Cofilin 1-Mediated Biphasic F-Actin Dynamics of Neuronal Cells Affect Herpes Simplex Virus 1 Infection and Replication

Xiang, Yangfei; Zheng, Kai; Ju, Huai-Qiang; Wang, Shaoxiang; Pei, Ying; Ding, Wei-Chao; Chen, Zhenping; Wang, Qiaoli; Qiu, Xiangyun; Zhong, Meigong; Zeng, Fanli; Ren, Zhe; Chen, Qian; Liu, Ge; Kitazato, Kaio; Wang, Yifei

doi:10.1128/jvi.00609-12

Cited by 55 publications

(75 citation statements)

References 49 publications

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“…122 Recently, Jacob and coworkers demonstrated that US3-and PAK-dependent cofilin activation plays a central role in the US3-induced actin rearrangements. 123,124 HSV-1 was also found to activate cofilin although this appeared restricted to the early stages of infection. 124 Interestingly, for HSV-1, US3 has recently been reported to stabilize microtubules, which further contributes to virus spread.…”

Section: Virus Assembly and Egressmentioning

confidence: 99%

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Rho’ing in and out of cells

2014

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These authors contributed equally to this work Keywords: Rho GTPase, actin, egress, entry, gene expression, immune system, transformation, virus Rho GTPases are key regulators of actin and microtubule dynamics and organization. increasing evidence shows that many viruses have evolved diverse interactions with Rho GTPase signaling and manipulate them for their own benefit. in this review, we discuss how Rho GTPase signaling interferes with many steps in the viral replication cycle, especially entry, replication, and spread. Seen the diversity between viruses, it is not surprising that there is considerable variability in viral interactions with Rho GTPase signaling. However, several largely common effects on Rho GTPases and actin architecture and microtubule dynamics have been reported. For some of these processes, the molecular signaling and biological consequences are well documented while for others we just begin to understand them. A better knowledge and identification of common threads in the different viral interactions with Rho GTPase signaling and their ultimate consequences for virus and host may pave the way toward the development of new antiviral drugs that may target different viruses.©2014 Landes Bioscience. Do not distribute. e28318-2Small GTPases volume 5effector of ROCK, which phosphorylates and inhibits cofilin.14 Cofilin is an F-actin-severing protein. Mainly depending on the local availability of G-actin monomers, cofilin activity may lead to net actin depolymerization or increased actin polymerization and branching. Other RhoA effectors include members of the ezrin/radixin/moesin (ERM) proteins 15 . Rac1 is thought to release WAVE from an inhibited complex, thereby activating the actin-polymerizing complex Arp2/3. 16,17 Active Arp2/3 mediates branching and elongation of existing actin filaments, generating a meshwork. Cdc42 also activates Arp2/3 through a direct interaction with the Arp2/3 activators Wiskott-Aldrich syndrome protein (WASP) or N-WASP.18 Both Rac1 and Cdc42 also activate group I serine/threonine p21 activating kinases (PAK). These different signalization branches are interconnected. In general, RhoA pathway signaling counteracts the Rac1 and Cdc42 signaling axes and vice versa.Because Rho GTPase signaling is involved in a plethora of cellular processes, it is perhaps not surprising that several viral gene products have evolved to interfere with and modulate these signaling axes. Indeed, several viruses interfere with the actin cytoskeleton and Rho GTPase signaling during many steps of their replication cycle. During entry and egress, these interactions may allow or facilitate viral particle passage across the cortical actin barrier and to rearrange actin to conformations that promote virus infection and spread, while other viral processes, such as intracellular movement, gene expression and latency, but also interaction with the immune system or oncogenesis may also depend to some extent on Rho GTPase signaling and associated actin rearrangements. In this review, the current kno...

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Section: Virus Assembly and Egressmentioning

confidence: 99%

“…123,124 HSV-1 was also found to activate cofilin although this appeared restricted to the early stages of infection. 124 Interestingly, for HSV-1, US3 has recently been reported to stabilize microtubules, which further contributes to virus spread. …”

Section: Virus Assembly and Egressmentioning

confidence: 99%

Rho’ing in and out of cells

2014

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“…Phosphorylation and dephosphorylation of cofilin at S3 is complexly regulated by multiple kinases and phosphatases (10). Increasing evidence indicates that cofilin constitutes an important cellular target affected by both bacterial and viral infections (11)(12)(13)(14)(15). With regard to alphaherpesviruses, herpes simplex virus 1 (HSV-1) has been reported to induce a cell-type-dependent upregulation of cofilin levels and modulation of cofilin activity (16,17).…”

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confidence: 99%

Alphaherpesviral US3 Kinase Induces Cofilin Dephosphorylation To Reorganize the Actin Cytoskeleton

Jacob

Broeke

Troys

et al. 2013

J Virol

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bThe conserved alphaherpesviral serine/threonine kinase US3 causes dramatic actin rearrangements, associated with increased viral spread. Here, we show that US3 of pseudorabies virus (PRV) leads to activation (dephosphorylation) of the central actin regulator cofilin. A mutation that impairs US3 kinase activity and the group I p21-activated kinase inhibitor IPA-3 inhibited US3-mediated cofilin activation. Additionally, expression of phosphomimetic S3D cofilin significantly suppressed the ability of US3 to cause cell projections and cell rounding. In conclusion, the US3 kinase of PRV leads to activation (dephosphorylation) of cofilin, and cofilin contributes to US3-mediated actin rearrangements.

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“…Cofilin-1 is deactivated by phosphorylation on Ser-3 by LIM-kinase1 (LIMK1), and results in an increase in F-actin [35,36]. Disruption of the LIMK1-cofilin pathway affected viral releases of Mason-Pfizer monkey virus (M-PMV) and HIV-1 [21], as well as the entry and replication of HSV-1 [22,23,24]. However, there are no reports on IAV.…”

Section: Discussionmentioning

confidence: 99%

“…HIV-1 inactivates cofilin to optimize immune evasion, replication, release, and cell-cell transmission [19,20,21]. We have previously reported that cofilin-1 play a crucial role in mediating biphasic F-actin dynamics to facilitate HSV-1 infection and replication [22,23]. Cofilin-1 mediates the inhibition of actincytoskeleton remodeling and the anti-HSV activity of pentagalloyl glucose (PGG) [24].…”

Section: Introductionmentioning

confidence: 99%

Cofilin-1 is involved in regulation of actin reorganization during influenza A virus assembly and budding

Liu

Xiang

Guo

et al. 2014

Biochemical and Biophysical Research Communications

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Influenza A virus (IAV) assembly and budding on host cell surface plasma membrane requires actin cytoskeleton reorganization. The underlying molecular mechanism involving actin reorganization remains unclarified. In this study, we found that the natural antiviral compound petagalloyl glucose (PGG) inhibits F-actin reorganization in the host cell membrane during the late stage of IAV infection, which are associated with the suppression of total cofilin-1 level and its phosphorylation. Knock-down of cofilin-1 reduces viral yields. These findings provide the first evidence that cofilin-1 plays an important role in regulating actin reorganization during IAV assembly and budding.

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Cofilin 1-Mediated Biphasic F-Actin Dynamics of Neuronal Cells Affect Herpes Simplex Virus 1 Infection and Replication

Cited by 55 publications

References 49 publications

Rho’ing in and out of cells

Rho’ing in and out of cells

Alphaherpesviral US3 Kinase Induces Cofilin Dephosphorylation To Reorganize the Actin Cytoskeleton

Cofilin-1 is involved in regulation of actin reorganization during influenza A virus assembly and budding

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