNA templates and mediate the switch from translation to negative-strand synthesis. Instead, the initiation of negative-strand synthesis appears to be coordinately regulated with the natural clearance of translating ribosomes to avoid the dilemma of ribosome-polymerase collisions.

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16

Green, T. J., R. Cox, J. Tsao, M. Rowse, S. Qiu, and M. Luo. "Common Mechanism for RNA Encapsidation by Negative-Strand RNA Viruses." Journal of Virology 88, no. 7 (2014): 3766–75. http://dx.doi.org/10.1128/jvi.03483-13.

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17

Banerjee, Rajeev, and Asim Dasgupta. "Specific Interaction of Hepatitis C Virus Protease/Helicase NS3 with the 3′-Terminal Sequences of Viral Positive- and Negative-Strand RNA." Journal of Virology 75, no. 4 (2001): 1708–21. http://dx.doi.org/10.1128/jvi.75.4.1708-1721.2001.

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ABSTRACT The hepatitis C virus (HCV)-encoded protease/helicase NS3 is likely to be involved in viral RNA replication. We have expressed and purified recombinant NS3 (protease and helicase domains) and ΔpNS3 (helicase domain only) and examined their abilities to interact with the 3′-terminal sequence of both positive and negative strands of HCV RNA. These regions of RNA were chosen because initiation of RNA synthesis is likely to occur at or near the 3′ untranslated region (UTR). The results presented here demonstrate that NS3 (and ΔpNS3) interacts efficiently and specifically with the 3′-terminal sequences of both positive- and negative-strand RNA but not with the corresponding complementary 5′-terminal RNA sequences. The interaction of NS3 with the 3′-terminal negative strand [called 3′(−) UTR127] was specific in that only homologous (and not heterologous) RNA competed efficiently in the binding reaction. A predicted stem-loop structure present at the 3′ terminus (nucleotides 5 to 20 from the 3′ end) of the negative-strand RNA appears to be important for NS3 binding to the negative-strand UTR. Deletion of the stem-loop structure almost totally impaired NS3 (and ΔpNS3) binding. Additional mutagenesis showed that three G-C pairs within the stem were critical for helicase-RNA interaction. The data presented here also suggested that both a double-stranded structure and the 3′-proximal guanosine residues in the stem were important determinants of protein binding. In contrast to the relatively stringent requirement for 3′(−) UTR binding, specific interaction of NS3 (or ΔpNS3) with the 3′-terminal sequences of the positive-strand RNA [3′(+) UTR] appears to require the entire 3′(+) UTR of HCV. Deletion of either the 98-nucleotide 3′-terminal conserved region or the 5′ half sequence containing the variable region and the poly(U) and/or poly(UC) stretch significantly impaired RNA-protein interaction. The implication of NS3 binding to the 3′-terminal sequences of viral positive- and negative-strand RNA in viral replication is discussed.

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18

Teterina, Natalya L., Mario S. Rinaudo, and Ellie Ehrenfeld. "Strand-Specific RNA Synthesis Defects in a Poliovirus with a Mutation in Protein 3A." Journal of Virology 77, no. 23 (2003): 12679–91. http://dx.doi.org/10.1128/jvi.77.23.12679-12691.2003.

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ABSTRACT Substitution of a methionine residue at position 79 in poliovirus protein 3A with valine or threonine caused defective viral RNA synthesis, manifested as delayed onset and reduced yield of viral RNA, in HeLa cells transfected with a luciferase-containing replicon. Viruses containing these same mutations produced small or minute plaques that generated revertants upon further passage, with either wild-type 3A sequences or additional nearby compensating mutations. Translation and polyprotein processing were not affected by the mutations, and 3AB proteins containing the altered amino acids at position 79 showed no detectable loss of membrane-binding activity. Analysis of individual steps of viral RNA synthesis in HeLa cell extracts that support translation and replication of viral RNA showed that VPg uridylylation and negative-strand RNA synthesis occurred normally from mutant viral RNA; however, positive-strand RNA synthesis was specifically reduced. The data suggest that a function of viral protein 3A is required for positive-strand RNA synthesis but not for production of negative strands.

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19

Kranzusch, Philip J., and Sean P. J. Whelan. "Architecture and regulation of negative-strand viral enzymatic machinery." RNA Biology 9, no. 7 (2012): 941–48. http://dx.doi.org/10.4161/rna.20345.

