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Journal articles on the topic 'Rotaviral Replication'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 September 2023

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1

Zhou, Yan, Linlin Chen, Jing Du, et al. "MicroRNA-7 Inhibits Rotavirus Replication by Targeting Viral NSP5 In Vivo and In Vitro." Viruses 12, no. 2 (2020): 209. http://dx.doi.org/10.3390/v12020209.

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Rotavirus (RV) is the major causes of severe diarrhea in infants and young children under five years of age. There are no effective drugs for the treatment of rotavirus in addition to preventive live attenuated vaccine. Recent evidence demonstrates that microRNAs (miRNAs) can affect RNA virus replication. However, the antiviral effect of miRNAs during rotavirus replication are largely unknown. Here, we determined that miR-7 is upregulated during RV replication and that it targets the RV NSP5 (Nonstructural protein 5). Results suggested that miR-7 affected viroplasm formation and inhibited RV r

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2

Cheung, Winsome, Michael Gill, Alessandro Esposito, et al. "Rotaviruses Associate with Cellular Lipid Droplet Components To Replicate in Viroplasms, and Compounds Disrupting or Blocking Lipid Droplets Inhibit Viroplasm Formation and Viral Replication." Journal of Virology 84, no. 13 (2010): 6782–98. http://dx.doi.org/10.1128/jvi.01757-09.

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ABSTRACT Rotaviruses are a major cause of acute gastroenteritis in children worldwide. Early stages of rotavirus assembly in infected cells occur in viroplasms. Confocal microscopy demonstrated that viroplasms associate with lipids and proteins (perilipin A, ADRP) characteristic of lipid droplets (LDs). LD-associated proteins were also found to colocalize with viroplasms containing a rotaviral NSP5-enhanced green fluorescent protein (EGFP) fusion protein and with viroplasm-like structures in uninfected cells coexpressing viral NSP2 and NSP5. Close spatial proximity of NSP5-EGFP and cellular pe

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3

Fenaux, M., M. A. Cuadras, N. Feng, M. Jaimes, and H. B. Greenberg. "Extraintestinal Spread and Replication of a Homologous EC Rotavirus Strain and a Heterologous Rhesus Rotavirus in BALB/c Mice." Journal of Virology 80, no. 11 (2006): 5219–32. http://dx.doi.org/10.1128/jvi.02664-05.

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ABSTRACT Although rotavirus infection has generally been felt to be restricted to the gastrointestinal tract, over the last two decades there have been sporadic reports of children with acute or fatal cases of rotavirus gastroenteritis testing positive for rotavirus antigen and/or nucleic acid in various extraintestinal locations such as serum, liver, kidney, bladder, testes, nasal secretions, cerebrospinal fluid, and the central nervous system. Recently, studies in animals and people have demonstrated that rotavirus antigenemia is a common event during natural infection. In this study, we ext

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4

Morris, Andrew P., and Mary K. Estes. "VIII. Pathological consequences of rotavirus infection and its enterotoxin." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 2 (2001): G303—G310. http://dx.doi.org/10.1152/ajpgi.2001.281.2.g303.

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Rotaviral infection in neonatal animals and young children leads to acute self-limiting diarrhea, but infected adults are mainly asymptomatic. Recently, significant in-roads have been made into our understanding of this disease: both viral infection and virally manufactured nonstructural protein (NSP)4 evoke intracellular Ca2+([Ca2+]i) mobilization in native and transformed gastrointestinal epithelial cells. In neonatal mouse pup mucosa models, [Ca2+]ielevation leads to age-dependent halide ion movement across the plasma membrane, transepithelial Cl−secretion, and, unlike many microbial entero

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5

Criglar, Jeanette M., Ramakrishnan Anish, Liya Hu, et al. "Phosphorylation cascade regulates the formation and maturation of rotaviral replication factories." Proceedings of the National Academy of Sciences 115, no. 51 (2018): E12015—E12023. http://dx.doi.org/10.1073/pnas.1717944115.

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The rotavirus (RV) genome is replicated and packaged into virus progeny in cytoplasmic inclusions called viroplasms, which require interactions between RV nonstructural proteins NSP2 and NSP5. How viroplasms form remains unknown. We previously found two forms of NSP2 in RV-infected cells: a cytoplasmically dispersed dNSP2, which interacts with hypophosphorylated NSP5; and a viroplasm-specific vNSP2, which interacts with hyperphosphorylated NSP5. Other studies report that CK1α, a ubiquitous cellular kinase, hyperphosphorylates NSP5, but requires NSP2 for reasons that are unclear. Here we show t

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6

Ramírez, María-Camila, Kelly Méndez, Alicia Castelblanco-Mora, Sandra Quijano, and Juan Ulloa. "In Vitro Evaluation of Anti-Rotaviral Activity and Intestinal Toxicity of a Phytotherapeutic Prototype of Achyrocline bogotensis (Kunth) DC." Viruses 14, no. 11 (2022): 2394. http://dx.doi.org/10.3390/v14112394.

