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PubMed2025

Computational Insights on the Assembly of the Dengue Virus Membrane-Capsid-RNA Complex.

Dengue virus, an arbovirus from the genus Flavivirus in the family Flaviviridae, forms a nucleocapsid structure through interactions between its genome and multiple copies of the capsid protein. Experimental studies have confirmed the interaction between the viral capsid protein and lipid droplets, indicating a protein-lipid interaction. Cryo-EM studies show that in immature viruses, the nucleocapsid is located close to the viral membrane. This study uses multiple MD simulations to explore the orientation of the capsid protein relative to the lipid membrane, focusing on how the protein's hydrophobic pocket interacts with the membrane. We also investigated the interaction between the capsid protein and RNA, considering the effects of sequence length and identity. Finally, we construct a model of the lipid-protein-RNA complex, demonstrating that the capsid protein's hydrophobic pocket interacts with the membrane, while the positively charged H4 helix interacts with the negatively charged RNA. This research may identify crucial interactions for immature virus particle formation and provide insights for future therapeutic interventions.

Dengue Virus↗
PubMed1978

Assembly intermediates among adenovirus type 5 temperature-sensitive mutants.

Temperature-sensitive mutants from three different complementation groups, ts5, ts19, and 6s58, have been shown to accumulate assembly intermediates at the restrictive temperature. The polypeptide composition of these intermediates is similar to that of the wild type, including the precursor polypeptides pVI, pVII, and pVIII. ts5 and ts19 also contained cleaved precursors, indicating assembly into defective virions. The increase of infectious virus after temperature shift-down of ts19 and ts58 was rapid when compared with that of ts24, which does not accumulate intermediates, suggesting that intermediates formed at nonpermissive temperature may be processed to mature virus. However, shift-down experiments reveal that only a fraction of the intermediates are utilized for virus assembly and that degradation of intermediates occurs at the restrictive temperature.

Adenoviruses, Human↗
PubMed2026

Virome of the Russian Grapevine Germplasm: A Final Study and Summary.

Ampelographic collections play an important role in the conservation of grapevine genetic resources and therefore require continuous phytosanitary monitoring. In this study, the virome of grapevines from the Magarach ampelographic collection in Russia was analyzed using total RNA high-throughput sequencing. A total of twenty-seven grapevine viruses and four viroids were identified. Two viruses were characterized as putative novel species: (+) ssRNA grapevine umbra-like virus 5 (GULV-5) and the bipartite (+) ssRNA grapevine Magarach secovirus (GMSV), which, together with related viruses, may represent a novel genus within the family Secoviridae. Among the economically important viruses, the most prevalent were grapevine fanleaf virus (76%), grapevine leafroll-associated virus 1 (39%), and grapevine virus A (33%). Mixed infections involving two or three of these viruses were detected in 50% of the analyzed grapevines. Grapevine virus D was detected in Russia for the first time. Phylogenetic analysis of 222 assembled virus and viroid genome sequences revealed high genetic diversity. The obtained results were summarized and compared with previous virome studies conducted on four Russian ampelographic collections.

RNA-Seq↗
PubMed1979

Effect of interferon on murine leukaemia virus infection. IV. Formation of non-infectious virus in chronically infected cells.

Interferon (150 units/ml) was used to treat SC-1 and AKR-2B cells which were chronically infected with murine leukaemia virus (MuLV). This led to a 100-fold decrease in the amount of infectious virus released into the medium and a 10-fold decrease in the number of virus particles measured by the virion-associated reverse transcriptase assay. However, there was little change in the amount of cell-associated infectious virus, though nearly twice as many cell-associated virions were counted in electron micrographs. With both types of cells, interferon blocked MuLV replication at the post-budding stage, but it did not change the morphology of the particles produced or their content of virion 70S RNA. Infectious virus assembled on the cell membranes of interferon-treated cells was less stable at 37 degrees C than that grown in the absence of interferon. Release of infectious virus from interferon-treated cells was not inhibited by actinomycin D or cycloheximide, though both agents inhibited virus production in controls. These results show that interferon inhibits MuLV replication through effects on virion assembly; these lead both to the formation of non-infectious particles and of fewer virions. Kinetic analysis further shows that interferon affects MuLV assembly rapidly and induction of an antiviral protein may not be required.

Cell Line↗
PubMed1977

Membrane-associated assembly of M13 phage in extracts of virus-infected Escherichia coli.