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20

Murray, Kenneth E., and David J. Barton. "Poliovirus CRE-Dependent VPg Uridylylation Is Required for Positive-Strand RNA Synthesis but Not for Negative-Strand RNA Synthesis." Journal of Virology 77, no. 8 (2003): 4739–50. http://dx.doi.org/10.1128/jvi.77.8.4739-4750.2003.

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ABSTRACT The cis-acting replication element (CRE) is a 61-nucleotide stem-loop RNA structure found within the coding sequence of poliovirus protein 2C. Although the CRE is required for viral RNA replication, its precise role(s) in negative- and positive-strand RNA synthesis has not been defined. Adenosine in the loop of the CRE RNA structure functions as the template for the uridylylation of the viral protein VPg. VPgpUpUOH, the predominant product of CRE-dependent VPg uridylylation, is a putative primer for the poliovirus RNA-dependent RNA polymerase. By examining the sequential synthesis of negative- and positive-strand RNAs within preinitiation RNA replication complexes, we found that mutations that disrupt the structure of the CRE prevent VPg uridylylation and positive-strand RNA synthesis. The CRE mutations that inhibited the synthesis of VPgpUpUOH, however, did not inhibit negative-strand RNA synthesis. A Y3F mutation in VPg inhibited both VPgpUpUOH synthesis and negative-strand RNA synthesis, confirming the critical role of the tyrosine hydroxyl of VPg in VPg uridylylation and negative-strand RNA synthesis. trans-replication experiments demonstrated that the CRE and VPgpUpUOH were not required in cis or in trans for poliovirus negative-strand RNA synthesis. Because these results are inconsistent with existing models of poliovirus RNA replication, we propose a new four-step model that explains the roles of VPg, the CRE, and VPgpUpUOH in the asymmetric replication of poliovirus RNA.

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21

Ertel, Kenneth J., Jo Ellen Brunner, and Bert L. Semler. "Mechanistic Consequences of hnRNP C Binding to Both RNA Termini of Poliovirus Negative-Strand RNA Intermediates." Journal of Virology 84, no. 9 (2010): 4229–42. http://dx.doi.org/10.1128/jvi.02198-09.

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ABSTRACT The poliovirus 3′ noncoding region (3′ NCR) is necessary for efficient virus replication. A poliovirus mutant, PVΔ3′NCR, with a deletion of the entire 3′ NCR, yielded a virus that was capable of synthesizing viral RNA, albeit with a replication defect caused by deficient positive-strand RNA synthesis compared to wild-type virus. We detected multiple ribonucleoprotein (RNP) complexes in extracts from poliovirus-infected HeLa cells formed with a probe corresponding to the 5′ end of poliovirus negative-strand RNA (the complement of the genomic 3′ NCR), and the levels of these RNP complexes increased during the course of viral infection. Previous studies have identified RNP complexes formed with the 3′ end of poliovirus negative-strand RNA, including one that contains a 36-kDa protein later identified as heterogeneous nuclear ribonucleoprotein C (hnRNP C). We report here that the 5′ end of poliovirus negative-strand RNA is capable of interacting with endogenous hnRNP C, as well as with poliovirus nonstructural proteins. Further, we demonstrate that the addition of recombinant purified hnRNP C proteins can stimulate virus RNA synthesis in vitro and that depletion of hnRNP C proteins in cultured cells results in decreased virus yields and a correspondingly diminished accumulation of positive-strand RNAs. We propose that the association of hnRNP C with poliovirus negative-strand termini acts to stabilize or otherwise promote efficient positive-strand RNA synthesis.

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22

Yanagi, Yusuke. "Negative-strand RNA viruses. Measles virus receptor CD46." Uirusu 45, no. 2 (1995): 159–64. http://dx.doi.org/10.2222/jsv.45.159.

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23

Kawaoka, Yoshihiro. "Molecular Aspects of Emerging Negative Strand RNA Viruses." Uirusu 53, no. 1 (2003): 57. http://dx.doi.org/10.2222/jsv.53.57.

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24

Kormelink, Richard, Maria Laura Garcia, Michael Goodin, Takahide Sasaya, and Anne-Lise Haenni. "Negative-strand RNA viruses: The plant-infecting counterparts." Virus Research 162, no. 1-2 (2011): 184–202. http://dx.doi.org/10.1016/j.virusres.2011.09.028.

