Nucleotide Sequences of the Joint between the L and S Segments of Herpes Simplex Virus Types 1 and 2

113

125

SUMMARYThe nucleotide sequence of 4 kilobases of DNA from within the short region of the genome of herpes simplex virus type 1 has been determined. This portion of DNA contains the junctions of the terminal and internal inverted repeat sequence components with the unique sequence component and the 5' regions of the genes which encode the Vmw 12, Vmw 68 and Vmw 175 immediate-early polypeptides. The transcription and translation initiation sites of all three genes and the 5' and 3' boundaries of the Vmw 12 and Vmw 68 gene introns have been localized on the DNA sequence and shown to be flanked by sequences which resemble those found in similar positions in other eukaryotic genes. For the Vmw 12 and Vmw 68 genes the promoters, the 5'-non-coding regions of the mRNAs, and the introns lie within the terminal and internal inverted repeats respectively while the polypeptide-coding regions lie in the short unique component. The introns consist largely of tandemly reiterated copies of a 22-nucleotide sequence: the Vmw 12 gene intron contains seven of these and the Vmw 68 gene intron five. The Vmw 175 gene is located entirely within the short repeats, of which those regions sequenced here have the extremely high G + C content of 78 %, in marked contrast to the value of 66 % obtained for the adjacent region of the unique sequence component. Prediction of the complete amino acid sequence of the Vmw 12 polypeptide, accounting for a mol. wt. of 9830, and of the first 523 amino-terminal amino acids of the Vmw 175 polypeptide has been made from the DNA sequence. The polypeptide-coding region of the Vmw 175 gene has an average G + C content of 80% but nevertheless specifies a wide range of amino acid types because of the maximal assignment of G and C residues to codon third base positions.

Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

DNA Sequence Anaylysis of an Immediate-Early Gene Region of the Herpes Simplex Virus Type 1 Genome (Map Coordinates 0.950 to 0.978)

Murchie

McGeoch

1982

113

125

“…Competing DNAs were obtained from plasmids containing HSV-1 DNA inserts. Plasmid DNA was prepared (Davison & Wilkie, 1981) and, after treatment with the appropriate restriction endonucleases, the cloned HSV-1 fragment was isolated on a 5 ~ non-denaturing polyacrylamide gel. Fragments were visualized by staining with ethidium bromide and an acrylamide slice containing the band of interest was excised.…”

Section: Methodsmentioning

confidence: 99%

Identification of Two Herpes Simplex Virus Type 1-induced Proteins (21K and 22K) which Interact Specifically with the a Sequence of Herpes Simplex Virus DNA

Dalziel

Marsden

1984

SUMMARYWe have used a DNA competition binding assay to search for herpes simplex virus (HSV) proteins which are able to bind to specific sequences of the genome of HSV. Cloned DNAs from different regions of the virus genome were tested. Two late polypeptides, one major of apparent molecular weight 21000 and one minor of 22 000, were preferentially bound by a variety of fragments containing the HSV-1 400 bp a sequence (a direct repeat present at the ends of the molecule and in inverted orientation between the long and short regions of the genome) but not by other competing DNAs including ones containing an origin of replication. We interpret our result as evidence that the HSV type 1-induced 21K and 22K polypeptides interact specifically with DNA sequences within this 400 bp HSV-1 a sequence.

“…RFLP analyses were performed as previously described Ozawa et al, 2006) using the restriction endonuclease maps of strain F as references (Hayward et al, 1975;Locker & Frenkel, 1979;Roizman, 1979; Roizman & Tognon, 1983). The terminal internal and 'joint' sequences containing the 280 bp repeat, consisting predominantly of the terminal reiterated sequence 'a' (Davison & Wilkie, 1981;Locker & Frenkel, 1979;Roizman, 1979) (Fig. 1), were excluded from the RFLP analyses (Locker & Frenkel, 1979;Roizman & Tognon, 1983;Wagner & Summers, 1978).…”

mentioning

confidence: 99%

Analysis of herpes simplex virus type 1 restriction fragment length polymorphism variants associated with herpes gladiatorum and Kaposi's varicelliform eruption in sumo wrestlers

Ban

Asano²,

Ozawa

et al. 2008

The geographical distribution of herpes simplex virus type 1 (HSV-1) restriction fragment length polymorphism (RFLP) variants BgK L and BgO L and the high relative frequency (RF) of BgK L in orolabial lesions has led to a dispersion-replacement hypothesis for these variants. The pathogenic properties of HSV-1 variants in mice and professional sumo wrestlers were examined here. The wrestlers herpes gladiatorum (HG) was caused by primary and non-primary HSV-1 infections and recurred in many wrestlers. HSV-1 neutralizing antibody titres in sera from wrestlers who did not develop HG were relatively high. HG was caused by distinct HSV-1 variants and strains from wrestlers living in the same sumo stable. The BgK L RF was significantly higher in HG cases, particularly in those with Kaposi's varicelliform eruption. These data indicated that reactivation and transmission of latent HSV-1 infections, especially BgK L , occurred frequently among wrestlers and was caused by severe skin damage. These results support the BgK L dispersion hypothesis.Herpes simplex virus type 1 (HSV-1) variant BgK L is a restriction fragment length polymorphism (RFLP) variant (Ozawa et al., 1988(Ozawa et al., , 1989a caused by loss of the BglII cleavage site between the BglII K and Q/13 fragments . BgK L is a good surrogate marker for the HSV-1 multiple mutant BgK L :SaCFJ M :SaE L :SaGH M :KpM S , where SaCFJ M denotes loss of SalI fragments C, F and J, SaE L denotes a larger SalI L fragment, SaGH M denotes loss of SalI G and H fragments and KpM S denotes a smaller KpnI M fragment Ozawa et al., 2006). The prevalence of BgK L in HSV-1 clinical isolates, referred to as its relative frequency (RF), is 27 % in Japan (Ozawa et al., 2006). Another HSV-1 RFLP variant BgO L (Ozawa et al., 1989b) has lost the BglII cleavage site between the BglII Q/ 13 and O fragments . It has been proposed that BgK L spread and replaced BgO L in Japan, based on the geographical distribution profiles of BgK L and BgO L Ozawa et al., 1989bOzawa et al., , 2006 and the high RF of BgK L in orolabial infections .In the present study, we compared the pathogenic and epidemiological properties of HSV-1 BgK L , BgO L and nonBgK L :non-BgO L variants in mice and sumo wrestlers with herpes gladiatorum (HG). Central nervous system (CNS) destruction is a major consequence of experimental murine disease induced by HSV-1 (Dix et al., 1983b; Goel et al., 2002;Mao & Rosenthal, 2003;Richards et al., 1981;Roizman & Knipe, 2001). HG has been documented among wrestlers and rugby players (Anderson, 2003;Becker, 1992;Belongia et al., 1991;De Bernardo, 1992;Turbeville et al., 2006;White & Grant-Kels, 1984 et al., 1990;Dix et al., 1983aDix et al., , 1983bMao & Rosenthal, 2003;Richards et al., 1981) and mutants (Roizman & Knipe, 2001).Clinical specimens and HSV-1 isolates from sumo wrestlers, described previously by Asano et al. (1994) et al., 1994) and HSV-2 was isolated from another wrestler (data not shown). Virus isolates were propagated on Vero cell (Yasumura & Kawakita, 1988) monolayers...