The molecular basis of herpes simplex virus pathogenicity

Fawl, Randall L.; Roizman, Bernard

doi:10.1006/smvy.1994.1029

Cited by 13 publications

(7 citation statements)

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“…Explantation of ganglia is a primary means of experimentally reactivating HSV from the latent state. Other stimuli, such as scarification of the infected animals' eyes, will also induce viral replication, although at a significantly lower frequency (22) and an altered reactivation time course. To explore further the correlation between C1 localization and HSV reactivation, ganglia were removed and immediately fixed at various times after eye scarification.…”

Section: Resultsmentioning

confidence: 99%

Nuclear localization of the C1 factor (host cell factor) in sensory neurons correlates with reactivation of herpes simplex virus from latency

Kristie

Vogel

Sears

1999

Proc. Natl. Acad. Sci. U.S.A.

112

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After a primary infection, herpes simplex virus is maintained in a latent state in neurons of sensory ganglia until complex stimuli reactivate viral lytic replication. Although the mechanisms governing reactivation from the latent state remain unknown, the regulated expression of the viral immediate early genes represents a critical point in this process. These genes are controlled by transcription enhancer complexes whose assembly requires and is coordinated by the cellular C1 factor (host cell factor). In contrast to other tissues, the C1 factor is not detected in the nuclei of sensory neurons. Experimental conditions that induce the reactivation of herpes simplex virus in mouse model systems result in rapid nuclear localization of the protein, indicating that the C1 factor is sequestered in these cells until reactivation signals induce a redistribution of the protein. The regulated localization suggests that C1 is a critical switch determinant of the viral lytic-latent cycle.

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Section: Resultsmentioning

confidence: 99%

Nuclear localization of the C1 factor (host cell factor) in sensory neurons correlates with reactivation of herpes simplex virus from latency

Kristie

Vogel

Sears

1999

Proc. Natl. Acad. Sci. U.S.A.

112

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“…Interestingly, the BVP22 gene is not considered an essential BHV-1 survival gene (17), but the HVP22 gene is essential for HSV-1 replication (12). A BVP22-deleted BHV-1 mutant was capable of replication in cell culture although at a significantly reduced yield (17).…”

Section: Discussionmentioning

confidence: 99%

“…Nevertheless, BVP22 predominantly localizes to the nucleus during BHV-1 infection (17), while HVP22 localizes primarily to the cytoplasm early during HSV-1 infection and accumulates in the nucleus late in HSV-1 infection (8,23). Further, the BVP22 gene is not considered an essential gene for viral replication (16), while the HVP22 gene is considered essential (12). These distinctions between the VP22 homologs suggest that BVP22 and HVP22 have different functional properties.…”

mentioning

confidence: 99%

Distinctions between Bovine Herpesvirus 1 and Herpes Simplex Virus Type 1 VP22 Tegument Protein Subcellular Associations