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25

Palese, P. "Genetic engineering of infectious negative-strand RNA viruses." Trends in Microbiology 3, no. 4 (1995): 123–25. http://dx.doi.org/10.1016/s0966-842x(00)88897-6.

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26

Ruigrok, Rob WH, Thibaut Crépin, and Dan Kolakofsky. "Nucleoproteins and nucleocapsids of negative-strand RNA viruses." Current Opinion in Microbiology 14, no. 4 (2011): 504–10. http://dx.doi.org/10.1016/j.mib.2011.07.011.

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27

Ziegler, Christopher M., and Jason W. Botten. "Defective Interfering Particles of Negative-Strand RNA Viruses." Trends in Microbiology 28, no. 7 (2020): 554–65. http://dx.doi.org/10.1016/j.tim.2020.02.006.

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28

Garcia-Sastre, A., and P. Palese. "Genetic Manipulation of Negative-Strand RNA Virus Genomes." Annual Review of Microbiology 47, no. 1 (1993): 765–90. http://dx.doi.org/10.1146/annurev.mi.47.100193.004001.

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29

Palese, P., H. Zheng, O. G. Engelhardt, S. Pleschka, and A. Garcia-Sastre. "Negative-strand RNA viruses: genetic engineering and applications." Proceedings of the National Academy of Sciences 93, no. 21 (1996): 11354–58. http://dx.doi.org/10.1073/pnas.93.21.11354.

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30

Banerjee, Amiya K., Sailen Barik, and Bishnu P. De. "Gene expression of nonsegmented negative strand RNA viruses." Pharmacology & Therapeutics 51, no. 1 (1991): 47–70. http://dx.doi.org/10.1016/0163-7258(91)90041-j.

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31

An, Sungwhan, Akihiko Maeda, and Shinji Makino. "Coronavirus Transcription Early in Infection." Journal of Virology 72, no. 11 (1998): 8517–24. http://dx.doi.org/10.1128/jvi.72.11.8517-8524.1998.

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ABSTRACT We studied the accumulation kinetics of murine coronavirus mouse hepatitis virus (MHV) RNAs early in infection by using cloned MHV defective interfering (DI) RNA that contained an intergenic sequence from which subgenomic DI RNA is synthesized in MHV-infected cells. Genomic DI RNA and subgenomic DI RNA accumulated at a constant ratio from 3 to 11 h postinfection (p.i.) in the cells infected with MHV-containing DI particles. Earlier, at 1 h p.i., this ratio was not constant; only genomic DI RNA accumulated, indicating that MHV RNA replication, but not MHV RNA transcription, was active during the first hour of MHV infection. Negative-strand genomic DI RNA and negative-strand subgenomic DI RNA were first detectable at 1 and 3 h p.i., respectively, and the amounts of both RNAs increased gradually until 6 h p.i. These data showed that at 2 h p.i., subgenomic DI RNA was undergoing synthesis in the cells in which negative-strand subgenomic DI RNA was undetectable. These data, therefore, signify that negative-strand genomic DI RNA, but not negative-strand subgenomic DI RNA, was an active template for subgenomic DI RNA synthesis early in infection.

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32

Nakada, Susumu. "Negative-strand RNA viruses. Functions of influenza virus RNA polymerase subunits." Uirusu 45, no. 2 (1995): 125–43. http://dx.doi.org/10.2222/jsv.45.125.

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33

Morasco, B. Joan, Nidhi Sharma, Jessica Parilla, and James B. Flanegan. "Poliovirus cre(2C)-Dependent Synthesis of VPgpUpU Is Required for Positive- but Not Negative-Strand RNA Synthesis." Journal of Virology 77, no. 9 (2003): 5136–44. http://dx.doi.org/10.1128/jvi.77.9.5136-5144.2003.

