Molecular biology of rubella virus structural proteins

1994 ◽  
Vol 72 (9-10) ◽  
pp. 349-356 ◽  
Author(s):  
Shirley Gillam
Keyword(s):  
Molecular Biology ◽  
Rubella Virus ◽  
Cell Biology ◽  
Intracellular Transport ◽  
Rna Virus ◽  
Viral Gene Expression ◽  
Proteolytic Processing ◽  
Structural Proteins ◽  
Viral Gene ◽  
Structural Protein

Rubella virus is a small, enveloped, positive-stranded RNA virus in the Togaviridae family and bears similarities to the prototype alphaviruses in terms of its genome organization and strategy for viral gene expression. Despite being an important human pathogen, the cell biology of rubella virus remains poorly characterized. This review focuses on the molecular biology of rubella virus structural proteins, with emphasis on the proteolytic processing and maturation of virus structural proteins, the glycosylation requirement for intracellular transport and function of glycoproteins, and the localization of hemagglutinin- and virus-neutralizing epitopes. A number of significant differences between rubella virus and alphavirus structural protein expression and maturation were discovered.Key words: rubella virus, N-linked glycosylation, epitope mapping, proteolytic processing.

scholarly journals Vaccinia Virus A6L Encodes a Virion Core Protein Required for Formation of Mature Virion

2006 ◽  
Vol 81 (3) ◽  
pp. 1433-1443 ◽  
Author(s):  
Xiangzhi Meng ◽  
Addie Embry ◽  
Debbi Sochia ◽  
Yan Xiang
Keyword(s):  
Vaccinia Virus ◽  
Core Protein ◽  
Viral Gene Expression ◽  
Recombinant Vaccinia Virus ◽  
Proteolytic Processing ◽  
Viral Gene ◽  
Temperature Sensitive ◽  
Virion Morphogenesis ◽  
Viral Factory ◽  
Virion Core

ABSTRACT Vaccinia virus A6L is a previously uncharacterized gene that is conserved in all sequenced vertebrate poxviruses. Here, we constructed a recombinant vaccinia virus encoding A6 with an epitope tag and showed that A6 was expressed in infected cells after viral DNA replication and packaged in the core of the mature virion. Furthermore, we showed that A6 was essential for vaccinia virus replication by performing clustered charge-to-alanine mutagenesis on A6, which resulted in two vaccinia virus mutants (vA6L-mut1 and vA6L-mut2) that displayed a temperature-sensitive phenotype. At 31°C, both mutants replicated efficiently; however, at 40°C, vA6L-mut1 grew to a low titer, while vA6L-mut2 failed to replicate. The A6 protein expressed by vA6L-mut2 exhibited temperature-dependent instability. At the nonpermissive temperature, vA6L-mut2 was normal at viral gene expression and viral factory formation, but it was defective for proteolytic processing of the precursors of several major virion proteins, a defect that is characteristic of a block in virion morphogenesis. Electron microscopy further showed that the morphogenesis of vA6L-mut2 was arrested before the formation of immature virion with nucleoid and mature virion. Taken together, our data show that A6 is a virion core protein that plays an essential role in virion morphogenesis.

scholarly journals Herpesviral Latency—Common Themes

Pathogens ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 125 ◽  
Author(s):  
Magdalena Weidner-Glunde ◽  
Ewa Kruminis-Kaszkiel ◽  
Mamata Savanagouder
Keyword(s):  
Cell Biology ◽  
Particle Production ◽  
Viral Gene Expression ◽  
Lytic Cycle ◽  
Latent Reservoir ◽  
Viral Gene ◽  
Target Cells ◽  
Viral Particle Production ◽  
The Family ◽  
The Common

Latency establishment is the hallmark feature of herpesviruses, a group of viruses, of which nine are known to infect humans. They have co-evolved alongside their hosts, and mastered manipulation of cellular pathways and tweaking various processes to their advantage. As a result, they are very well adapted to persistence. The members of the three subfamilies belonging to the family Herpesviridae differ with regard to cell tropism, target cells for the latent reservoir, and characteristics of the infection. The mechanisms governing the latent state also seem quite different. Our knowledge about latency is most complete for the gammaherpesviruses due to previously missing adequate latency models for the alpha and beta-herpesviruses. Nevertheless, with advances in cell biology and the availability of appropriate cell-culture and animal models, the common features of the latency in the different subfamilies began to emerge. Three criteria have been set forth to define latency and differentiate it from persistent or abortive infection: 1) persistence of the viral genome, 2) limited viral gene expression with no viral particle production, and 3) the ability to reactivate to a lytic cycle. This review discusses these criteria for each of the subfamilies and highlights the common strategies adopted by herpesviruses to establish latency.

scholarly journals Identification of Novel Antipoxviral Agents: Mitoxantrone Inhibits Vaccinia Virus Replication by Blocking Virion Assembly