Harms

Ren

Oliveira

et al. 2000

J Virol

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The alphaherpesvirus tegument protein VP22 has been characterized with multiple traits including microtubule reorganization, nuclear localization, and nonclassical intercellular trafficking. However, all these data were derived from studies using herpes simplex virus type 1 (HSV-1) and may not apply to VP22 homologs of other alphaherpesviruses. We compared subcellular attributes of HSV-1 VP22 (HVP22) with bovine herpesvirus 1 (BHV-1) VP22 (BVP22) using green fluorescent protein (GFP)-fused VP22 expression vectors. Fluorescence microscopy of cell lines transfected with these constructs revealed differences as well as similarities between the two VP22 homologs. Compared to that of HVP22, the BVP22 microtubule interaction was much less pronounced. The VP22 nuclear interaction varied, with a marbled or halo appearance for BVP22 and a speckled or nucleolus-bound appearance for HVP22. Both VP22 homologs associated with chromatin at various stages of mitosis and could traffic from expressing cells to the nuclei of nonexpressing cells. However, distinct qualitative differences in microtubule, nuclear, and chromatin association as well as trafficking were observed. The differences in VP22 homolog characteristics revealed in this study will help define VP22 function within HSV-1 and BHV-1 infection.As with those of other alphaherpesviruses, the bovine herpesvirus 1 (BHV-1) virion contains a complex structure called the tegument located between the nucleocapsid and the virus envelope (21). Limited data elucidating the functions of the various BHV-1 tegument proteins exist. In fact, practically all information about this crucial alphaherpesvirus virion structure has been obtained from studies with herpes simplex virus type 1 (HSV-1). Tegument proteins are first to encounter the intracellular environment and provide essential functions to subjugate the host cell (20). The tegument can assemble into a stable structure without capsid interaction, and its assembly or dissociation depends on the phosphorylation state of its structural proteins (15,21). However, the site and mechanisms of tegument assembly and the functions of its protein components are largely unknown.Homologs of the major HSV-1 tegument proteins VP13/14, VP16, and VP22 are found in BHV-1. Available information suggests similar as well as distinct roles for each BHV-1 and HSV-1 tegument homolog. The BHV-1 homolog to HSV-1 VP13/14 (HVP13/14) is BHV-1 VP8 (BVP8), the most abundant BHV-1 protein (14). Like HVP13/14, BVP8 contains Olinked carbohydrates acquired during transport of tegumented nucleocapsids through the Golgi (27). Compared to HVP13/ 14, BVP8 has less affinity for the nucleocapsid (19). Whether BVP8 can modulate alpha gene expression as does HVP13/14 is not known (30). HVP16 and BVP16 are both transcription activators that can recruit host homeodomain proteins Oct-1 and HCF into a transcriptional regulatory complex. However, they differ in DNA recognition, binding to HSV-1-or BHV-1-specific response element sequences (13). BVP22, like HVP22, is a phosp...

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“…These features have been taken as indications of a regulatory role for this viral protein in virus replication (6). For HSV, UL49 is classified as an essential gene (7). In this study, we constructed a partial UL49h gene deletion mutant.…”

Section: Nuclear Localization Of Ul49h Proteinmentioning

confidence: 99%

Characterization of bovine herpesvirus 1 UL49 homolog gene and product: bovine herpesvirus 1 UL49 homolog is dispensable for virus growth

Liang

Chow

et al. 1995

J Virol

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The sequence of the bovine herpesvirus 1 (BHV-1) gene that is homologous to the herpes simplex virus UL49 gene was determined. The BHV-1 UL49 homolog open reading frame consists of 774 bp and is capable of encoding 258 amino acids. Northern (RNA) blot analysis showed that the BHV-1 UL49 homolog is transcribed into a 1.1-kb RNA which is coterminal with the transcripts of an upstream UL49.5 homolog gene. Rabbit antisera produced against synthetic peptides of the predicted UL49 homolog gene product recognized a polypeptide of 33 to 35 kDa in both virus-infected cells and isolated virions. Further analysis by unionicdetergent partition of isolated virions suggested that the UL49 homolog gene product is a virion tegument protein. Indirect immunofluorescence assay revealed that the UL49 homolog gene product was predominantly localized in the nuclei of BHV-1-infected cells. A mutant virus with the UL49 homolog gene deleted was produced, and it was able to replicate in noncomplementing cells. Nevertheless, the yield of mutant virus was significantly reduced. The results from this study suggest that the BHV-1 UL49 homolog gene encodes a nuclear protein which constitutes a tegument component in mature virions and that it is dispensable for virus growth in cell culture.

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The molecular basis of herpes simplex virus pathogenicity

Cited by 13 publications

References 0 publications

Nuclear localization of the C1 factor (host cell factor) in sensory neurons correlates with reactivation of herpes simplex virus from latency

Nuclear localization of the C1 factor (host cell factor) in sensory neurons correlates with reactivation of herpes simplex virus from latency

Distinctions between Bovine Herpesvirus 1 and Herpes Simplex Virus Type 1 VP22 Tegument Protein Subcellular Associations

Characterization of bovine herpesvirus 1 UL49 homolog gene and product: bovine herpesvirus 1 UL49 homolog is dispensable for virus growth

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