Further characterization of virus obtained from herpes simplex virus type 1 recurrences and primary infections. Influence of the temperature of incubation upon glycoprotein synthesis and virus release

Costanzo, F.; Borgatti, M.; Bartoletti, Anna Maria; Foà-Tomasi, Laura; Cassai, Enzo; Mannini-Palenzona, A

doi:10.1007/bf01310883

Cited by 7 publications

(3 citation statements)

References 5 publications

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“…Small-plaque production by clinical isolates (14,15,17,27) and its correlation with limited virion release and a block in processing of multiple glycoproteins have been described for other low-passage HSV-1 isolates (15). HSV glycoproteins are incorporated into the envelope within the endoplasmic reticulum and are processed from the high-mannose precursor form to the sialylated mature form as the virion progresses through the Golgi apparatus, and then the virus is released by exocytosis or cell lysis (36).…”

Section: Discussionmentioning

confidence: 99%

Intrastrain Variants of Herpes Simplex Virus Type 1 Isolated from a Neonate with Fatal Disseminated Infection Differ in the ICP34.5 Gene, Glycoprotein Processing, and Neuroinvasiveness

Bower

Mao

Durishin

et al. 1999

J Virol

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Two intrastrain variants of herpes simplex virus type 1 (HSV-1) were isolated from a newborn with fatal disseminated infection. A small-plaque-producing variant (SP7) was the predominant virus (>99%) in the brain, and a large-plaque-producing variant (LP5) was the predominant virus (>99%) in the lung and gastrointestinal tract. EcoRI and BamHI restriction fragment patterns indicated that SP7 and LP5 are related strains. The large-plaque variants produced plaques similar in size to those produced by HSV-1 KOS. Unlike LP5 or KOS, SP7 was highly cell associated and processing of glycoprotein C and glycoprotein D was limited to precursor forms in infected Vero cells. The large-plaque phenotype from KOS could be transferred into SP7 by cotransfection of plasmids containing the EK or JK EcoRI fragment or a 3-kb plasmid with the UL34.5 gene of HSV-1 KOS together with SP7 DNA. PCR analysis using primers from within the ICP34.5 gene indicated differences for SP7, LP5, and KOS. Sequencing data indicated two sets of deletions in the UL34.5 gene that distinguish SP7 from LP5. Both SP7 and LP5 variants were neurovirulent (lethal following intracranial inoculation of young BALB/c mice); however, the LP5 variant was much less able to cause lethal neuroinvasive disease (footpad inoculation) whereas KOS caused no disease. Passage of SP7 selected for viruses (SLP-5 and SLP-10) which were attenuated for lethal neuroinvasive disease, were not cell-associated, and differed in the UL34.5 gene. UL34.5 from SLP-5 or SLP-10 resembled that of KOS. These findings support a role for UL34.5 in promoting virus egress and for neuroinvasive disease.

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Section: Discussionmentioning

confidence: 99%

Intrastrain Variants of Herpes Simplex Virus Type 1 Isolated from a Neonate with Fatal Disseminated Infection Differ in the ICP34.5 Gene, Glycoprotein Processing, and Neuroinvasiveness

Bower

Mao

Durishin

et al. 1999

J Virol

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“…Consequently, a high degree of virulence is generally the rule (Dix et al, 1983). Such virulence in mice may possibly be due to alterations in the virus resulting from tissue culture passage (Costanzo et al, 1986;Rajcani & Szanto, 1973). In any case, HSV is generally benign in the human population, and even given infection ofthe brain (Adams & Victor, 1981), survival is higher than in most animal studies, where 100% mortality is often the rule.…”