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ABSTRACT The cre(2C) hairpin is a cis-acting replication element in poliovirus RNA and serves as a template for the synthesis of VPgpUpU. We investigated the role of the cre(2C) hairpin on VPgpUpU synthesis and viral RNA replication in preinitiation RNA replication complexes isolated from HeLa S10 translation-RNA replication reactions. cre(2C) hairpin mutations that block VPgpUpU synthesis in reconstituted assays with purified VPg and poliovirus polymerase were also found to completely inhibit VPgpUpU synthesis in preinitiation replication complexes. Surprisingly, blocking VPgpUpU synthesis by mutating the cre(2C) hairpin had no significant effect on negative-strand synthesis but completely inhibited positive-strand synthesis. Negative-strand RNA synthesized in these reactions immunoprecipitated with anti-VPg antibody and demonstrated that it was covalently linked to VPg. This indicated that VPg was used to initiate negative-strand RNA synthesis, although the cre(2C)-dependent synthesis of VPgpUpU was inhibited. Based on these results, we concluded that the cre(2C)-dependent synthesis of VPgpUpU was required for positive- but not negative-strand RNA synthesis. These findings suggest a replication model in which negative-strand synthesis initiates with VPg uridylylated in the 3′ poly(A) tail in virion RNA and positive-strand synthesis initiates with VPgpUpU synthesized on the cre(2C) hairpin. The pool of excess VPgpUpU synthesized on the cre(2C) hairpin should support high levels of positive-strand synthesis and thereby promote the asymmetric replication of poliovirus RNA.

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34

Steil, Benjamin P., and David J. Barton. "Poliovirus cis-Acting Replication Element-Dependent VPg Uridylylation Lowers the Km of the Initiating Nucleoside Triphosphate for Viral RNA Replication." Journal of Virology 82, no. 19 (2008): 9400–9408. http://dx.doi.org/10.1128/jvi.00427-08.

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ABSTRACT Initiation of RNA synthesis by RNA-dependent RNA polymerases occurs when a phosphodiester bond is formed between the first two nucleotides in the 5′ terminus of product RNA. The concentration of initiating nucleoside triphosphates (NTPi) required for RNA synthesis is typically greater than the concentration of NTPs required for elongation. VPg, a small viral protein, is covalently attached to the 5′ end of picornavirus negative- and positive-strand RNAs. A cis-acting replication element (CRE) within picornavirus RNAs serves as a template for the uridylylation of VPg, resulting in the synthesis of VPgpUpUOH. Mutations within the CRE RNA structure prevent VPg uridylylation. While the tyrosine hydroxyl of VPg can prime negative-strand RNA synthesis in a CRE- and VPgpUpUOH-independent manner, CRE-dependent VPgpUpUOH synthesis is absolutely required for positive-strand RNA synthesis. As reported herein, low concentrations of UTP did not support negative-strand RNA synthesis when CRE-disrupting mutations prevented VPg uridylylation, whereas correspondingly low concentrations of CTP or GTP had no negative effects on the magnitude of CRE-independent negative-strand RNA synthesis. The experimental data indicate that CRE-dependent VPg uridylylation lowers the Km of UTP required for viral RNA replication and that CRE-dependent VPgpUpUOH synthesis was required for efficient negative-strand RNA synthesis, especially when UTP concentrations were limiting. By lowering the concentration of UTP needed for the initiation of RNA replication, CRE-dependent VPg uridylylation provides a mechanism for a more robust initiation of RNA replication.

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35

Steil, Benjamin P., Brian J. Kempf, and David J. Barton. "Poly(A) at the 3′ End of Positive-Strand RNA and VPg-Linked Poly(U) at the 5′ End of Negative-Strand RNA Are Reciprocal Templates during Replication of Poliovirus RNA." Journal of Virology 84, no. 6 (2010): 2843–58. http://dx.doi.org/10.1128/jvi.02620-08.

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ABSTRACT A 3′ poly(A) tail is a common feature of picornavirus RNA genomes and the RNA genomes of many other positive-strand RNA viruses. We examined the manner in which the homopolymeric poly(A) and poly(U) portions of poliovirus (PV) positive- and negative-strand RNAs were used as reciprocal templates during RNA replication. Poly(A) sequences at the 3′ end of viral positive-strand RNA were transcribed into VPg-linked poly(U) products at the 5′ end of negative-strand RNA during PV RNA replication. Subsequently, VPg-linked poly(U) sequences at the 5′ ends of negative-strand RNA templates were transcribed into poly(A) sequences at the 3′ ends of positive-strand RNAs. The homopolymeric poly(A) and poly(U) portions of PV RNA products of replication were heterogeneous in length and frequently longer than the corresponding homopolymeric sequences of the respective viral RNA templates. The data support a model of PV RNA replication wherein reiterative transcription of homopolymeric templates ensures the synthesis of long 3′ poly(A) tails on progeny RNA genomes.