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Viruses represent the primary etiologic agents (70–80%) of acute diarrheal disease (ADD), and rotavirus (RV) is the most relevant one. Currently, four rotavirus vaccines are available. However, these vaccines do not protect against emerging viral strains or are not available in low-income countries. To date, there are no approved drugs available against rotavirus infection. In this study, we evaluated the in vitro anti-rotaviral activity and intestinal toxicity of a phytotherapeutic prototype obtained from Achyrocline bogotensis (Kunth) DC. (PPAb); medicinal plant that contains compounds that

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7

Jafri, Mubeen, Bryan Donnelly, Monica McNeal, Richard Ward, and Greg Tiao. "MAPK signaling contributes to rotaviral-induced cholangiocyte injury and viral replication." Surgery 142, no. 2 (2007): 192–201. http://dx.doi.org/10.1016/j.surg.2007.03.008.

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8

Viskovska, M., R. Anish, L. Hu, et al. "Probing the Sites of Interactions of Rotaviral Proteins Involved in Replication." Journal of Virology 88, no. 21 (2014): 12866–81. http://dx.doi.org/10.1128/jvi.02251-14.

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9

Komoto, Satoshi, Saori Fukuda, Takayuki Murata, and Koki Taniguchi. "Human Rotavirus Reverse Genetics Systems to Study Viral Replication and Pathogenesis." Viruses 13, no. 9 (2021): 1791. http://dx.doi.org/10.3390/v13091791.

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Human rotaviruses (HuRVAs) are highly important causes of acute gastroenteritis in infants and young children worldwide. A lack of reliable and reproducible reverse genetics systems for HuRVAs has limited a proper understanding of HuRVA biology and also the rational design of live-attenuated vaccines. Since the development of the first reverse genetics system for RVAs (partially plasmid-based reverse genetics system) in 2006, there have been many efforts with the goal of generating infectious recombinant HuRVAs entirely from cloned cDNAs. However, the establishment of a HuRVA reverse genetics

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10

Montero, Hilda, Carlos F. Arias, and Susana Lopez. "Rotavirus Nonstructural Protein NSP3 Is Not Required for Viral Protein Synthesis." Journal of Virology 80, no. 18 (2006): 9031–38. http://dx.doi.org/10.1128/jvi.00437-06.

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ABSTRACT Initiation is the rate-limiting step in protein synthesis and therefore an important target for regulation. For the initiation of translation of most cellular mRNAs, the cap structure at the 5′ end is bound by the translation factor eukaryotic initiation factor 4E (eIF4E), while the poly(A) tail, at the 3′ end, is recognized by the poly(A)-binding protein (PABP). eIF4G is a scaffold protein that brings together eIF4E and PABP, causing the circularization of the mRNA that is thought to be important for an efficient initiation of translation. Early in infection, rotaviruses take over th

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11

Campagna, Michela, Catherine Eichwald, Fulvia Vascotto, and Oscar R. Burrone. "RNA interference of rotavirus segment 11 mRNA reveals the essential role of NSP5 in the virus replicative cycle." Journal of General Virology 86, no. 5 (2005): 1481–87. http://dx.doi.org/10.1099/vir.0.80598-0.

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Rotavirus genomes contain 11 double-stranded (ds) RNA segments. Genome segment 11 encodes the non-structural protein NSP5 and, in some strains, also NSP6. NSP5 is produced soon after viral infection and localizes in cytoplasmic viroplasms, where virus replication takes place. RNA interference by small interfering (si) RNAs targeted to genome segment 11 mRNA of two different strains blocked production of NSP5 in a strain-specific manner, with a strong effect on the overall replicative cycle: inhibition of viroplasm formation, decreased production of other structural and non-structural proteins,

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12

Vascotto, Fulvia, Michela Campagna, Michela Visintin, Antonino Cattaneo, and Oscar R. Burrone. "Effects of intrabodies specific for rotavirus NSP5 during the virus replicative cycle." Journal of General Virology 85, no. 11 (2004): 3285–90. http://dx.doi.org/10.1099/vir.0.80075-0.

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Intracellular antibodies or intrabodies (ICAbs) have great potential in protein knockout strategies for intracellular antigens. In this study, they have been used to investigate the role of the rotavirus non-structural protein NSP5 in the virus replication cycle. Intracellular antibody-capture technology was used to select single-chain Fv format (scFv) ICAbs against an NSP5 mutant. Five different specific ICAbs were selected and expressed in MA104 cells, in the scFv format, as cytoplasmic- and nuclear-tagged forms. By confocal microscopy, it was found that three of these ICAbs recognized the f

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13

Holloway, Gavan, and Barbara S. Coulson. "Innate cellular responses to rotavirus infection." Journal of General Virology 94, no. 6 (2013): 1151–60. http://dx.doi.org/10.1099/vir.0.051276-0.

