Glycoproteins Specified by Herpes Simplex Viruses

Spear, Patricia G.

doi:10.1007/978-1-4613-2383-9_7

Cited by 233 publications

(234 citation statements)

References 158 publications

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“…HSV-2 gB has a central role in adsorption of virus as well as the penetration of the virus into the host cell (39). Collectively, the transgene reduces the spread as well as the replication of the virus from the vaginal tissue to peripheral and, ultimately, central nervous systems based on a reduction in viral yields in the vagina and spinal cord in line with the progression of the disease.…”

Section: Figurementioning

confidence: 99%

The Application of a Plasmid DNA Encoding IFN-α1 Postinfection Enhances Cumulative Survival of Herpes Simplex Virus Type 2 Vaginally Infected Mice

Härle

Noisakran

Carr

2001

The Journal of Immunology

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Using a hormonally induced susceptibility mouse model to investigate vaginal HSV type 2 (HSV-2) infection, a study was undertaken to determine the efficacy of a plasmid DNA encoding IFN-α1 introduced into the vaginal lumen postinfection (PI). Mice infected with HSV-2 intravaginally and treated intravaginally 24 h later with 100 μg DNA encoding IFN-α1 showed enhanced survival (10/15) in comparison to mice treated with 100 μg plasmid DNA vector alone (3/10) or vehicle (4/27). In contrast, mice receiving recombinant IFN-αA (5–500 U/vagina) 24 h PI showed no significant survival in comparison to the vehicle (saline)-treated group. The protective effect was time dependent in that mice receiving the IFN-α1 transgene 48 h PI succumbed at a rate similar to the plasmid DNA vector-treated group. The increase in cumulative survival elicited by the transgene corresponded with a reduction in viral replication and Ag expressed in the vaginal epithelium early (i.e., 3 days PI) during acute infection and replicating virus recovered in the spinal cord day 7 PI. By day 7 PI, HSV-2 glycoprotein B transcript expression was no longer detectable in vaginal tissue from the IFN-α1 transgene-treated group (0/8) compared with levels expressed in plasmid vector-treated controls (4/6 mice surveyed were positive). Collectively, these results suggest the application of DNA encoding type I IFN is an effective and alternative approach to currently prescribed therapies in controlling vaginal HSV-2 infection by antagonizing viral replication.

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Section: Figurementioning

confidence: 99%

The Application of a Plasmid DNA Encoding IFN-α1 Postinfection Enhances Cumulative Survival of Herpes Simplex Virus Type 2 Vaginally Infected Mice

Härle

Noisakran

Carr

2001

The Journal of Immunology

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“…On the basis of electron microscopic studies it has been suggested that enveloped herpesviruses in the perinuclear space are released into the cytoplasm as nucleocapsids as a result of fusion of the virion envelope with the outer lamella of the nuclear envelope, and that egress results from subsequent re-envelopment at cytoplasmic membranes (Sirninoff & Menefee, 1966). However, the weight of biochemical and electron microscopic evidence favours a single envelopment process followed by egress via a process of reverse endocytosis (reviewed by Spear, 1984), and on this basis the phenotype of tsQ26 is more readily explained by degradation of gH during transport of the enveloped particle to the cell surface.…”

mentioning

confidence: 99%

Excretion of Non-infectious Virus Particles Lacking Glycoprotein H by a Temperature-sensitive Mutant of Herpes Simplex Virus Type 1: Evidence that gH Is Essential for Virion Infectivity

Desai

Schaffer

Minson

1988

Journal of General Virology

170

130

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SUMMARYA temperature-sensitive mutant of herpes simplex virus type 1, tsQ26, was shown to contain an amino acid substitution in glycoprotein H (gH). The mutant entered cells efficiently at the non-permissive temperature and replicated to give nearly normal yields of intracellular infectivity. The intracellular virions contained, predominantly, an immature form ofgH and no gH was found on the surface of infected cells. Excreted virions were devoid of gH and were not infectious. Virions excreted at the permissive temperature were infectious and contained gH and no loss of gH resulted from incubation of these virions at the non-permissive temperature. The temperaturesensitive phenotype apparently results from the loss of gH from virions during their transport to the cell surface, and since loss of gH is accompanied by loss of infectivity we conclude that gH is an essential component of the infectious virion.

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“…The membranes of the virions and infected cells contain a number of virus-specified glycoproteins which contain N-and/or O-glycosylated oligosaccharides (Spear, 1985). The two common types of HSV, facial (HSV-1) and genital (HSV-2) are closely related (Person et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

“…The two common types of HSV, facial (HSV-1) and genital (HSV-2) are closely related (Person et al, 1985). The genes of four antigenically distinct glycoproteins gB, gC, gD and gE map colinearly in the HSV-1 and HSV-2 genomes (Spear, 1985). The glycoprotein gG-2 encoded by the S component of the HSV-2 genome (Marsden et al, 1984) also has a smaller sized counterpart mapped in the US4 region of the HSV-1 genome (Frame et al, 1986;Richman et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

“…The glycoprotein gG-2 encoded by the S component of the HSV-2 genome (Marsden et al, 1984) also has a smaller sized counterpart mapped in the US4 region of the HSV-1 genome (Frame et al, 1986;Richman et al, 1986). The HSV-1 glycoproteins have been studied extensively to elucidate their biogenesis, glycosylation, processing and intracellular transport (Spear, 1985). The genes for the glycoproteins gB-1, gC-1, gD-1 and gE-1 have also been cloned and sequenced and the deduced amino acid sequences have been reported (Bzik et al, 1984;Frink et al, 1983: McGeoch et al, 1985Watson et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

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Herpes Simplex Virus Type 2 Glycoprotein Biogenesis: Effect of Monensin on Glycoprotein Maturation, Intracellular Transport and Virus Infectivity

Ghosh‐Choudhury

Graham

Ghosh

1987

Journal of General Virology

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SUMMARYThe ionophore monensin inhibited the formation of herpes simplex virus type 2 (HSV-2) particles by about 30~ but the yields of infectious particles were reduced to 5~ and 1 ~ for cell-associated and extracellular virus, respectively. The presence of monensin did not affect the processing of the two viral glycoproteins gB-2 and gG-2. However, two other glycoproteins, gC-2 and gD-2, were not processed to their fully mature forms in the monensin-treated cells and only the faster moving pgC-2 and pgD-2 were detected. The cell-associated virus particles contained the glycoproteins gB-2, gC-2, gD-2 and gG-2, whereas the extracellular virus particles contained only gG-2 glycoprotein. These results suggest that HSV

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Glycoproteins Specified by Herpes Simplex Viruses

Cited by 233 publications

References 158 publications

The Application of a Plasmid DNA Encoding IFN-α1 Postinfection Enhances Cumulative Survival of Herpes Simplex Virus Type 2 Vaginally Infected Mice

The Application of a Plasmid DNA Encoding IFN-α1 Postinfection Enhances Cumulative Survival of Herpes Simplex Virus Type 2 Vaginally Infected Mice

Excretion of Non-infectious Virus Particles Lacking Glycoprotein H by a Temperature-sensitive Mutant of Herpes Simplex Virus Type 1: Evidence that gH Is Essential for Virion Infectivity

Herpes Simplex Virus Type 2 Glycoprotein Biogenesis: Effect of Monensin on Glycoprotein Maturation, Intracellular Transport and Virus Infectivity

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