Assembly of coliphage M13 is known to occur as the viral DNA crosses the cytoplasmic membrane, shedding its virus-coded DNA unwinding protein and acquiring from the membrane approximately 2400 copies of the major coat protein. Conditions are described in which extracts of M13-infected E. coli and membranes prepared from such extracts will support virus assembly at a rate equivalent to that of intact cells. Extracts prepared from cells infected with temperature-sensitive M13 mutants in genes 1, 3, 4, or 5 are temperature-sensitive in this cell-free assembly reaction. Phage assembly in vitro requires magnesium and as yet an unidentified heat-stable cofactor of low molecular weight. The rate of virus assembly is approximately linear with respect to extract concentration over a 10(4)-fold range, consistent with the observation that the entire M13 assembly activity copurifies with the cell membrane fraction.

Cell Membrane↗
PubMed1977

Kinetics of assembly of a parvovirus, minute virus of mice, in synchronized rat brain cells.

The rates of assembly of the three classes of particles of minute virus of mice were examined in synchronized rat brain cells by a combination of electron microscopy and biochemical techniques. We observed a burst of virus assembly beginning about 8 h after the end of cellular S phase. Labeled thymidine incorporated into the 1.46 g/cm3 class of full virus particles was transferred almost quantitatively to the 1.42 g/cm3 class. The 1.46 g/cm3 virus appeared to be an immediate precursor to the 1.42 g/cm3 class. Conversion of the 1.46 density virus to the 1.42 density particles was observed at the time of virus assembly. The processing was rapid and occurred primarily in the nucleus. Infected cells did not contain significant pools of viral DNA in a form that could be encapsulated in the absence of DNA synthesis. The role of the empty virus capsids in the assembly process is discussed.

Animals↗
PubMedDate not supplied

Inhibition of herpes simplex virus multiplication by 2,3-bis(acetyl mercaptomethyl)-quinoxalin.

The drug 2,3-bis(acetyl mercaptomethyl)-quinoxalin (BAMMQ) was 99.9% inhibitory for herpes simplex virus (HSV) multiplication in cell cultures at concentrations of 1.6 X 10(-5) M or less. The drug was not inactivating for the virus, did not interfere with adsorption and penetration of the virus, and was still active when added as late as 12 h after infection with HSV. BAMMQ did not prevent HSV DNA replication, but interfered with a late stage of virus assembly and/or maturation.

Cell Line↗
PubMed1977

Interferon inhibits mouse leukaemia virus release: an electron microscope study.

Scanning electron microscopy of AKR cells chronically infected with AKR mouse leukaemia virus revealed that the number of budding virions was greatly increased in interferon-treated cells. These results, together with previous biochemical findings, suggest that in this system, interferon inhibits a late stage of virus assembly or release.

AKR murine leukemia virus↗
PubMed1976

Incomplete viral synthesis in Friend leukemia virus-induced reticulum cell sarcomas.

Tissue-culture-passaged, Friend leukemia virus (FV)-induced reticulum cell sarcomas from BALB/c mice (FVTCT-BALB) did not produce infectious FV, although retrieval of infectious FV occurred when these cells were co-cultivated with cell lines replicating non-defective murine leukemia viruses (MLVs). The level of FV expression in the FVTCT-BALB cell line was studied to understand better the process of FV retrieval. 3H-uridine labelling techniques and reverse transcriptase assays showed that FVTCT-BALB cells did not release C-type virus particles. Nucleic acid hybridization techniques demonstrated that the level of viral RNA synthesis in the FVTCT-BALB non-producer cell line was indistinguishable from that in cell lines productively infected with MLVs. These data suggest that in the FVTCT-BALB cell line the synthesis of FV is blocked in some late stage of virus assembly.

Animals↗
PubMed1978

Cross-linking of Newcastle disease virus (NDV) proteins.

The proxomity and spatial relationships of the structural proteins of Newcastle disease virus (NDV) were studied by chemical cross-linking with a series of imidoesters. When the virions were reacted by the cross-linker with a distance 6.1A or longer between the functional groups and analyzed by polyacrylamide gel electrophoresis, remarkable changes were observed in the migration patterns of the viral proteins. The most striking one was the extensive decrease in the intensity of the M protein band, and although not so strikingly, glycoprotein and nucleocapsid protein bands were reduced significantly. Instead, several protein complexes appeared at and near the top of the gels. The protein complexes formed by a reversible cross-linker, dimethyl-3,3'-dithiobispropionimidate (DTBP), were analyzed by two dimensional electrophoresis; the complexes on the first-dimension cylindrical gels were cleaved by reduction with 2-mercaptoethanol and electrophoresed laterally on the second-dimension slab gels. The results indicated that homodimers of glycoprotein, nucleocapsid protein and M protein were generated under the condition of the most gentle cross-linking employed. At the same time, however, trimer and higher homopolymers of M protein were already detectable. Under the more extensive conditions, the bulk of M protein was cross-linked to form a large protein complex with very high molecular weight. Further, small but significant amounts of glycoprotein and nucleocapsid protein were always detected in this complex. These results suggest that M protein may be present in the virion in close enough proximity to interact with each other and may further have some interactions with glycoprotein and nucleocapsid protein. On the basis of these findings possible roles of M protein in virus assembly were discussed.