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König, Katja Marie Kjara, Aminu S. Jahun, Komal Nayak, et al. "Design, development, and validation of a strand-specific RT-qPCR assay for GI and GII human Noroviruses." Wellcome Open Research 6 (September 23, 2021): 245. http://dx.doi.org/10.12688/wellcomeopenres.17078.1.

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Human noroviruses (HuNoV) are the major cause of viral gastroenteritis worldwide. Similar to other positive-sense single-stranded RNA viruses, norovirus RNA replication requires the formation of a negative strand RNA intermediate. Methods for detecting and quantifying the viral positive or negative sense RNA in infected cells and tissues can be used as important tools in dissecting virus replication. In this study, we have established a sensitive and strand-specific Taqman-based quantitative polymerase chain reaction (qPCR) assay for both genogroups GI and GII HuNoV. This assay shows good reproducibility, has a broad dynamic range and is able to detect a diverse range of isolates. We used tagged primers containing a non-viral sequence for the reverse transcription (RT) reaction and targeted this tag in the succeeding qPCR reaction to achieve strand specificity. The specificity of the assay was confirmed by the detection of specific viral RNA strands in the presence of high levels of the opposing strands, in both RT and qPCR reactions. Finally, we further validated the assay in norovirus replicon-bearing cell lines and norovirus-infected human small intestinal organoids, in the presence or absence of small-molecule inhibitors. Overall, we have established a strand-specific qPCR assay that can be used as a reliable method to understand the molecular details of the human norovirus life cycle.

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Tomita, Yuriko, Tomomitsu Mizuno, Juana Díez, Satoshi Naito, Paul Ahlquist, and Masayuki Ishikawa. "Mutation of Host dnaJ Homolog Inhibits Brome Mosaic Virus Negative-Strand RNA Synthesis." Journal of Virology 77, no. 5 (2003): 2990–97. http://dx.doi.org/10.1128/jvi.77.5.2990-2997.2003.

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ABSTRACT The replication of positive-strand RNA viruses involves not only viral proteins but also multiple cellular proteins and intracellular membranes. In both plant cells and the yeast Saccharomyces cerevisiae, brome mosaic virus (BMV), a member of the alphavirus-like superfamily, replicates its RNA in endoplasmic reticulum (ER)-associated complexes containing viral 1a and 2a proteins. Prior to negative-strand RNA synthesis, 1a localizes to ER membranes and recruits both positive-strand BMV RNA templates and the polymerase-like 2a protein to ER membranes. Here, we show that BMV RNA replication in S. cerevisiae is markedly inhibited by a mutation in the host YDJ1 gene, which encodes a chaperone Ydj1p related to Escherichia coli DnaJ. In the ydj1 mutant, negative-strand RNA accumulation was inhibited even though 1a protein associated with membranes and the positive-strand RNA3 replication template and 2a protein were recruited to membranes as in wild-type cells. In addition, we found that in ydj1 mutant cells but not wild-type cells, a fraction of 2a protein accumulated in a membrane-free but insoluble, rapidly sedimenting form. These and other results show that Ydj1p is involved in forming BMV replication complexes active in negative-strand RNA synthesis and suggest that a chaperone system involving Ydj1p participates in 2a protein folding or assembly into the active replication complex.

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SCHNEEMANN, ANETTE, PATRICK A. SCHNEIDER, and W. IAN LIPKIN. "Negative-strand RNA viruses. The atypical strategies used for gene expression of Borna disease virus, a nonsegmented, negative-strand RNA virus." Uirusu 45, no. 2 (1995): 165–74. http://dx.doi.org/10.2222/jsv.45.165.

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Banerjee, Rajeev, and Asim Dasgupta. "Interaction of picornavirus 2C polypeptide with the viral negative-strand RNA." Journal of General Virology 82, no. 11 (2001): 2621–27. http://dx.doi.org/10.1099/0022-1317-82-11-2621.

