Processing of Glycoproteins Induced by Herpes Simplex Virus Type 1: Sulphation and Nature of the Oligosaccharide Linkages

Hope, RM; Marsden, Howard S.

doi:10.1099/0022-1317-64-9-1943

Cited by 16 publications

(14 citation statements)

References 16 publications

(19 reference statements)

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“…As expected from the calculation of size, the deletion does not extend into the coding region for gE (US8) in HG52X163X12, which has been shown to make gE in normal amounts in SDS-PAGE analysis of sulphated polypeptides (Hope & Marsden, 1983). Due to the lack of an antiserum or antibody against the HSV-2 equivalent of the 30K (US9) mol.…”

Section: Discussionmentioning

confidence: 96%

Three Mutants of Herpes Simplex Virus Type 2: One Lacking the Genes US10, US11 and US12 and Two in which RS Has Been Extended by 6 kb to 0{middle dot}91 Map Units with Loss of US Sequences between 0{middle dot}94 and the US/TRS Junction

Brown¹,

Harland²

1987

Journal of General Virology

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SUMMARYin the process of generating restriction endonuclease site deletion mutants, we have isolated and characterized three mutants of herpes simplex virus type 2 (HSV-2), strain HG52, with large genomic deletions in Us and TRs. The deleted sequences (7.5 kb) extend from 0-94 map coordinates (m.c.) to 0-99 m.c. and are presumed to contain the HSV-2 gene equivalents of US10, 11 and 12, one copy of immediate early (IE) gene 3 and one copy of an origin of replication (ORls). One of the mutants (HG52X163X12) has a simple deletion whereas in the two others (HG52X 163X14 and HG52X163X21) the deleted sequences have been replaced by inverted duplications of Us/IRs sequences between 0.83 and 0-91 m.c. such that the molecules have short region inverted repeats extended by 6 kb on either side. All three are viable, stable and grow in tissue culture indicating that the polypeptides coded by the HSV-2 genes equivalent to US10, 11 and 12 are n0n-essential for lytic growth in BHK21/C13 cells. In addition the lack of one copy of the HSV-2 equivalent of IE gene 3 and ORIs in HG52X163X12 shows that only one copy of each suffices for viability. However the temperature restriction of the mutants at 38-5 °C suggests that one or more of the polypeptides coded by the deleted sequences may be required in conjunction with another polypeptide(s) for viral growth or stability at the higher temperature. INTRODUCTIONDeletions in one copy of the long repeat sequences of herpes simplex virus type 2 (HSV-2) strain HG52 occur at a frequency of 24~o by passage eight from the original field isolation (Harland & Brown, 1985). The described deletions range in size with the maximum being 9 kb and encompass the entire long repeat with the exception of the 'a' sequences. Other strains of HSV-2 exhibit simdar deletions showing that the HG52 strain is not exceptional. Deletions in the long repeat had been observed previously in intertypic reeombinants when Davison et al. (1981) suggested that they probably arose as a consequence of heterotypic repetitive regions. Our observations show that this could not be the explanation but that deletions within one copy of the long repeats of the HG52 genome are relatively common. These deletion variants do not have a selective disadvantage (Harland & Brown, 1985); thus only one copy of immediate early (IE) gene 1 and the other coding information within the long repeats is sufficient for viable growth in tissue culture. The product of IE gene 1, i.e. Vm,~ IE 110, in conjunction with V mw IE175 has an enhancing effect on early polypeptide transcription (Everett, 1984) but it has not been shown whether V~wlE110 is essential for lytic growth.The high frequency of spontaneous deletions within the long repetitive sequences raises the question of whether similar deletions could occur in the short repetitive sequences of the genome. The repeat (TRs) and unique short (Us) regions of the HSV-l genome have been fully sequenced (Murchie & McGeoch, 1982;McGeoch et al., 1985), The IE3 gene coding for

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Section: Discussionmentioning

confidence: 96%

Three Mutants of Herpes Simplex Virus Type 2: One Lacking the Genes US10, US11 and US12 and Two in which RS Has Been Extended by 6 kb to 0{middle dot}91 Map Units with Loss of US Sequences between 0{middle dot}94 and the US/TRS Junction

Brown¹,

Harland²

1987

Journal of General Virology

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“…Inorganic sulfate is incorporated into all the major HSV-1 and HSV-2 glycoproteins, particularly into gE-1 and gE-2 (Hope et a1., 1982;Hope and Marsden, 1983). The nature of the linkage between sulfate and the glycoproteins is not known and, as pointed out by these authors, several possibilities exist.…”