2007 ◽  
Vol 81 (24) ◽  
pp. 13392-13402 ◽  
Author(s):  
Liang Deng ◽  
Peihong Dai ◽  
Anthony Ciro ◽  
Donald F. Smee ◽  
Hakim Djaballah ◽  
...  
Keyword(s):  
Vaccinia Virus ◽  
Virus Replication ◽  
Viral Gene Expression ◽  
Maximum Tolerated Dose ◽  
Structural Proteins ◽  
Dna Ligase ◽  
Viral Gene ◽  
Whole Genome ◽  
Missense Mutations ◽  
Virion Assembly

ABSTRACT The bioterror threat of a smallpox outbreak in an unvaccinated population has mobilized efforts to develop new antipoxviral agents. By screening a library of known drugs, we identified 13 compounds that inhibited vaccinia virus replication at noncytotoxic doses. The anticancer drug mitoxantrone is unique among the inhibitors identified in that it has no apparent impact on viral gene expression. Rather, it blocks processing of viral structural proteins and assembly of mature progeny virions. The isolation of mitoxantrone-resistant vaccinia strains underscores that a viral protein is the likely target of the drug. Whole-genome sequencing of mitoxantrone-resistant viruses pinpointed missense mutations in the N-terminal domain of vaccinia DNA ligase. Despite its favorable activity in cell culture, mitoxantrone administered intraperitoneally at the maximum tolerated dose failed to protect mice against a lethal intranasal infection with vaccinia virus.

scholarly journals Induced Packaging of Cellular MicroRNAs into HIV-1 Virions Can Inhibit Infectivity

mBio ◽  
2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Hal P. Bogerd ◽  
Edward M. Kennedy ◽  
Adam W. Whisnant ◽  
Bryan R. Cullen
Keyword(s):  
Viral Genome ◽  
Rna Viruses ◽  
Rna Virus ◽  
Viral Gene Expression ◽  
Fold Increase ◽  
Significant Inhibition ◽  
Viral Gene ◽  
Cellular Mirnas ◽  
Target Sites ◽  
Hiv 1

ABSTRACT Analysis of the incorporation of cellular microRNAs (miRNAs) into highly purified HIV-1 virions revealed that this largely, but not entirely, mirrored the level of miRNA expression in the producer CD4 + T cells. Specifically, of the 58 cellular miRNAs detected at significant levels in the producer cells, only 5 were found in virions at a level 2- to 4-fold higher than that predicted on the basis of random cytoplasmic sampling. Of note, these included two miRNAs, miR-155 and miR-92a, that were reported previously to at least weakly bind HIV-1 transcripts. To test whether miRNA binding to the HIV-1 genome can induce virion incorporation, artificial miRNA target sites were introduced into the viral genome and a 10- to 40-fold increase in the packaging of the cognate miRNAs into virions was then observed, leading to the recruitment of up to 1.6 miRNA copies per virion. Importantly, this high level of incorporation significantly inhibited HIV-1 virion infectivity. These results suggest that target sites for cellular miRNAs can inhibit RNA virus replication at two distinct steps, i.e., during infection and during viral gene expression, thus explaining why a range of different RNA viruses appear to have evolved to avoid cellular miRNA binding to their genome. IMPORTANCE The genomes of RNA viruses have the potential to interact with cellular miRNAs, which could lead to their incorporation into virions, with unknown effects on virion function. Here, it is demonstrated that wild-type HIV-1 virions essentially randomly incorporate low levels of the miRNAs expressed by infected cells. However, the specific incorporation of high levels of individual cellular miRNAs can be induced by insertion of cognate target sites into the viral genome. Of note, this results in a modest but significant inhibition of virion infectivity. These data imply that cellular miRNAs have the potential to inhibit viral replication by interfering with not only viral mRNA function but also virion infectivity.

scholarly journals Autographa californica M nucleopolyhedrovirus early GP64 synthesis mitigates developmental resistance in orally infected noctuid hosts

2004 ◽  
Vol 85 (4) ◽  
pp. 833-842 ◽  
Author(s):  
Ji-Hong Zhang ◽  
Jan O. Washburn ◽  
Donald L. Jarvis ◽  
Loy E. Volkman
Keyword(s):  
Trichoplusia Ni ◽  
Viral Gene Expression ◽  
Autographa Californica ◽  
Viral Gene ◽  
Structural Protein ◽  
Baculovirus Infection ◽  
Two Factors ◽  
Control Virus ◽  
Developmental Resistance ◽  
Budded Virus

