scholarly journals Neuroprotective effect of herpes simplex virus-mediated gene transfer of erythropoietin in hyperglycemic dorsal root ganglion neurons

Brain ◽  
2008 ◽  
Vol 132 (4) ◽  
pp. 879-888 ◽  
Author(s):  
M. Chattopadhyay ◽  
C. Walter ◽  
M. Mata ◽  
D. J. Fink
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Gene Transfer ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Neuroprotective Effect ◽  
Dorsal Root Ganglion Neurons ◽  
Simplex Virus ◽  
Ganglion Neurons

scholarly journals Anterograde Transport of Herpes Simplex Virus Type 1 in Cultured, Dissociated Human and Rat Dorsal Root Ganglion Neurons

2000 ◽  
Vol 74 (4) ◽  
pp. 1827-1839 ◽  
Author(s):  
Monica Miranda-Saksena ◽  
Patricia Armati ◽  
Ross A. Boadle ◽  
David J. Holland ◽  
Anthony L. Cunningham
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
De Novo ◽  
Brefeldin A ◽  
Dorsal Root Ganglion Neurons ◽  
Anterograde Transport ◽  
Simplex Virus ◽  
Ganglion Neurons

ABSTRACT The mechanism of anterograde transport of herpes simplex virus was studied in cultured dissociated human and rat dorsal root ganglion neurons. The neurons were infected with HSV-1 to examine the distribution of capsid (VP5), tegument (VP16), and glycoproteins (gC and gB) at 2, 6, 10, 13, 17, and 24 h postinfection (p.i.) with or without nocodazole (a microtubule depolymerizer) or brefeldin A (a Golgi inhibitor). Retrogradely transported VP5 was detected in the cytoplasm of the cell body up to the nuclear membrane at 2 h p.i. It was first detected de novo in the nucleus and cytoplasm at 10 h p.i., the axon hillock at 13 h p.i., and the axon at 15 to 17 h p.i. gC and gB were first detected de novo in the cytoplasm and the axon hillock at 10 h p.i. and then in the axon at 13 h p.i., which was always earlier than the detection of VP5. De novo-synthesized VP16 was first detected in the cytoplasm at 10 to 13 h p.i. and in the axon at 16 to 17 h p.i. Nocodazole inhibited the transport of all antigens, VP5, VP16, and gC or gB. The kinetics of inhibition of VP5 and gC could be dissociated. Brefeldin A inhibited the transport of gC or gB and VP16 but not VP5 into axons. Transmission immunoelectron microscopy confirmed that there were unenveloped nucleocapsids in the axon with or without brefeldin A. These findings demonstrate that glycoproteins and capsids, associated with tegument proteins, are transported by different pathways with slightly differing kinetics from the nucleus to the axon. Furthermore, axonal anterograde transport of the nucleocapsid can proceed despite the loss of most VP16.

scholarly journals In Rat Dorsal Root Ganglion Neurons, Herpes Simplex Virus Type 1 Tegument Forms in the Cytoplasm of the Cell Body

2002 ◽  
Vol 76 (19) ◽  
pp. 9934-9951 ◽  
Author(s):  
Monica Miranda-Saksena ◽  
Ross A. Boadle ◽  
Patricia Armati ◽  
Anthony L. Cunningham
Keyword(s):  
Herpes Simplex ◽  
Dorsal Root Ganglion ◽  
Cell Body ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Tegument Proteins ◽  
Viral Egress ◽  
Simplex Virus ◽  
Ganglion Neurons

ABSTRACT The herpes simplex virus type 1 (HSV-1) tegument is the least understood component of the virion, and the mechanism of tegument assembly and incorporation into virions during viral egress has not yet been elucidated. In the present study, the addition of tegument proteins (VP13/14, VP16, VP22, and US9) and envelope glycoproteins (gD and gH) to herpes simplex virions in the cell body of rat dorsal root ganglion neurons was examined by immunoelectron microscopy. All tegument proteins were detected diffusely spread in the nucleus within 10 to 12 h and, at these times, nucleocapsids were observed budding from the nucleus. The majority (96%) of these nucleocapsids had no detectable label for tegument and glycoproteins despite the presence of tegument proteins in the nucleus and glycoproteins adjacent to the nuclear membrane. Immunolabeling for tegument proteins and glycoproteins was found abundantly in the cytoplasm of the cell body in multiple discrete vesicular areas: on unenveloped, enveloped, or partially enveloped capsids adjacent to these vesicles and in extracellular virions. These vesicles and intracytoplasmic and extracellular virions also labeled with Golgi markers, giantin, mannosidase II, and TGN38. Treatment with brefeldin A from 2 to 24 h postinfection markedly inhibited incorporation into virions of VP22 and US9 but to a lesser degree with VP16 and VP13/14. These results suggest that, in the cell body of neurons, most tegument proteins are incorporated into unenveloped nucleocapsids prior to envelopment in the Golgi and the trans-Golgi network. These findings give further support to the deenvelopment-reenvelopment hypothesis for viral egress. Finally, the addition of tegument proteins to unenveloped nucleocapsids in the cell body allows access to these unenveloped nucleocapsids to one of two pathways: egress through the cell body or transport into the axon.

Apoptosis induced in the spinal cord and dorsal root ganglion by infection of herpes simplex virus type 2 in the mouse

1997 ◽  
Vol 228 (2) ◽  
pp. 99-102 ◽  
Author(s):  
Noriyuki Ozaki ◽  
Yasuo Sugiura ◽  
Mitsuaki Yamamoto ◽  
Sachihiko Yokoya ◽  
Akio Wanaka ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Dorsal Root Ganglion ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Dorsal Root ◽  
Simplex Virus
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