Dimethyl Adipimidate↗
PubMed1975

Assembly of the enveloped bacteriophage phi 6 in environments which perturb the host cell membranes.

The effects of known membrane-perturbing agents (pH, Na+, Ca2+, and a small lipid-soluble molecule) on the enveloped bacteriophage phi 6 host cell system were investigated at the levels of cellular growth, virus assembly and stability, and the physical and chemical properties of host cell membranes. Spin-label probes of cellular membranes indicate that growth in high levels of Na+ or the small spherical hydrophobic molecule adamantanone results in membranes having increased "fluidity," while growth in high levels of Ca2+ results in slightly greater rigidity of the membranes. In addition, the phospholipid composition of the cellular membranes is dependent on the NaCl concentration in the growth medium. None of these membrane alterations, however, prevent the production of infectious phi 6 virus particles.

Adamantane↗
PubMed1977

Effect of concanavalin A on vesicular stomatitis virus maturation.

Addition of concanavalin A to BHK cell monolayers infected with vesicular stomatitis virus prevented the formation of mature virus particles. In these cells the virus glycoprotein (G) was inserted into the plasma membrane and the protein that is in close association with the ribonucleic acid, protein N, was found in the cytoplasm. At times when cells infected in the absence of the lectin were liberating virus into the supernatant medium, the M or matrix protein was found in association with the plasma membrane of the lectin-treated cells. The removal of the lectin from the cells with alpha-methyl-D-glucoside 3 h after infection was followed by the immediate release of mature virus particles. The rate of virus release from these cells was the same as that from cells infected in the absence of the lectin. Addition of cycloheximide, and inhibitor of protein synthesis, immediately after alpha-methyl-D-glucoside treatment of the cells did not alter the rate of virus production, suggesting that the proteins required for virus synthesis were available in the lectin-treated cells and that virus assembly took place without further protein synthesis on removal of the lectin.

Cell Line↗
PubMed1976

Comparative study of the milk fat globule membrane and the mouse mammary tumour virus prepared from the milk of an infected strain of Swiss albino mice.

Milk fat globule membranes and mammary tumour virus particles (d=1.17 g/cm3) have been obtained from the milk of a Swiss albino mice strain. Comparative biochemistry shows that these two structures differ significantly in the phospholipid, polypeptide and glycopolypeptide patterns and enzymatic activities. However, the lipid profile and the morphology of both structures suggest a filiation with the plasma membrane. Density fractions obtained from the crude virus preparation have been thoroughly investigated. The results suggest that most of these fractions represent degraded virus and/or atypical virus assembly.

Animals↗
PubMed1975

Interferon-directed inhibition of chronic murine leukemia virus production in cell cultures: lack of effect on intracellular viral markers.

Extracellular murine leukemia virus (MLV) reverse transcriptase activity was decreased by interferon treatment in four interferon-sensitive mouse cell lines which were chronic MLV producers. In three cell lines which were relatively insensitive to interferon, extracellular enzyme activity remained unchanged by interferon treatment. The concentrations of interferon used had no effect on DNA synthesis or cell replication of AKR,C+ cells which were chronic producers of AKR-MLV. In AKR,C+ cultures interferon treatment also had no effect on the level of intracellular viral reverse transcriptase activity in spite of an inhibition of extracellular enzyme activity. Treatment of AKRC+ cultures with interferon for 9 days inhibited extracellular viral reverse transcriptase levels throughout the period of treatment; however, the intracellular enzyme activity remained unchanged, and concentrations of viral p30 (gs) antigen were increased in the interferon-treated cells. When the cells were washed to remove interferon, however, virus production rapidly rose and intracellular p30 antigen fell to the levels of untreated AKR,C+ cells. These and previously reported results suggested that in interferon-treated AKR,C+ cells virus production is inhibited at a late step in the MLV replication cycle, either directly or through the inhibition of the production of a protein required for virus assembly.

Animals↗
PubMed1977

Phosphorylation and nucleic acid binding properties of m1 Moloney murine sarcoma virus-specific pP60gag.