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Rotavirus is a leading cause of severe dehydrating diarrhoea in infants and young children. Following rotavirus infection in the intestine an innate immune response is rapidly triggered. This response leads to the induction of type I and type III interferons (IFNs) and other cytokines, resulting in a reduction in viral replication. Here we review the current literature describing the detection of rotavirus infection by pattern recognition receptors within host cells, the subsequent molecular mechanisms leading to IFN and cytokine production, and the processes leading to reduced rotavirus repli

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14

Schnepf, Daniel, Pedro Hernandez, Tanel Mahlakõiv, et al. "Rotavirus susceptibility of antibiotic-treated mice ascribed to diminished expression of interleukin-22." PLOS ONE 16, no. 8 (2021): e0247738. http://dx.doi.org/10.1371/journal.pone.0247738.

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The commensal microbiota regulates susceptibility to enteric pathogens by fine-tuning mucosal innate immune responses, but how susceptibility to enteric viruses is shaped by the microbiota remains incompletely understood. Past reports have indicated that commensal bacteria may either promote or repress rotavirus replication in the small intestine of mice. We now report that rotavirus replicated more efficiently in the intestines of germ-free and antibiotic-treated mice compared to animals with an unmodified microbiota. Antibiotic treatment also facilitated rotavirus replication in type I and t

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15

Campagna, Michela, Mauricio Budini, Francesca Arnoldi, Ulrich Desselberger, Jorge E. Allende та Oscar R. Burrone. "Impaired hyperphosphorylation of rotavirus NSP5 in cells depleted of casein kinase 1α is associated with the formation of viroplasms with altered morphology and a moderate decrease in virus replication". Journal of General Virology 88, № 10 (2007): 2800–2810. http://dx.doi.org/10.1099/vir.0.82922-0.

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The rotavirus (RV) non-structural protein 5, NSP5, is encoded by the smallest of the 11 genomic segments and localizes in ‘viroplasms’, cytoplasmic inclusion bodies in which viral RNA replication and packaging take place. NSP5 is essential for the replicative cycle of the virus because, in its absence, viroplasms are not formed and viral RNA replication and transcription do not occur. NSP5 is produced early in infection and undergoes a complex hyperphosphorylation process, leading to the formation of proteins differing in electrophoretic mobility. The role of hyperphosphorylation of NSP5 in th

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16

Ruiz, Marie Christine, Theresa Leon, Yuleima Diaz, and Fabian Michelangeli. "Molecular Biology of Rotavirus Entry and Replication." Scientific World JOURNAL 9 (2009): 1476–97. http://dx.doi.org/10.1100/tsw.2009.158.

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Rotavirus is a nonenveloped, double-stranded, RNA virus belonging to the Reoviridae family and is the major etiological agent of viral gastroenteritis in young children and young animals. Remarkable progress in the understanding of the rotavirus cycle has been made in the last 10 years. The knowledge of viral replication thus far acquired is based on structural studies, the expression and coexpression of individual viral proteins, silencing of individual genes by siRNAs, and the effects that these manipulations have on the physiology of the infected cell. The functions of the individual rotavi

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17

Ciarlet, Max, Mary K. Estes, Christopher Barone, Robert F. Ramig, and Margaret E. Conner. "Analysis of Host Range Restriction Determinants in the Rabbit Model: Comparison of Homologous and Heterologous Rotavirus Infections." Journal of Virology 72, no. 3 (1998): 2341–51. http://dx.doi.org/10.1128/jvi.72.3.2341-2351.1998.

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ABSTRACT The main limitation of both the rabbit and mouse models of rotavirus infection is that human rotavirus (HRV) strains do not replicate efficiently in either animal. The identification of individual genes necessary for conferring replication competence in a heterologous host is important to an understanding of the host range restriction of rotavirus infections. We recently reported the identification of the P type of the spike protein VP4 of four lapine rotavirus strains as being P[14]. To determine whether VP4 is involved in host range restriction in rabbits, we evaluated infection in

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18

Crawford, Sue E., Dinesh G. Patel, Elly Cheng, et al. "Rotavirus Viremia and Extraintestinal Viral Infection in the Neonatal Rat Model." Journal of Virology 80, no. 10 (2006): 4820–32. http://dx.doi.org/10.1128/jvi.80.10.4820-4832.2006.