The unusual early synthesis of the Autographa californica M nucleopolyhedrovirus (AcMNPV) budded virus (BV) structural protein GP64 is an important virulence factor during oral infection of Heliothis virescens larvae. Considering the breadth of the AcMNPV host range, the importance of early GP64 synthesis in orally infected permissive hosts (Trichoplusia ni and Spodoptera exigua) from subfamilies other than that of H. virescens was assessed. An AcMNPV recombinant, having wild-type early and late GP64 synthesis, was compared with one in which only late GP64 synthesis occurred. Early GP64 synthesis was found to have more of an effect on virulence in orally inoculated T. ni than S. exigua and that virulence was dependent on two factors: the ability of the host to slough occlusion-derived virus (ODV)-infected midgut cells and the rapidity with which BV was transmitted to the tracheal cells. In both host species, insects inoculated orally with the control virus transmitted BV to tracheal cells hours before those inoculated with the gp64 temporal mutant. Moreover, with early GP64 synthesis, the lag between the onset of viral gene expression in midgut and tracheal cells was only 3–4 h, supporting the conclusion that in these insects, the first systemic infections arose from ODV-derived nucleocapsids repackaged as BV. These results provide further empirical proof that early GP64 synthesis is a component of a unique and selectively advantageous baculovirus infection strategy for exploiting larval lepidopterans by counteracting developmental resistance.

scholarly journals Function of Anti-CoV Structure Using INH [1-6]- Tyr160-Met161-His162 Complex

2021 ◽  
Vol 11 (6) ◽  
pp. 14433-14450
Keyword(s):  
Hydrogen Bonding ◽  
Theoretical Calculations ◽  
Wide Spectrum ◽  
Normal Modes ◽  
Viral Gene Expression ◽  
Heat Of Formation ◽  
Electronic Energy ◽  
Proteolytic Processing ◽  
Viral Gene ◽  
Multiple Species

Coronaviruses (CoVs), positive-stranded RNA viruses, can infect humans and multiple species of animals, cause enteric, respiratory, and central nervous system diseases in many species, and are attractive targets for anti-CoV drug design through a pivotal role in viral gene expression and replication through the proteolytic processing of replicase polyproteins. In this work, it has been investigated the junction of six inhibitors including N-[[4-(4-methylpiperazin-1-yl)phenyl]methyl]-1,2-oxazole-5-carboxamide (INH1), NSC 158362 (INH2), JMF 1586 (INH3), (N-(2-aminoethyl)-1-1ziridine-ethanamine) (INH4), [(Z)-1-thiophen-2-ylethylideneamino]thiourea (INH5), and Vanillinbananin (INH6) to coronavirus by forming the complexes of inhibitor-CoV through the hydrogen bonding using the physicochemical properties of the heat of formation, Gibbs free energy, electronic energy, the charge distribution of active parts in the hydrogen bonding, NMR estimation of inhibitor jointed to the database amino acids fragment of Tyr-Met-His as the selective zone of the CoV, positive frequency and intensity of different normal modes of these structures. The theoretical calculations were done at various levels of theory to gain more accurate equilibrium geometrical results. A comparison of these structures with two configurations provides new insights for the design of substrate-based inhibitors targeting CoV. This indicates a feasible model for designing wide-spectrum inhibitors against CoV-associated diseases. The structure-based optimization of these structures has yielded two more efficacious lead compounds, N and O atoms, through forming the hydrogen bonding (H-bonding) with potent inhibition against CoV (Tyr160-Met161-His162), which has been abbreviated as TMH in this work.

Helical polymers of the REV protein of human immunodeficiency virus 1

1992 ◽  
Vol 50 (1) ◽  
pp. 456-457
Author(s):  
Manoj Misra ◽  
Benes L. Trus ◽  
Paul Wingfield ◽  
Alasdair C. Steven
Keyword(s):  
Rna Virus ◽  
Viral Gene Expression ◽  
Viral Gene ◽  
Helical Polymers ◽  
Immunodeficiency Virus ◽  
Viral Gene Product ◽  
Active Proliferation ◽  
Hiv 1 ◽  
Rev Protein

The pattern of viral gene expression in cells infected with HIV-1 is orchestrated by several regulatory proteins. One such viral gene product is Rev (regulator of expression of virus), a 13 kDa basic protein that plays a crucial role in determining whether full-length transcripts coding for the major structural proteins of HIV-1 are exported intact from the nucleus into the cytoplasm, so that active proliferation of the virus can ensue. Purified Rov has been shown to polymerize in vitro into long filamentous polymers. Based on this and other observations, it has been hypothesized that Rev functions rather like the nucleocapsid protein of a filamentous RNA virus, and that coating of the transcripts in question by Rev is the mechanism whereby they are protected from splicing. To explore this hypothesis further, we have studied the structure of these Rev polymers in greater detail.

scholarly journals Processing and intracellular transport of rubella virus structural proteins in COS cells

Virology ◽  
1990 ◽  
Vol 178 (1) ◽  
pp. 122-133 ◽  
Author(s):  
Tom C. Hobman ◽  
Marita L. Lundstrom ◽  
Shirley Gillam
Keyword(s):  
Rubella Virus ◽  
Intracellular Transport ◽  
Structural Proteins ◽  
Cos Cells
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