The pP60gag polyprotein of the feline leukemia virus pseudotype of m1 Moloney murine sarcoma virus [m1MSV(FeLV)] was previously shown to be MSV specific and to contain murine p30 and smaller structural polypeptides. This protein was detected in m1MSV-transformed cells, and in pulse-chase studies it was found to be stable. In this study virion P60 was shown to contain murine pp12, to be phosphorylated, and to bind to nucleic acids. 32P-labeled m1MSV[FeLV) was fractionated by guanidine agarose chromatography and analyzed by gel electrophoresis. Both P60 and pp12 were found to be the major phosphoproteins, phosphorylated in both serine and threonine residues. Virion P60 bound preferentially to single-stranded DNA and RNA in a competition filter binding assay, using 125I-labeled single-stranded calf thymus DNA and various unlabeled nucleic acids. Similar phosphorylation and DNA binding properties were demonstrated for cellular P60. Thus, immunoprecipitation of cellular extracts showed that P60 was phosphorylated in both producer and nonproducer transformed cells, indicating that phosphorylation occurs independently of virus assembly. Moreover, P60 from cytoplasmic extracts was retained on single-stranded DNA-Sepharose columns, demonstrating that cellular P60 binds to DNA.

DNA↗
PubMed1978

Expression of "early" and "late" viral functions in a somatic cell hybrid between a mouse cell and a spontaneous yielder SV 40-transformed Chinese hamster cell.

A somatic cell hybrid (Cl. 6d) was originated from the fusion of mouse 3T3-4E) and spontaneous yielder SV 40-transformed Chinese hamster (CHK/SVLP AG) cells. During the early stages of its history, the C1. 6d hybrid underwent a rapid chromosome loss, preferentially loosing hamster chromosomes. This was not a constant tendency of the hybrid cells. As the parental CHK)SVLP AG cells, the hybrid cells were always found 100 per cent SV40 T-antigen positive. While CHK/SVLP AG cells infectious SV 40 DNA, V-antigen and virus were regularly detected, in the hybrid cells only infectious DNA was occasionally detected. This was not due either to the loww of an essential Chinese hamster gene(s) or to the presence of an inhibiting mouse cell component(s); it was apparently the consequence of inability of the cells to properly activate the resident SV 40 genome(s). After superinfection with SV 40 DNA, the hybrid cells-though capable of synthesizing SV 40 V-antigen--were unable to ensure virus assembly. Experimental evidence was obtained suggesting that SV 40 maturation is dependent of a cellular function(s).

Animals↗
PubMed1978

Cycloleucine blocks 5'-terminal and internal methylations of avian sarcoma virus genome RNA.

Cycloleucine, a competitive inhibitor of ATP: L-methionine S-adenosyltransferase in vitro, has been used to reduce intracellular concentrations of S-adenosylmethionine and by this means to inhibit virion RNA methylation in chicken embryo cells that are infected with B77 avian sarcoma virus. Under conditions of cycloleucine treatment, where virus production as measured by incorporation of radioactive precursors or by number of infectious particles is not significantly affected, the internal m6A methylations of the avian sarcoma virus genome RNA are inhibited greater than 90%. The predominant 5'-terminal structure in viral RNA produced by treated cells in m7G(5')pppG (cap zero) rather than m7G-(5')pppGm (cap 1). It appears from these results that internal m6A and penultimate ribose methylations are not required for avian sarcoma RNA synthesis and function. Furthermore, these methylations are apparently not required for transport of genome RNA to virus assembly sites. The insensitivity of the 5'-terminal m7G methylation to inhibition by cycloleucine suggests that the affinity of S-adenosylmethionine for 7-methylguanosine methyltransferase is significantly greater than for the 2'-0-methyltransferases or the N6-methyltransferases.

Amino Acids↗
PubMed1979

The errors in assembly of MuLV in interferon treated cells.

Interferon treatment of JLSV-6 cells chronically infected with Rauscher MuLV leads to the formation of noninfectious particles (interferon virions) containing the structural proteins of env and gag genes as well as additional viral polypeptides. In the control virions the major glycoprotein detected is gp71, interferon virions contain in addition to gp71 and 85k dalton (gp85) glucosamine-containing, fucose-deficient glycoprotein which is recognized by antiserum to MuLV but not by the gp71 antiserum. The surface iodination of the intact virions indicates that both gp71 and gp85 are the major components of the external virions envelope. However, unlike the control virions in which gp71 associates with p15E (gp90), the gp71-p15E complex was not detected in interferon virions. The analysis of the iodinated proteins of the disrupted interferon virions revealed the presence of 85k and 65k dalton polypeptides preciptable with antiserum against MuLV, which are not present in the control virions. The difference in the polypeptide pattern of virions produced in the presence of interferon does not seem to be a consequence of the slowdown in the synthesis of viral proteins or their processing in the interferon-treated cells. Both the structural proteins of env and gag genes seem to be synthesized and processed at a comparable rate in the interferon-treated and -untreated cells. These results indicate an alteration of virus assembly in the presence of interferon.

Animals↗