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ABSTRACT Rotaviruses infect mature, differentiated enterocytes of the small intestine and, by an unknown mechanism, escape the gastrointestinal tract and cause viremia. The neonatal rat model of rotavirus infection was used to determine the kinetics of viremia, spread, and pathology of rotavirus in extraintestinal organs. Five-day-old rat pups were inoculated intragastrically with an animal (RRV) or human (HAL1166) rotavirus or phosphate-buffered saline. Blood was collected from a subset of rat pups, and following perfusion to remove residual blood, organs were removed and homogenized to analy

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19

Boshuizen, Jos A., Johan H. J. Reimerink, Anita M. Korteland-van Male, et al. "Changes in Small Intestinal Homeostasis, Morphology,and Gene Expression during Rotavirus Infection of InfantMice." Journal of Virology 77, no. 24 (2003): 13005–16. http://dx.doi.org/10.1128/jvi.77.24.13005-13016.2003.

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ABSTRACT Rotavirus is the most important cause of infantile gastroenteritis. Since in vivo mucosal responses to a rotavirus infection thus far have not been extensively studied, we related viral replication in the murine small intestine to alterations in mucosal structure, epithelial cell homeostasis, cellular kinetics, and differentiation. Seven-day-old suckling BALB/c mice were inoculated with 2 × 104 focus-forming units of murine rotavirus and were compared to mock-infected controls. Diarrheal illness and viral shedding were recorded, and small intestinal tissue was evaluated for rotavirus

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20

Feng, N., A. Sen, H. Nguyen, et al. "Variation in Antagonism of the Interferon Response to Rotavirus NSP1 Results in Differential Infectivity in Mouse Embryonic Fibroblasts." Journal of Virology 83, no. 14 (2009): 6987–94. http://dx.doi.org/10.1128/jvi.00585-09.

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ABSTRACT Rotavirus NSP1 has been shown to function as an E3 ubiquitin ligase that mediates proteasome-dependent degradation of interferon (IFN) regulatory factors (IRF), including IRF3, -5, and -7, and suppresses the cellular type I IFN response. However, the effect of rotavirus NSP1 on viral replication is not well defined. Prior studies used genetic analysis of selected reassortants to link NSP1 with host range restriction in the mouse, suggesting that homologous and heterologous rotaviruses might use their different abilities to antagonize the IFN response as the basis of their host tropism

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21

Civra, Andrea, Rachele Francese, Manuela Donalisio, et al. "Human Colostrum and Derived Extracellular Vesicles Prevent Infection by Human Rotavirus and Respiratory Syncytial Virus in Vitro." Journal of Human Lactation 37, no. 1 (2021): 122–34. http://dx.doi.org/10.1177/0890334420988239.

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Background It is known that breastfeeding protects the infant from enteric and respiratory infections; however, the antiviral properties of human milk against enteric and respiratory viruses are largely unexplored. Research aims To explore the antiviral activity of human preterm colostrum against rotavirus and respiratory syncytial virus and to assess whether the derived extracellular vesicle contribute to this activity. Methods We used a cross-sectional, prospective two-group non-experimental design. Colostra were collected from mothers of preterm newborns ( N = 10) and extracellular vesicles

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22

Ramesh, Mao, Lei, et al. "Parenterally Administered P24-VP8* Nanoparticle Vaccine Conferred Strong Protection against Rotavirus Diarrhea and Virus Shedding in Gnotobiotic Pigs." Vaccines 7, no. 4 (2019): 177. http://dx.doi.org/10.3390/vaccines7040177.

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Current live rotavirus vaccines are costly with increased risk of intussusception due to vaccine replication in the gut of vaccinated children. New vaccines with improved safety and cost-effectiveness are needed. In this study, we assessed the immunogenicity and protective efficacy of a novel P24-VP8* nanoparticle vaccine using the gnotobiotic (Gn) pig model of human rotavirus infection and disease. Three doses of P24-VP8* (200 μg/dose) intramuscular vaccine with Al(OH)3 adjuvant (600 μg) conferred significant protection against infection and diarrhea after challenge with virulent Wa strain ro

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Long, Courtney P., and Sarah M. McDonald. "Rotavirus genome replication: Some assembly required." PLOS Pathogens 13, no. 4 (2017): e1006242. http://dx.doi.org/10.1371/journal.ppat.1006242.

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Ciarlet, Max, Mary K. Estes, and Margaret E. Conner. "Simian rhesus rotavirus is a unique heterologous (non-lapine) rotavirus strain capable of productive replication and horizontal transmission in rabbits." Microbiology 81, no. 5 (2000): 1237–49. http://dx.doi.org/10.1099/0022-1317-81-5-1237.

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Simian rhesus rotavirus (RRV) is the only identified heterologous (non-lapine) rotavirus strain capable of productive replication at a high inoculum dose of virus (>108 p.f.u.) in rabbits. To evaluate whether lower doses of RRV would productively infect rabbits and to obtain an estimate of the 50% infectious dose, rotavirus antibody-free rabbits were inoculated orally with RRV at inoculum doses of 103, 105 or 107 p.f.u. Based on faecal virus antigen or infectious virus shedding, RRV replication was observed with inoculum doses of 107 and 105 p.f.u., but not 103 p.f.u. Horizontal transmissio

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Holloway, Gavan, Rebecca I. Johnson, Yilin Kang, Vi T. Dang, Diana Stojanovski та Barbara S. Coulson. "Rotavirus NSP6 localizes to mitochondria via a predicted N-terminal α-helix". Journal of General Virology 96, № 12 (2015): 3519–24. http://dx.doi.org/10.1099/jgv.0.000294.