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The picornavirus membrane-associated polypeptide 2C is believed to be required for viral RNA synthesis. Hepatitis A virus (HAV)- and human rhinovirus (HRV)-encoded recombinant 2C proteins have been expressed, purified and examined for their ability to interact with the terminal sequences of viral positive- and negative-strand RNAs. The results demonstrate that both the HAV- and the HRV-encoded 2C polypeptide specifically interact with the 3′-terminal sequences of the negative-strand RNA, but not with the complementary sequences at the 5′ terminus of the positive-strand RNA. This interaction was detected by both mobility gel shift and UV cross-linking assays. Furthermore, complex formation exhibited dose-dependency and competition assays confirmed specificity. These results are consistent with our previous observation using the poliovirus 2C protein. The implication of the picornavirus 2C protein binding to the 3′-terminal sequence of the negative-strand untranslated region in viral RNA synthesis is discussed.

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40

Sharma, Nidhi, Brian J. O'Donnell, and James B. Flanegan. "3′-Terminal Sequence in Poliovirus Negative-Strand Templates Is the Primary cis-Acting Element Required for VPgpUpU-Primed Positive-Strand Initiation." Journal of Virology 79, no. 6 (2005): 3565–77. http://dx.doi.org/10.1128/jvi.79.6.3565-3577.2005.

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ABSTRACT The 5′ cloverleaf in poliovirus RNA has a direct role in regulating the stability, translation, and replication of viral RNA. In this study, we investigated the role of stem a in the 5′ cloverleaf in regulating the stability and replication of poliovirus RNA in HeLa S10 translation-replication reactions. Our results showed that disrupting the duplex structure of stem a destabilized viral RNA and inhibited efficient negative-strand synthesis. Surprisingly, the duplex structure of stem a was not required for positive-strand synthesis. In contrast, altering the primary sequence at the 5′-terminal end of stem a had little or no effect on negative-strand synthesis but dramatically reduced positive-strand initiation and the formation of infectious virus. The inhibition of positive-strand synthesis observed in these reactions was most likely a consequence of nucleotide alterations in the conserved sequence at the 3′ ends of negative-strand RNA templates. Previous studies suggested that VPgpUpU synthesized on the cre(2C) hairpin was required for positive-strand synthesis. Therefore, these results are consistent with a model in which preformed VPgpUpU serves as the primer for positive-strand initiation on the 3′AAUUUUGUC5′ sequence at the 3′ ends of negative-strand templates. Our results suggest that this sequence is the primary cis-acting element that is required for efficient VPgpUpU-primed positive-strand initiation.

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Lerat, Hervé, Sylvie Rumin, François Habersetzer, et al. "In Vivo Tropism of Hepatitis C Virus Genomic Sequences in Hematopoietic Cells: Influence of Viral Load, Viral Genotype, and Cell Phenotype." Blood 91, no. 10 (1998): 3841–49. http://dx.doi.org/10.1182/blood.v91.10.3841.

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Abstract Extrahepatic sites capable of supporting hepatitis C virus (HCV) replication have been suggested. We analyzed the influence of virological factors such as viral genotype and viral load, and cellular factors such as cell phenotype, on the detection rate of HCV sequences in hematopoietic cells of infected patients. Thirty-eight chronically infected patients were included in the study: 19 infected by genotype 1 isolates (1a and 1b), 13 by nongenotype 1 isolates (including genotypes 2 a/c, 3a, and 4), and 6 coinfected by genotype 1 and 6 isolates. Polymerase chain reaction (PCR) detection efficiency of viral genomic sequences, both the positive and negative strand RNA, was evaluated using RNA transcripts derived from genotype 1, 2, 3, and 4 cloned sequences and found to be equivalent within one log unit. The serum viral load, ranging from less than 2 × 105 Eq/mL to 161 × 105 Eq/mL, did not influence the detection rate of either strand of RNA in patients' peripheral blood mononuclear cells (PBMCs). Positive and negative strand RNA were found in PBMCs of all 3 cohorts of patients with a detection rate ranging from 15% to 100% and from 8% to 83.3% for the positive and negative strand RNA, respectively. Coinfected patients showed a detection rate in all cases greater than 80%. Patients infected with genotype 1 isolates showed a higher detection rate of either strands of RNA when compared with patients infected with other genotypes (P < .001 andP < .04). Both strands were found restricted to polymorphonuclear leukocytes, monocytes/macrophages, and B (but not T) lymphocytes. These data show that HCV genomic sequences, possibly reflecting viral replication, can be detected in PBMCs of chronically infected patients independent of the viral load and that specific associated cell subsets are implicated in the harboring of such sequences.

