This experimental system is based upon the properties of the HSV mutant strain tsProt.A, which carries a reversible temperature-sensitive lesion in its UL26 protease gene. Each a sequence is flanked by direct repeats (DR1) of 17 to 20 bp, with single copies of DR1 separating tandem a sequences. Below about 100 kbp, the packaged amplicon molecules exhibited an abundance and size distribution similar to those generated using wt HSV-1 as a helper, but the mutant was relatively impaired in packaging longer amplicon molecules. The analysis of herpesvirus cleavage packaging signals has employed two principal approaches. It has further been proposed that UL15 could actually be an accessory component of the DNA replication machinery (34) and may couple the process of DNA replication to that of genome cleavage and packaging. The genome isomers are found in equimolar ratios, reflecting a high frequency of homologous recombination. I have examined the packaging of the KUL25NS genome and an HSV-1 amplicon in cells infected with the mutant virus.
A decade ago, Kosz-Vnenchak et al. Conversely, during infection it must be unstable enough to allow efficient genome release into the host cell. H., Watson, D. DNA-dependent activator of interferon (IFN) regulatory factor (DAI), which is also referred to as Z-DNA binding protein 1 (ZBP1) or DLM-1, was initially identified as a highly upregulated protein in mouse tumor stromal cells and in macrophages treated by gamma IFN (IFN-γ) or lipopolysaccharide (1). Geldanamycin, an inhibitor of Hsp90, results in decreased HSV-1 yields and blocks viral DNA synthesis. Get a printable copy (PDF file) of the complete article (2.1M), or click on a page image below to browse page by page. This may not be the complete list of references from this article.
Links to PubMed are also available for Selected References. Similar to the 3′-to-5′-exonuclease of procaryotic DNA polymerases and mammalian DNA polymerase delta, the HSV-polymerase-associated exonuclease catalyzed the removal of 3′-terminal nucleotides from the primer/template as well as the template-dependent conversion of deoxynucleoside triphosphates to monophosphates. Importantly, this provides a simple mechanism for generating a two-polymerase replisome at the replication fork. DNA molecules consisting of tandem duplications of the complete plasmid, suggesting that replication was occurring by a rolling-circle mechanism. Mutants tsD and tsK appear to be defective in early regulatory functions. B capsids lacking UL25 contained about twofold-less UL17 than wt capsids, raising the possibilities that UL25 is important for stabilizing UL17 in capsids and that the two proteins interact in the capsid. The fibers most probably correspond to multiple, laterally aligned DNA segments, as their diameters are nearly all greater than that of a single DNA double helix.
Analysis of the three potential open reading frames within the 1,147-base-pair fragment and comparison with the amino acid sequence of DNA polymerase of HSV type 1 indicated that the Aphr mutant polymerase had an amino acid substitution from a tyrosine to a histidine in the well-conserved region of the DNA polymerase. There was no statistically significant change in the number of HSV genomes or the number of neuronal cells expressing LAT in these ganglia between 20 and 360 days after infection. The sequestration of endogenous hyperphosphorylated RPA away from replicating viral DNA suggests that HSV-1 prevents the normal ATR-signaling response. Rabbit eyes were infected with either the McKrae strain or the l7Syn+ strain of HSV-1. Rabbits were sacrificed between 5 and 360 days after infection and their trigeminal ganglia were analyzed for the number of HSV DNA genomes and the number of neuronal cells expressing LAT. HSV type 1 (HSV-1) is commonly associated with oropharyngeal infections, keratoconjunctivitis, and infections of the central nervous system, whereas HSV-2 commonly produces genital infections that are considered one of the most important sexually transmitted diseases. The physical map limits for the Aphr mutation were contained in a 1.1-kilobase pair region within the HSV DNA polymerase locus.
In 21 children for whom both cerebrospinal fluid and sera were available, HSV DNA was found in one or both specimens in 19 (90%). This “endless” herpes simplex virus DNA is both qualitatively and quantitatively stable in mouse neural tissue analyzed over a 4-month period. To clarify the function of UL25, we have examined capsids with the goal of defining where it is located. Currently, though India’s Free Trade Act with Thailand is yet to be inked, both countries are bound by the Early Harvest Scheme. Bacteria? The existence of latent HSV-1 DNA in the trigeminal ganglia of infected BALB/c mice was examined using a direct in situ PCR technique, based on Digoxigenin-11-dUTP detection system with anti-digoxigenin-peroxidase and 3,3′-diaminobenzidine (DAB) substrate. ↵1 To whom correspondence should be addressed: Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, 450 West Dr., Chapel Hill, NC 27599-7295.
Unrepaired DNA lesions and deficit in pathways repairing DNA have been documented in several neurodegenerative diseases, including Alzheimer’s disease (AD; Robison et al., 1987; Mullaart et al., 1990; Adamec et al., 1999; Shackelford, 2006; Weissman et al., 2007).