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Specific roles have been ascribed to each of the 12 known rotavirus proteins apart from the non-structural protein 6 (NSP6). However, NSP6 may be present at sites of viral replication within the cytoplasm. Here we report that NSP6 from diverse species of rotavirus A localizes to mitochondria via conserved sequences in a predicted N-terminal α-helix. This suggests that NSP6 may affect mitochondrial functions during rotavirus infection.

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Taraporewala, Zenobia F., Xiaofang Jiang, Rodrigo Vasquez-Del Carpio, Hariharan Jayaram, B. V. Venkataram Prasad, and John T. Patton. "Structure-Function Analysis of Rotavirus NSP2 Octamer by Using a Novel Complementation System." Journal of Virology 80, no. 16 (2006): 7984–94. http://dx.doi.org/10.1128/jvi.00172-06.

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ABSTRACT Viral inclusion bodies, or viroplasms, that form in rotavirus-infected cells direct replication and packaging of the segmented double-stranded RNA (dsRNA) genome. NSP2, one of two rotavirus proteins needed for viroplasm assembly, possesses NTPase, RNA-binding, and helix-unwinding activities. NSP2 of the rotavirus group causing endemic infantile diarrhea (group A) was shown to self-assemble into large doughnut-shaped octamers with circumferential grooves and deep clefts containing nucleotide-binding histidine triad (HIT)-like motifs. Here, we demonstrate that NSP2 of group C rotavirus,

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Gozalbo-Rovira, Roberto, Cristina Santiso-Bellón, Javier Buesa, et al. "Microbiota Depletion Promotes Human Rotavirus Replication in an Adult Mouse Model." Biomedicines 9, no. 7 (2021): 846. http://dx.doi.org/10.3390/biomedicines9070846.

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Intestinal microbiota-virus-host interaction has emerged as a key factor in mediating enteric virus pathogenicity. With the aim of analyzing whether human gut bacteria improve the inefficient replication of human rotavirus in mice, we performed fecal microbiota transplant (FMT) with healthy infants as donors in antibiotic-treated mice. We showed that a simple antibiotic treatment, irrespective of FMT, resulted in viral shedding for 6 days after challenge with the human rotavirus G1P[8] genotype Wa strain (RVwa). Rotavirus titers in feces were also significantly higher in antibiotic-treated ani

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Chang-Graham, Alexandra L., Jacob L. Perry, Melinda A. Engevik, et al. "Rotavirus induces intercellular calcium waves through ADP signaling." Science 370, no. 6519 (2020): eabc3621. http://dx.doi.org/10.1126/science.abc3621.

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Rotavirus causes severe diarrheal disease in children by broadly dysregulating intestinal homeostasis. However, the underlying mechanism(s) of rotavirus-induced dysregulation remains unclear. We found that rotavirus-infected cells produce paracrine signals that manifested as intercellular calcium waves (ICWs), observed in cell lines and human intestinal enteroids. Rotavirus ICWs were caused by the release of extracellular adenosine 5′-diphosphate (ADP) that activated P2Y1 purinergic receptors on neighboring cells. ICWs were blocked by P2Y1 antagonists or CRISPR-Cas9 knockout of the P2Y1 recept

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Patton, John, Rodrigo Carpio, and Eugenio Spencer. "Replication and Transcription of the Rotavirus Genome." Current Pharmaceutical Design 10, no. 30 (2004): 3769–77. http://dx.doi.org/10.2174/1381612043382620.

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Garba, Salisu, Malami Dikko, Barga Isiyaka Bala, Abdullahi Aliyu, and Yusuf Sarkingobir. "Relating a Conceptual Overview of Vaccines Utilization for the Prevention of Rotavirus in Children." Journal of Multidisciplinary Science: MIKAILALSYS 1, no. 2 (2023): 226–39. http://dx.doi.org/10.58578/mikailalsys.v1i2.1736.

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Rotavirus infection is an emphatic health concern that when left unabated elicits hospitalizations, and deaths of many children due to diarrhea, even in developed countries; let one in poor settings. Likewise, the virus can affect older youngsters and adults resulting in mild infection. The consequences of the rotavirus could not be unconnected with the levels of poor prevention ploys put in place, including the inability of the body of children to counteract the rotavirus with a substantial immunity due to earlier invasion. Thus, it is important to seek for vaccines, because vaccination use i

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Lundstrom, Kenneth. "Are Viral Vectors Any Good for RNAi Antiviral Therapy?" Viruses 12, no. 10 (2020): 1189. http://dx.doi.org/10.3390/v12101189.

