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A conserved alpha-herpesvirus protein necessary for axonal localization of viral membrane proteins.

Tomishima MJ, Enquist LW - J. Cell Biol. (2001)

Bottom Line: We conclude that the Us9 membrane protein controls axonal localization of diverse viral membrane proteins but not that of capsid or tegument proteins.The data support a model where virion subassemblies but not complete virions are transported in the axon.Our results provide new insight into the process of virion assembly and exit from neurons that leads to directional spread of herpesviruses in the nervous system.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.

ABSTRACT
Pseudorabies virus, an alpha-herpesvirus, is capable of infecting the nervous system and spreading between synaptically connected neurons in diverse hosts. At least three viral membrane proteins (gE, gI, and Us9) are necessary for the spread of infection from presynaptic to postsynaptic neurons (anterograde spread) in infected rodents. To understand how these proteins effect anterograde spread between neurons, we analyzed the subcellular localization of viral proteins after infection of cultured rat sympathetic neurons with wild-type or mutant viruses. After Us9- mutant infections but not gE- mutant infections, only a subset of the viral structural proteins had entered axons. Surprisingly, capsid and tegument proteins but not viral membrane proteins were detected in axons. The spread of Us9 missense mutants in the rodent nervous system correlated with the amount of viral membrane proteins localized to axons. We conclude that the Us9 membrane protein controls axonal localization of diverse viral membrane proteins but not that of capsid or tegument proteins. The data support a model where virion subassemblies but not complete virions are transported in the axon. Our results provide new insight into the process of virion assembly and exit from neurons that leads to directional spread of herpesviruses in the nervous system.

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Related in: MedlinePlus

Colocalization of Us9 with other viral membrane proteins within the axon. Neurons were infected with the wild-type virus such that every neuron was infected for 6 h, and then antibodies to Us9 (A, D, and G) and gB (B), gC (E), or gE (H) were added. The merged images are shown in C, F, and I with Us9 in green and the corresponding membrane protein in red. Bar, 10 μm.
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fig6: Colocalization of Us9 with other viral membrane proteins within the axon. Neurons were infected with the wild-type virus such that every neuron was infected for 6 h, and then antibodies to Us9 (A, D, and G) and gB (B), gC (E), or gE (H) were added. The merged images are shown in C, F, and I with Us9 in green and the corresponding membrane protein in red. Bar, 10 μm.

Mentions: We examined the colocalization of Us9 and other viral membrane proteins during wild-type infections. Us9 was observed on vesicles close to the cell body of an infected neuron (Fig. 6 , A–C, gB; D–F, gC; and G–I, gE) but often did not colocalize with viral membrane proteins containing vesicles in the distal axon.


A conserved alpha-herpesvirus protein necessary for axonal localization of viral membrane proteins.

Tomishima MJ, Enquist LW - J. Cell Biol. (2001)

Colocalization of Us9 with other viral membrane proteins within the axon. Neurons were infected with the wild-type virus such that every neuron was infected for 6 h, and then antibodies to Us9 (A, D, and G) and gB (B), gC (E), or gE (H) were added. The merged images are shown in C, F, and I with Us9 in green and the corresponding membrane protein in red. Bar, 10 μm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196449&req=5

fig6: Colocalization of Us9 with other viral membrane proteins within the axon. Neurons were infected with the wild-type virus such that every neuron was infected for 6 h, and then antibodies to Us9 (A, D, and G) and gB (B), gC (E), or gE (H) were added. The merged images are shown in C, F, and I with Us9 in green and the corresponding membrane protein in red. Bar, 10 μm.
Mentions: We examined the colocalization of Us9 and other viral membrane proteins during wild-type infections. Us9 was observed on vesicles close to the cell body of an infected neuron (Fig. 6 , A–C, gB; D–F, gC; and G–I, gE) but often did not colocalize with viral membrane proteins containing vesicles in the distal axon.

Bottom Line: We conclude that the Us9 membrane protein controls axonal localization of diverse viral membrane proteins but not that of capsid or tegument proteins.The data support a model where virion subassemblies but not complete virions are transported in the axon.Our results provide new insight into the process of virion assembly and exit from neurons that leads to directional spread of herpesviruses in the nervous system.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.

ABSTRACT
Pseudorabies virus, an alpha-herpesvirus, is capable of infecting the nervous system and spreading between synaptically connected neurons in diverse hosts. At least three viral membrane proteins (gE, gI, and Us9) are necessary for the spread of infection from presynaptic to postsynaptic neurons (anterograde spread) in infected rodents. To understand how these proteins effect anterograde spread between neurons, we analyzed the subcellular localization of viral proteins after infection of cultured rat sympathetic neurons with wild-type or mutant viruses. After Us9- mutant infections but not gE- mutant infections, only a subset of the viral structural proteins had entered axons. Surprisingly, capsid and tegument proteins but not viral membrane proteins were detected in axons. The spread of Us9 missense mutants in the rodent nervous system correlated with the amount of viral membrane proteins localized to axons. We conclude that the Us9 membrane protein controls axonal localization of diverse viral membrane proteins but not that of capsid or tegument proteins. The data support a model where virion subassemblies but not complete virions are transported in the axon. Our results provide new insight into the process of virion assembly and exit from neurons that leads to directional spread of herpesviruses in the nervous system.

Show MeSH
Related in: MedlinePlus