Section: Su1fationmentioning

confidence: 90%

Glycoproteins Specified by Herpes Simplex Viruses

1985

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“…Unfortunately, the functions of most of the proteins coded by the HSV-1 and VZV S segments are unknown. Two of the genes in the VZV S segment encode glycoproteins: VZV US4 encodes a major envelope glycoprotein (Ellis et al, 1985) which is homologous to the product of HSV-1 US8, also an envelope glycoprotein, gE Lee et al, 1982;Para et al, 1982;Hope & Marsden, 1983;McGeoch et al, 1985); VZV US3 is a glycoprotein gene and its counterpart, HSV-1 US7, has been predicted to encode a glycoprotein (McGeoch et al, 1985;McGeoch, 1985). The hydrophobicity plot for each of these proteins exhibits a hydrophobic region near the amino terminus, corresponding to a signal sequence for translation on membrane-bound ribosomes, and towards the carboxy terminus there is a region containing a highly hydrophobic domain followed by basic residues, which is thought to be a transmembrane anchor sequence.…”

Section: Methodsmentioning

confidence: 99%

Evolutionary Comparisons of the S Segments in the Genomes of Herpes Simplex Virus Type 1 and Varicella-Zoster Virus

Davison

McGeoch

1986

Journal of General Virology

122

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SUMMARYThe genomes of herpes simplex virus type 1 (HSV-1) and varicella-zoster virus (VZV) consist of two covalently joined segments, L and S.,Each segment comprises an unique sequence flanked by inverted repeats. We have reported previously the DNA sequences of the S segments in these two genomes, and have identified protein-coding regions therein. In HSV-1, the unique sequence of S contains ten entire genes plus the major parts of two more, and each inverted repeat contains one entire gene; in VZV, the unique sequence of S contains two entire genes plus the major parts of two more, and each inverted repeat contains three entire genes. In this report, an examination of polypeptide sequence homology has shown that each VZV gene has an HSV-1 counterpart, but that six of the HSV-1 genes have no VZV homologues. Thus, although these regions of the two genomes differ in gene layout, they are related to a significant degree. The analysis indicates that the inverted repeats are evidently capable of largescale expansion or contraction during evolution. The differences in gene layout can be understood as resulting from a small number of recombinational events during the descent of HSV-1 and VZV from a common ancestor. INTRODUCTIONMembers of the family Herpesviridae are classified into three subfamilies: the Alpha-, Betaand Gamma-herpesvirinae. This subclassification is based on properties of the virus particle, on features of the replication cycle and on biological aspects, such as host range and site of latency (Matthews, 1982). These criteria have proved useful but, despite some attempts to include genome organization as an additional taxonomical factor, the evidence for relationships between the subfamilies has been circumstantial. Comparisons of currently emerging herpesvirus DNA sequences will allow the relationships to be investigated precisely and directly at the genetic level. For example, recent comparisons of sequences from herpes simplex virus type l (HSV-1) and Epstein-Barr virus, which are members of the Alpha-and Gammaherpesvirinae, respectively, have demonstrated a degree of conservation in the predicted amino acid sequences of at least three virus-coded proteins: the two subunits of the ribonucleotide reductase , the DNA polymerase (Quinn & McGeoch, 1985;Baer et al., 1984) and the major DNA-binding protein (Quinn & McGeoch, 1985). Nevertheless, the available evidence indicates that the Alphaherpesvirinae and Gammaherpesvirinae are rather distantly related. There are as yet no sequence data indicating the degree of relationship between the Betaherpesvirinae and the other subfamilies.In contrast, studies of antigenic relatedness and DNA homology have shown members of the same subfamily to be much more closely related. For example, Davison & Wilkie (1983), using the technique of DNA-DNA hybridization, detected conservation of several genes in five members of the Alphaherpesvirinae. They proposed from the colinear arrangement of conserved

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Processing of Glycoproteins Induced by Herpes Simplex Virus Type 1: Sulphation and Nature of the Oligosaccharide Linkages

Cited by 16 publications

References 16 publications

Three Mutants of Herpes Simplex Virus Type 2: One Lacking the Genes US10, US11 and US12 and Two in which RS Has Been Extended by 6 kb to 0{middle dot}91 Map Units with Loss of US Sequences between 0{middle dot}94 and the US/TRS Junction

Three Mutants of Herpes Simplex Virus Type 2: One Lacking the Genes US10, US11 and US12 and Two in which RS Has Been Extended by 6 kb to 0{middle dot}91 Map Units with Loss of US Sequences between 0{middle dot}94 and the US/TRS Junction

Glycoproteins Specified by Herpes Simplex Viruses

Evolutionary Comparisons of the S Segments in the Genomes of Herpes Simplex Virus Type 1 and Varicella-Zoster Virus

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