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RNA interference (RNAi) represents a novel approach for alternative antiviral therapy. However, issues related to RNA delivery and stability have presented serious obstacles for obtaining good therapeutic efficacy. Viral vectors are capable of efficient delivery of RNAi as short interfering RNA (siRNA), short hairpin RNA (shRNA) and micro-RNA (miRNA). Efficacy in gene silencing for therapeutic applications against viral diseases has been demonstrated in various animal models. Rotavirus (RV) miR-7 can inhibit rotavirus replication by targeting the RV nonstructural protein 5. Viral gene silencin

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Xia, Ming, Pengwei Huang, and Ming Tan. "A Pseudovirus Nanoparticle-Based Trivalent Rotavirus Vaccine Candidate Elicits High and Cross P Type Immune Response." Pharmaceutics 14, no. 8 (2022): 1597. http://dx.doi.org/10.3390/pharmaceutics14081597.

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Rotavirus infection continues to cause significant morbidity and mortality globally. In this study, we further developed the S60-VP8* pseudovirus nanoparticles (PVNPs) displaying the glycan receptor binding VP8* domains of rotavirus spike proteins as a parenteral vaccine candidate. First, we established a scalable method for the large production of tag-free S60-VP8* PVNPs representing four rotavirus P types, P[8], P[4], P[6], and P[11]. The approach consists of two major steps: selective precipitation of the S-VP8* proteins from bacterial lysates using ammonium sulfate, followed by anion excha

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Ciarlet, Max, Sue E. Crawford, Elly Cheng та ін. "VLA-2 (α2β1) Integrin Promotes Rotavirus Entry into Cells but Is Not Necessary for Rotavirus Attachment". Journal of Virology 76, № 3 (2002): 1109–23. http://dx.doi.org/10.1128/jvi.76.3.1109-1123.2002.

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ABSTRACT In an attempt to identify the rotavirus receptor, we tested 46 cell lines of different species and tissue origins for susceptibility to infection by three N-acetyl-neuraminic (sialic) acid (SA)-dependent and five SA-independent rotavirus strains. Susceptibility to SA-dependent or SA-independent rotavirus infection varied depending on the cell line tested and the multiplicity of infection (MOI) used. Cells of renal or intestinal origin and transformed cell lines derived from breast, stomach, bone, or lung were all susceptible to rotavirus infection, indicating a wider host tissue range

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Genthe, B., G. K. Idema, R. Kfir, and W. O. K. Grabow. "Detection of Rotavirus in South African Waters: A Comparison of a Cytoimmunolabelling Technique with Commercially Available Immunoassays." Water Science and Technology 24, no. 2 (1991): 241–44. http://dx.doi.org/10.2166/wst.1991.0066.

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A cytoimmunolabelling technique was compared with commercially available immunoassays for the detection of the simian rotavirus SA11 and human rotavirus in various environmental samples. The technique is based on labelling MA104 cells with antibody conjugated with an enzyme for the detection of rotavirus. Water samples were concentrated by ultrafiltration and inoculated on trypsin-treated MA104 cells. After 18 h incubation, evidence of viral replication was determined by immunolabelling of viral antigen using antibodies tagged with horseradish peroxidase. The cytoimmunolabelling method was sho

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Feng, N., B. Kim, M. Fenaux, et al. "Role of Interferon in Homologous and Heterologous Rotavirus Infection in the Intestines and Extraintestinal Organs of Suckling Mice." Journal of Virology 82, no. 15 (2008): 7578–90. http://dx.doi.org/10.1128/jvi.00391-08.

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ABSTRACT Recent studies demonstrated that viremia and extraintestinal rotavirus infection are common in acutely infected humans and animals, while systemic diseases appear to be rare. Intraperitoneal infection of newborn mice with rhesus rotavirus (RRV) results in biliary atresia (BA), and this condition is influenced by the host interferon response. We studied orally inoculated 5-day-old suckling mice that were deficient in interferon (IFN) signaling to evaluate the role of interferon on the outcome of local and systemic infection after enteric inoculation. We found that systemic replication

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Warfield, Kelly L., Sarah E. Blutt, Sue E. Crawford, Gagandeep Kang, and Margaret E. Conner. "Rotavirus Infection Enhances Lipopolysaccharide-Induced Intussusception in a Mouse Model." Journal of Virology 80, no. 24 (2006): 12377–86. http://dx.doi.org/10.1128/jvi.01185-06.

