Vimentin Rearrangement during African Swine Fever Virus Infection Involves Retrograde Transport along Microtubules and Phosphorylation of Vimentin by Calcium Calmodulin Kinase II

Stefanovic, Sandra; Windsor, Miriam; Nagata, Koh-ici; Inagaki, Masaki; Wileman, Thomas

doi:10.1128/jvi.79.18.11766-11775.2005

Cited by 122 publications

(111 citation statements)

References 50 publications

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“…Upon viral entry and virion release from the endosome-lysosome system into the cytoplasm, the ASFV core is transported to the MTOC (36). Meanwhile, transcription of early genes and posttranscriptional modification of the mRNA occur inside the virion; this is ensured by packaged proteins such as the viral RNA polymerase and, hence, independent of cellular enzymes (37)(38)(39)(40)(41).…”

mentioning

confidence: 99%

“…Similar to other viruses, cytoplasmic ASFV factories have been compared with aggresomes, since emerging viral factories form at the MTOC and become surrounded by vimentin and recruit cellular chaperones, ubiquitin, proteasomes, and mitochondria. Furthermore, similar to aggresomes, ASFV factories require microtubules and dynein motor proteins for their formation (36,46).…”

mentioning

confidence: 99%

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DNA Virus Replication Compartments

Schmid

Speiseder

Dobner

et al. 2014

J Virol

158

142

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bViruses employ a variety of strategies to usurp and control cellular activities through the orchestrated recruitment of macromolecules to specific cytoplasmic or nuclear compartments. Formation of such specialized virus-induced cellular microenvironments, which have been termed viroplasms, virus factories, or virus replication centers, complexes, or compartments, depends on molecular interactions between viral and cellular factors that participate in viral genome expression and replication and are in some cases associated with sites of virion assembly. These virus-induced compartments function not only to recruit and concentrate factors required for essential steps of the viral replication cycle but also to control the cellular mechanisms of antiviral defense. In this review, we summarize characteristic features of viral replication compartments from different virus families and discuss similarities in the viral and cellular activities that are associated with their assembly and the functions they facilitate for viral replication.

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confidence: 99%

mentioning

confidence: 99%

DNA Virus Replication Compartments

Schmid

Speiseder

Dobner

et al. 2014

J Virol

158

142

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“…This specialized site, close to the microtubule organizing center, contains mostly viral DNA, most of the viral proteins, immature and mature virions, and also abundant virus-induced membranes. Microtubule motors have also been proposed to be involved in at least three other events that occur in the ASFV replication cycle, namely, vimentin rearrangement into a cage that finally surrounds the viral factory (57), the recruitment of virustargeted membranes to the virus factory (54), and the transport of fully assembled virions to the plasma membrane before their release from an infected cell by budding (36).…”

mentioning

confidence: 99%

Small Rho GTPases and Cholesterol Biosynthetic Pathway Intermediates in African Swine Fever Virus Infection

Quetglas

Hernáez

Galindo

et al. 2012

J Virol

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The integrity of the cholesterol biosynthesis pathway is required for efficient African swine fever virus (ASFV) infection. Incorporation of prenyl groups into Rho GTPases plays a key role in several stages of ASFV infection, since both geranylgeranyl and farnesyl pyrophosphates are required at different infection steps. We found that Rho GTPase inhibition impaired virus morphogenesis and resulted in an abnormal viral factory size with the accumulation of envelope precursors and immature virions. Furthermore, abundant defective virions reached the plasma membrane, and filopodia formation in exocytosis was abrogated. Rac1 was activated at early ASFV infection stages, coincident with microtubule acetylation, a process that stabilizes microtubules for virus transport. Rac1 inhibition did not affect the viral entry step itself but impaired subsequent virus production. We found that specific Rac1 inhibition impaired viral induced microtubule acetylation and viral intracellular transport. These findings highlight that viral infection is the result of a carefully orchestrated modulation of Rho family GTPase activity within the host cell; this modulation results critical for virus morphogenesis and in turn, triggers cytoskeleton remodeling, such as microtubule stabilization for viral transport during early infection.

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“…They also suggest that in addition to building a protective cage, modified vimentin could play a more dynamic role, such as organizing the interior of viroplasm foci or facilitating egress and incorporation of viral proteins inside immature viral particles. 27,28 A recent study by Nitahara-Kasahara and colleagues 28,29 suggested that modulation of hepatic vimentin expression might enable the control of hepatitis C virus (HCV) production. Comparative proteomic studies of proteins in HCV core-expressing and non-expressing Huh7 cell lines, Uc39-6 and Uc321, respectively, showed that coreexpressing Uc39-6 cells had much lower vimentin content than Uc321 cells.…”

Section: Dovepressmentioning

confidence: 99%

Viral interactions with intermediate filaments: Paths less explored

Sripada¹

2010

CHC

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Vimentin Rearrangement during African Swine Fever Virus Infection Involves Retrograde Transport along Microtubules and Phosphorylation of Vimentin by Calcium Calmodulin Kinase II

Cited by 122 publications

References 50 publications

DNA Virus Replication Compartments

DNA Virus Replication Compartments

Small Rho GTPases and Cholesterol Biosynthetic Pathway Intermediates in African Swine Fever Virus Infection

Viral interactions with intermediate filaments: Paths less explored

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