Section: Discussionmentioning

confidence: 99%

Temporal development of the behavioral effects of herpes encephalitis in mice

McFarland

1989

Psychobiology

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The temporal development of behavioral effects due to central nervous system infection with the herpes simplex type 1 virus was examined in two mouse models. Following infection of adult female NY AlNylar mice with the HF strain of herpes, or adult female BALB/c mice with the F strain, the majority of animals survived. An increase in motor activity observed 7 days following infection of NY AlNylar mice coincided in time with a decline in brain virus titers. Likewise, an increase in errors occurring during serial-reversal performance in a water Y-maze was observed 8 days following infection of Balb/c mice and coincided with the declining phase of the viral growth curve. Taken together, these results suggest that processes involved in the elimination ofthe virus from the brain, such as the cellular immune response, may be important in the development of behavioral effects produced by nonfatal herpes encephalitis.A variety of model systems have been used to examine the development of virus-induced pathology. Cell-culture models are currently popular in the field ofvirology (e.g., Heeg, Dienes, Muller, & Falke, 1986), and in the case of neurotropic viruses, celliines with neuronal properties have been used (e.g., Rubenstein & Price, 1983). Although such simplified systems may at times aid in the analysis ofthe nature ofthe pathological process, in vivo systems offer an added advantage when factors such as the immune response ofthe host are considered. The impact of virus infection may be indexed by parameters such as biochemical alterations in the target organ system (e.g., Seegal & McFarland, 1988). However, the consequences of virus infection on the functioning of the target organ system represents an index that is more meaningful to the survival of the organism. In the case of neurotropic viruses, the target organ system is the brain and the appropriate functional index is the behavior of the organism.The herpes simplex type 1 virus (HSV) is one of the more common causes of sporadic viral encephalitis in the human population and is noted for severe neurobehavioral disturbances (Adams & Victor, 1981). Ofthese, a postencephalitic amnesic syndrome is perhaps best known (Hierons, Janota, & Corsellis, 1978). Behavioral effects of HSV infection have been examined in several animal model systems (Lycke & Roos, 1974;McFarland & Hotchin, 1983;Seegal & Hotchin, 1978).Lycke and Roos (1974) examined young mice inoculated with fatal strains of HSV. They observed a gradual increase in the level of motor activity starting on the second day after intracerebral inoculaton and continuing until death occurred starting on the fourth day postinoculation. There is a considerable degree of variation in mortality and the rate of virus growth in the brain following infection with different strains of HSV (Dix, McKendall, & Baringer, 1983). Although it is very likely that very high brain virus titers were rapidly reached in the study by Lycke and Roos (1974), this information was not reported in that publication. Accordingly, the present ...

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“…Although these viruses are replication competent, they exhibit very different tissue culture and biochemical behaviors than KOS, F and other large plaque strains [9,14,23]. KOS is also a model attenuated HSV-1 strain [18,36,38].…”

Section: Introductionmentioning

confidence: 99%

A block in glycoprotein processing correlates with small plaque morphology and virion targetting to cell-cell junctions for an oral and an anal strain of herpes simplex virus type-1

Dick

Rosenthal

1995

Archives of Virology

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The characteristics of two clinical isolates of HSV-1 obtained from an oral (424) and an anal (490) lesion were compared with the highly passaged KOS strain. In contrast to KOS, the clinical isolates produced small plaques, were more cell-associated and the predominant viral glycoprotein species for gC and gD in infected cell lysates was the precursor, high mannose glycoform. Total virus production in Vero cells was equivalent for the three virus strains in one-step growths. Pulse-chase studies of glycoprotein C processing showed a reduction in rate at 7.5 h post infection and a significant block in processing at 10.5 h post infection for 424 and 490 but not KOS. Similar results were obtained for gD. The significant reduction in glycoprotein processing for 424 and 490 suggests a block in transport of viral glycoproteins or virions to and through the Golgi apparatus. Extracellular virions and the cell surface, prior to cell lysis, contained the processed gC glycoform suggesting a competent cellular glycan processing system. Upon co-infection of 424 or 490 with KOS or a gC- KOS strain, gC was processed to levels equivalent to KOS indicating that 424 and 490 are not inhibitory but that an activity(s) encoded by KOS facilitates maturation of gC from 424 and 490. Unlike KOS infected Vero cells, virion-containing vacuoles were observed in the cytoplasm at 12 h p.i. and extracellular virions were concentrated at cell-cell junctions of 424 or 490 infected cells but not in the perinuclear region. These results suggest that intracellular transport of viral glycoproteins and virions in 424 and 490 infected cells is different from KOS infected cells. The reduced level of viral glycoprotein maturation, virus release, cell surface presence and presence of virions at cell-cell junctions are consistent with small plaque production in tissue culture cells.

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Further characterization of virus obtained from herpes simplex virus type 1 recurrences and primary infections. Influence of the temperature of incubation upon glycoprotein synthesis and virus release

Cited by 7 publications

References 5 publications

Intrastrain Variants of Herpes Simplex Virus Type 1 Isolated from a Neonate with Fatal Disseminated Infection Differ in the ICP34.5 Gene, Glycoprotein Processing, and Neuroinvasiveness

Intrastrain Variants of Herpes Simplex Virus Type 1 Isolated from a Neonate with Fatal Disseminated Infection Differ in the ICP34.5 Gene, Glycoprotein Processing, and Neuroinvasiveness

Temporal development of the behavioral effects of herpes encephalitis in mice

A block in glycoprotein processing correlates with small plaque morphology and virion targetting to cell-cell junctions for an oral and an anal strain of herpes simplex virus type-1

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