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ABSTRACT Unexpected reports of intussusception after vaccination with the live tetravalent rotavirus vaccine RotaShield resulted in voluntary withdrawal of the vaccine. Intussusception, a condition in which the intestine acutely invaginates upon itself, is the most common cause of intestinal obstruction in children. We report here the development of a mouse model to study rotavirus-induced intussusception. In this model, both homologous murine and heterologous simian rotavirus strains significantly enhanced the rate of lipopolysaccharide (LPS)-induced intussusception, and this enhancement was

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Brunet, Jean-Philippe, Nathalie Jourdan, Jacqueline Cotte-Laffitte, et al. "Rotavirus Infection Induces Cytoskeleton Disorganization in Human Intestinal Epithelial Cells: Implication of an Increase in Intracellular Calcium Concentration." Journal of Virology 74, no. 22 (2000): 10801–6. http://dx.doi.org/10.1128/jvi.74.22.10801-10806.2000.

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ABSTRACT Rotavirus infection is the most common cause of severe infantile gastroenteritis worldwide. In vivo, rotavirus exhibits a marked tropism for the differentiated enterocytes of the intestinal epithelium. In vitro, differentiated and undifferentiated intestinal cells can be infected. We observed that rotavirus infection of the human intestinal epithelial Caco-2 cells induces cytoskeleton alterations as a function of cell differentiation. The vimentin network disorganization detected in undifferentiated Caco-2 cells was not found in fully differentiated cells. In contrast, differentiated

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Papa, Guido, Alexander Borodavka, and Ulrich Desselberger. "Viroplasms: Assembly and Functions of Rotavirus Replication Factories." Viruses 13, no. 7 (2021): 1349. http://dx.doi.org/10.3390/v13071349.

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Viroplasms are cytoplasmic, membraneless structures assembled in rotavirus (RV)-infected cells, which are intricately involved in viral replication. Two virus-encoded, non-structural proteins, NSP2 and NSP5, are the main drivers of viroplasm formation. The structures (as far as is known) and functions of these proteins are described. Recent studies using plasmid-only-based reverse genetics have significantly contributed to elucidation of the crucial roles of these proteins in RV replication. Thus, it has been recognized that viroplasms resemble liquid-like protein–RNA condensates that may be f

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Sagher, F. A., J. A. Dodge, D. H. Simpson, and P. Evans. "Kinetics of Viral Replication in Experimental Rotavirus Infection." Journal of Pediatric Gastroenterology and Nutrition 13, no. 1 (1991): 83–89. http://dx.doi.org/10.1097/00005176-199107000-00015.

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Chen, D., C. Q. Zeng, M. J. Wentz, M. Gorziglia, M. K. Estes, and R. F. Ramig. "Template-dependent, in vitro replication of rotavirus RNA." Journal of Virology 68, no. 11 (1994): 7030–39. http://dx.doi.org/10.1128/jvi.68.11.7030-7039.1994.

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Boudreaux, Crystal E., Deborah F. Kelly, and Sarah M. McDonald. "Electron microscopic analysis of rotavirus assembly-replication intermediates." Virology 477 (March 2015): 32–41. http://dx.doi.org/10.1016/j.virol.2015.01.003.

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Arnoldi, Francesca, and Oscar R. Burrone. "Role of viral nonstructural proteins in rotavirus replication." Future Virology 4, no. 2 (2009): 185–96. http://dx.doi.org/10.2217/17460794.4.2.185.

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Feng, Ningguo, Jeffrey A. Lawton, Joana Gilbert, et al. "Inhibition of rotavirus replication by a non-neutralizing, rotavirus VP6–specific IgA mAb." Journal of Clinical Investigation 109, no. 9 (2002): 1203–13. http://dx.doi.org/10.1172/jci14397.

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Donker, Nicole C., Michael Foley, Debra C. Tamvakis, Ruth Bishop, and Carl D. Kirkwood. "Identification of an antibody-binding epitope on the rotavirus A non-structural protein NSP2 using phage display analysis." Journal of General Virology 92, no. 10 (2011): 2374–82. http://dx.doi.org/10.1099/vir.0.032599-0.

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The non-structural protein 2 (NSP2) of rotavirus has important roles in rotavirus replication associated with RNA binding, hydrolysis of NTPs and RNA, and helix destabilizing properties. A cell-culture assay using an NSP2-specific mAb and polyclonal antiserum to block virus replication showed a 73 and 96 % reduction in the amount of virus produced during replication, respectively. Phage display technology was used to identify the antibody-binding region on the NSP2 protein with the motif 244T-(Y/F)-Ø-Ø-Ø-X-K-Ø-G252, where Ø is a hydrophilic residue and X is any amino acid. This region was mapp

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Abid, Nabil, Giovanni Chillemi, and Marco Salemi. "Coding-Gene Coevolution Analysis of Rotavirus Proteins: A Bioinformatics and Statistical Approach." Genes 11, no. 1 (2019): 28. http://dx.doi.org/10.3390/genes11010028.