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42

Lerat, Hervé, Sylvie Rumin, François Habersetzer, et al. "In Vivo Tropism of Hepatitis C Virus Genomic Sequences in Hematopoietic Cells: Influence of Viral Load, Viral Genotype, and Cell Phenotype." Blood 91, no. 10 (1998): 3841–49. http://dx.doi.org/10.1182/blood.v91.10.3841.3841_3841_3849.

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Extrahepatic sites capable of supporting hepatitis C virus (HCV) replication have been suggested. We analyzed the influence of virological factors such as viral genotype and viral load, and cellular factors such as cell phenotype, on the detection rate of HCV sequences in hematopoietic cells of infected patients. Thirty-eight chronically infected patients were included in the study: 19 infected by genotype 1 isolates (1a and 1b), 13 by nongenotype 1 isolates (including genotypes 2 a/c, 3a, and 4), and 6 coinfected by genotype 1 and 6 isolates. Polymerase chain reaction (PCR) detection efficiency of viral genomic sequences, both the positive and negative strand RNA, was evaluated using RNA transcripts derived from genotype 1, 2, 3, and 4 cloned sequences and found to be equivalent within one log unit. The serum viral load, ranging from less than 2 × 105 Eq/mL to 161 × 105 Eq/mL, did not influence the detection rate of either strand of RNA in patients' peripheral blood mononuclear cells (PBMCs). Positive and negative strand RNA were found in PBMCs of all 3 cohorts of patients with a detection rate ranging from 15% to 100% and from 8% to 83.3% for the positive and negative strand RNA, respectively. Coinfected patients showed a detection rate in all cases greater than 80%. Patients infected with genotype 1 isolates showed a higher detection rate of either strands of RNA when compared with patients infected with other genotypes (P < .001 andP < .04). Both strands were found restricted to polymorphonuclear leukocytes, monocytes/macrophages, and B (but not T) lymphocytes. These data show that HCV genomic sequences, possibly reflecting viral replication, can be detected in PBMCs of chronically infected patients independent of the viral load and that specific associated cell subsets are implicated in the harboring of such sequences.

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43

Banerjee, Amiya K. "Response to “Non-segmented negative-strand RNA virus RNA synthesis in vivo”." Virology 371, no. 2 (2008): 231–33. http://dx.doi.org/10.1016/j.virol.2007.11.026.

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Whelan, Sean P. J. "Response to “Non-segmented negative-strand RNA virus RNA synthesis in vivo”." Virology 371, no. 2 (2008): 234–37. http://dx.doi.org/10.1016/j.virol.2007.11.027.

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45

Li, Y., and L. A. Ball. "Nonhomologous RNA recombination during negative-strand synthesis of flock house virus RNA." Journal of Virology 67, no. 7 (1993): 3854–60. http://dx.doi.org/10.1128/jvi.67.7.3854-3860.1993.

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Schneider, P. A., A. Schneemann, and W. I. Lipkin. "RNA splicing in Borna disease virus, a nonsegmented, negative-strand RNA virus." Journal of Virology 68, no. 8 (1994): 5007–12. http://dx.doi.org/10.1128/jvi.68.8.5007-5012.1994.

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47

Rehwinkel, Jan, Choon Ping Tan, Delphine Goubau, et al. "RIG-I Detects Viral Genomic RNA during Negative-Strand RNA Virus Infection." Cell 140, no. 3 (2010): 397–408. http://dx.doi.org/10.1016/j.cell.2010.01.020.

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Kondo, Hideki, Sotaro Chiba, Kazuhiro Toyoda, and Nobuhiro Suzuki. "Evidence for negative-strand RNA virus infection in fungi." Virology 435, no. 2 (2013): 201–9. http://dx.doi.org/10.1016/j.virol.2012.10.002.

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Wang, Y. F., S. G. Sawicki, and D. L. Sawicki. "Sindbis virus nsP1 functions in negative-strand RNA synthesis." Journal of Virology 65, no. 2 (1991): 985–88. http://dx.doi.org/10.1128/jvi.65.2.985-988.1991.

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50

Conzelmann, K. K. "Genetic manipulation of non-segmented negative-strand RNA viruses." Journal of General Virology 77, no. 3 (1996): 381–89. http://dx.doi.org/10.1099/0022-1317-77-3-381.

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