The Herpesvirus Capsid Surface Protein, VP26, and the Majority of the Tegument Proteins Are Dispensable for Capsid Transport toward the Nucleus

Antinone, Sarah E.; Shubeita, George T.; Coller, Kelly E.; Lee, Joy I.; Haverlock-Moyns, Sarah; Gross, Steven P.; Smith, Greg

doi:10.1128/jvi.00026-06

Cited by 68 publications

(65 citation statements)

References 26 publications

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“…This centripetal cytoplasmic transport in association with microtubules was shown in HSV-1 infected cells and is most likely conserved in alphaherpesviruses [41]. However, the virus protein(s) that mediate(s) this transport is (are) still unknown but is (are) expected to be either viral tegument proteins, or a surface component of the capsid itself [4,165].…”

Section: Bohv-1 Replication In the Cellmentioning

confidence: 79%

Bovine herpesvirus 1 infection and infectious bovine rhinotracheitis

et al. 2007

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-Bovine herpesvirus 1 (BoHV-1), classified as an alphaherpesvirus, is a major pathogen of cattle. Primary infection is accompanied by various clinical manifestations such as infectious bovine rhinotracheitis, abortion, infectious pustular vulvovaginitis, and systemic infection in neonates. When animals survive, a life-long latent infection is established in nervous sensory ganglia. Several reactivation stimuli can lead to viral re-excretion, which is responsible for the maintenance of BoHV-1 within a cattle herd. This paper focuses on an updated pathogenesis based on a molecular characterization of BoHV-1 and the description of the virus cycle. Special emphasis is accorded to the impact of the latency and reactivation cycle on the epidemiology and the control of BoHV-1. Several European countries have initiated BoHV-1 eradication schemes because of the significant losses incurred by disease and trading restrictions. The vaccines used against BoHV-1 are described in this context where the differentiation of infected from vaccinated animals is of critical importance to achieve BoHV-1 eradication.

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Section: Bohv-1 Replication In the Cellmentioning

confidence: 79%

Bovine herpesvirus 1 infection and infectious bovine rhinotracheitis

et al. 2007

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“…In addition, removal of outer tegument proteins to expose inner tegument proteins has been shown to enhance the in vitro MT-dependent transport of HSV-1 capsids [70]. These tegument proteins are therefore the likely complementary candidates to pUL35 for engaging the dynein/ dynactin complex [65,66,70]. In the case of pUL36 and pUL37, our laboratory has failed to detect a direct interaction with the subunits of dynein using the yeast two-hybrid assay [62].…”

Section: Dynein Cofactor: Dynactinmentioning

confidence: 99%

“…Recently, two studies with both PrV and HSV-1 lacking pUL35 have shown no significant effect on dynein-dependent retrograde viral transport in cell culture [65,66]. The relative contribution of other tegument or capsid proteins to HSV-1 transport is not known, although it has been suggested that the major tegument protein pUL36, or one of the minor capsid proteins such as pUL25, may also contribute to dynein binding in vivo [51,67].…”

Section: Dynein Cofactor: Dynactinmentioning

confidence: 99%

Transport and egress of herpes simplex virus in neurons

Diefenbach

Miranda-Saksena

Douglas

et al. 2007

Reviews in Medical Virology

166

150

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The mechanisms of axonal transport of the alphaherpesviruses, HSV and pseudorabies virus (PrV), in neuronal axons are of fundamental interest, particularly in comparison with other viruses, and offer potential sites for antiviral intervention or development of gene therapy vectors. These herpesviruses are transported rapidly along microtubules (MTs) in the retrograde direction from the axon terminus to the dorsal root ganglion and then anterogradely in the opposite direction. Retrograde transport follows fusion and deenvelopment of the viral capsid at the axonal membrane followed by loss of most of the tegument proteins and then binding of the capsid via one or more viral proteins (VPs) to the retrograde molecular motor dynein. The HSV capsid protein pUL35 has been shown to bind to the dynein light chain Tctex1 but is likely to be accompanied by additional dynein binding of an inner tegument protein. The mechanism of anterograde transport is much more controversial with different processes being claimed for PrV and HSV: separate transport of HSV capsid/tegument and glycoproteins versus PrV transport as an enveloped virion. The controversy has not been resolved despite application, in several laboratories, of confocal microscopy (CFM), realtime fluorescence with viruses dual labelled on capsid and glycoprotein, electron microscopy in situ and immunoelectron microscopy. Different processes for each virus seem counterintuitive although they are the most divergent in the alphaherpesvirus subfamily. Current hypotheses suggest that unenveloped HSV capsids complete assembly in the axonal growth cones and varicosities, whereas with PrV unenveloped capsids are only found travelling in a retrograde direction.

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“…In the axons of sensory neurons, incoming HSV capsids are moved by retrograde transport, whereas newly assembled capsids undergo bidirectional and salutatory motions, indicating a modulation of the plus-end directed motility 46 . This modulation involves HSV tegument proteins [47][48][49][50][51] , the removal of which precedes the retrograde transport of the incoming capsids to the cell body, whereas the addition is coupled to anterograde transport of progeny capsids to the distal axon 52,53 . Important signalling events might occur during viral transport.…”

Section: Viral Transportmentioning

confidence: 99%

Virus trafficking – learning from single-virus tracking

2007

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What could be a better way to study virus trafficking than 'miniaturizing oneself' and 'taking a ride with the virus particle' on its journey into the cell? Single-virus tracking in living cells potentially provides us with the means to visualize the virus journey. This approach allows us to follow the fate of individual virus particles and monitor dynamic interactions between viruses and cellular structures, revealing previously unobservable infection steps. The entry, trafficking and egress mechanisms of various animal viruses have been elucidated using this method. The combination of single-virus trafficking with systems approaches and state-of-the-art imaging technologies should prove exciting in the future.

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The Herpesvirus Capsid Surface Protein, VP26, and the Majority of the Tegument Proteins Are Dispensable for Capsid Transport toward the Nucleus

Cited by 68 publications

References 26 publications

Bovine herpesvirus 1 infection and infectious bovine rhinotracheitis

Bovine herpesvirus 1 infection and infectious bovine rhinotracheitis

Transport and egress of herpes simplex virus in neurons

Virus trafficking – learning from single-virus tracking

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