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Rotavirus remains a major cause of diarrhea in infants and young children worldwide. The permanent emergence of new genotypes puts the potential effectiveness of vaccines under serious question. The distribution of unusual genotypes subject to viral fitness is influenced by interactions among viral proteins. The present work aimed at analyzing the genetic constellation and the coevolution of rotavirus coding genes for the available rotavirus genotypes. Seventy-two full genome sequences of different genetic constellations were analyzed using a genetic algorithm. The results revealed an extensiv

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Berkova, Z., S. E. Crawford, G. Trugnan, T. Yoshimori, A. P. Morris, and M. K. Estes. "Rotavirus NSP4 Induces a Novel Vesicular Compartment Regulated by Calcium and Associated with Viroplasms." Journal of Virology 80, no. 12 (2006): 6061–71. http://dx.doi.org/10.1128/jvi.02167-05.

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ABSTRACT Rotavirus is a major cause of infantile viral gastroenteritis. Rotavirus nonstructural protein 4 (NSP4) has pleiotropic properties and functions in viral morphogenesis as well as pathogenesis. Recent reports show that the inhibition of NSP4 expression by small interfering RNAs leads to alteration of the production and distribution of other viral proteins and mRNA synthesis, suggesting that NSP4 also affects virus replication by unknown mechanisms. This report describes studies aimed at correlating the localization of intracellular NSP4 in cells with its functions. To be able to follow

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Holloway, Gavan, and Barbara S. Coulson. "Rotavirus Activates JNK and p38 Signaling Pathways in Intestinal Cells, Leading to AP-1-Driven Transcriptional Responses and Enhanced Virus Replication." Journal of Virology 80, no. 21 (2006): 10624–33. http://dx.doi.org/10.1128/jvi.00390-06.

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ABSTRACT Rotavirus infection is known to regulate transcriptional changes in many cellular genes. The transcription factors NF-κB and AP-1 are activated by rotavirus infection, but the upstream processes leading to these events are largely unidentified. We therefore studied the activation state during rotavirus infection of c-Jun NH2-terminal kinase (JNK) and p38, which are kinases known to activate AP-1. As assessed by Western blotting using phospho-specific antibodies, infection with rhesus rotavirus (RRV) or exposure to UV-psoralen-inactivated RRV (I-RRV) resulted in the activation of JNK i

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Chen, Sunrui, Cui Feng, Yan Fang, et al. "The Eukaryotic Translation Initiation Factor 4F Complex Restricts Rotavirus Infection via Regulating the Expression of IRF1 and IRF7." International Journal of Molecular Sciences 20, no. 7 (2019): 1580. http://dx.doi.org/10.3390/ijms20071580.

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The eIF4F complex is a translation initiation factor that closely regulates translation in response to a multitude of environmental conditions including viral infection. How translation initiation factors regulate rotavirus infection remains poorly understood. In this study, the knockdown of the components of the eIF4F complex using shRNA and CRISPR/Cas9 were performed, respectively. We have demonstrated that loss-of-function of the three components of eIF4F, including eIF4A, eIF4E and eIF4G, remarkably promotes the levels of rotavirus genomic RNA and viral protein VP4. Consistently, knockdown

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López, Tomás, Margarito Rojas, Camilo Ayala-Bretón, Susana López, and Carlos F. Arias. "Reduced expression of the rotavirus NSP5 gene has a pleiotropic effect on virus replication." Journal of General Virology 86, no. 6 (2005): 1609–17. http://dx.doi.org/10.1099/vir.0.80827-0.

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Rotavirus RRV gene 11 encodes two non-structural proteins, NSP5 and NSP6. NSP5 is a phosphorylated non-structural protein that binds single- and double-stranded RNA in a non-specific manner. Transient expression of this protein in uninfected cells has provided evidence for its participation in the formation of electron-dense cytoplasmic structures, known as viroplasms, which are thought to be key structures for the replication of the virus. NSP6 is a protein of unknown function that seems not to be essential for virus replication in cell culture. To study the function of NSP5 in the context of

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Berois, Mabel, Catherine Sapin, Inge Erk, Didier Poncet, and Jean Cohen. "Rotavirus Nonstructural Protein NSP5 Interacts with Major Core Protein VP2." Journal of Virology 77, no. 3 (2003): 1757–63. http://dx.doi.org/10.1128/jvi.77.3.1757-1763.2003.

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ABSTRACT Rotavirus is a nonenveloped virus with a three-layered capsid. The inner layer, made of VP2, encloses the genomic RNA and two minor proteins, VP1 and VP3, with which it forms the viral core. Core assembly is coupled with RNA viral replication and takes place in definite cellular structures termed viroplasms. Replication and encapsidation mechanisms are still not fully understood, and little information is available about the intermolecular interactions that may exist among the viroplasmic proteins. NSP2 and NSP5 are two nonstructural viroplasmic proteins that have been shown to intera

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