Disease relevance of Sindbis Virus

• Structure of Sindbis virus core protein reveals a chymotrypsin-like serine proteinase and the organization of the virion [1].
• Sense and antisense genome sequences from La Crosse virus (LAC) (a member of the Bunyaviridae) and dengue viruses serotypes 1 to 4 (DEN-1 to DEN-4) (members of the Flaviviridae) were expressed in mosquito cells from double-subgenomic and replicon vectors based on Sindbis virus (a member of the Togaviridae) [2].
• To determine the role of glutamate excitotoxicity in fatal alphavirus-induced paralytic encephalomyelitis, we treated mice infected with neuroadapted Sindbis virus (NSV) with antagonists of N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) subtypes of glutamate receptors [3].
• Cytochalasin B completely blocked ingestion of Sindbis virus particles or latex spheres by BHK cells but had no effect on the ability of Sindbis virus or vesicular stomatitis virus to infect or replicate in BHK cells [4].
• The envelopment of the Sindbis virus nucleocapsid in the modified cell plasma membrane involves a highly specific interaction between the capsid (C) protein and the endodomain of the E2 glycoprotein [5].

High impact information on Sindbis Virus

• Moreover, MEF from Usp18(-/-) mice showed enhanced interferon-mediated resistance to the cytopathic effect caused by VSV and Sindbis virus (SNV) [6].
• Di-and trimethylated congeners of 7-methylguanine in Sindbis virus mRNA [7].
• A Sindbis virus expressing the SpiC protein interfered with normal trafficking of the transferrin receptor in vivo [8].
• Here we use a recombinant Sindbis virus as a tool to silence BR-C expression in the silkmoth Bombyx mori [9].
• An assay using Sindbis virus (SV) as a cell death inducer revealed that, like Notch, EBNA2 also has antiapoptotic activity [10].

Chemical compound and disease context of Sindbis Virus

• Using recombinant viruses, we show that a single amino acid change in the E2 glycoprotein of Sindbis virus confers both neurovirulence and the ability to kill cells expressing bcl-2 [11].
• Other studies have shown that the sialic acid content of Sindbis virus is determined by the host in which it is propagated [12].
• Engineered defective interfering RNAs of Sindbis virus express bacterial chloramphenicol acetyltransferase in avian cells [13].
• Selective binding of lipid to glycoprotein was detected when [3H]palmitate-labeled Sindbis virus particles or viral-infected cells were disrupted by heating with sodium dodecyl sulfate, and glycoproteins were isolated by electrophoresis in sodium dodecyl sulfate/10% polyacrylamide gels [14].
• In the case of Sindbis virus, interferon is produced, its production being independent of the presence of vitamin A [15].

Biological context of Sindbis Virus

• The nucleotide sequence of the glycoprotein genes of fully virulent Sindbis virus and derived mutants that have reduced neurovirulence for neonatal mice (attenuated mutants) has been determined [16].
• Natural immunity to Sindbis virus is influenced by host tissue sialic acid content [12].
• The pluripotency of recombinant arginase was demonstrated by its ability to inhibit apoptosis in multiple paradigms including rat cortical neurons induced to die by glutathione depletion and oxidative stress, by 100 nM staurosporine treatment, or by Sindbis virus infection [17].
• In addition, fragments of eps15 (encompassing its EH domains or the COOH-terminal region that binds to adaptor protein 2) inhibit EGF internalization or endocytosis of Sindbis virus [18].
• Host-dependent variation of asparagine-linked oligosaccharides at individual glycosylation sites of Sindbis virus glycoproteins [19].

Anatomical context of Sindbis Virus

• To investigate the mechanism responsible for the inhibition of glucose transport by dibutyryl cAMP (Bt2cAMP), two different transporter isoforms (GLUT1 and GLUT4) and several GLUT1/4 chimeric transporters were expressed in Chinese hamster ovary (CHO) cells by using a Sindbis virus expression system [20].
• During Sindbis virus infection class I and II MHC antigens are expressed extensively on microglia which may present viral antigen produced by the infected neurons [21].
• Hexagonal glycoprotein arrays from Sindbis virus membranes [22].
• Indirect fluorescent-antibody studies of living and fixed chick cells infected with temperature-sensitive mutants of Sindbis virus suggest that functional envelope glycoprotein E1 must be inserted through the plasma membrane before E2 [23].
• Pretreatment with the Col-4 and Col-14 antibodies did not block Sindbis virus replication in HepG2 cells or MHV infection in DBT cells, suggesting that one or more CEA glycoproteins likely functioned as receptors for V51B entry into human cell lines [24].

Gene context of Sindbis Virus

• When Sindbis virus is used, these cells show high susceptibility to human IFN-gamma [25].
• Some of these adaptive mutations (e.g., in hepatitis C virus) increase the ability of RNA replication to resist the antiviral action of alpha/beta interferon (IFN-alpha/beta); others (e.g., in Sindbis virus) may also lead to more efficient IFN production [26].
• ISG15 expression protected against Sindbis virus-induced lethality and decreased Sindbis virus replication in multiple organs without inhibiting the spread of virus throughout the host [27].
• Differential regulation of Bcl-2 and Bax expression in cells infected with virulent and nonvirulent strains of sindbis virus [28].
• The brains of mice infected with SIN/beclin had fewer Sindbis virus RNA-positive cells, fewer apoptotic cells, and lower viral titers than the brains of mice infected with SIN/beclinDeltaBcl-2BD or SIN/beclinstop [29].

Analytical, diagnostic and therapeutic context of Sindbis Virus

• Partial NH2-terminal sequence analysis has been performed on some products that result from the translation of 26 S mRNA of Sindbis virus either in vivo or in vitro [30].
• A mutation at E2 position 1 (Arg to Asn) was placed into Sindbis virus AR339 by site-directed mutagenesis of a full-length AR339 cDNA clone, pTRSB, to produce pTRSB-N [31].
• To explore whether Sindbis virus genomes persist in mouse brain after the clearance of infectious virus, we used reverse transcriptase-polymerase chain reaction amplification methods to detect Sindbis virus RNA in brain samples from immunocompetent BALB/c and antibody-treated immunodeficient scid/CB17 mice [32].
• The plaque-reduction neutralization test (PRNT) was used to compare 15 isolates of Ockelbo virus from Sweden, one isolate of Ockelbo virus from Russia, the Egyptian prototype Sindbis virus, and Sindbis-like viruses from Slovakia, South Africa, Cameroon, and Australia. Strains from northern Europe (Sweden and Russia) were indistinguishable by PRNT [33].
• Indeed, validation studies have demonstrated that each immuno-affinity, ion-exchange, and heparin affinity chromatography step can eliminate 1 to 5 log of HIV-1, or of several model viruses, enveloped or non-enveloped, such as sindbis virus, pseudorabies virus, vesicular stomatitis virus, reovirus 3, or simian virus 40 [34].

References