A novel role for phagocytosis-like uptake in herpes simplex virus entry

Clément, Christian; Tiwari, Vaibhav; Scanlan, P.M.; Vályi-Nagy, Tibor; Yue, Beatrice Y.J.T.; Shukla, Deepak

doi:10.1084/jem20310oia25

Cited by 47 publications

(85 citation statements)

References 26 publications

(28 reference statements)

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“…In support of Cdc42 signaling during alphaherpesvirus entry, entry of HSV-1 into primary corneal fibroblasts, Madin-Darby canine kidney II (MDCKII) cells and nectin-1-overexpressing CHO cells results in a temporary activation of Cdc42 [12,22]. In nectin-1-overexpressing CHO cells, brief Cdc42 activation was accompanied with a more extended RhoA activation and the induction of filopodia-like structures within 30 min of virus attachment [12] (Figure 1).…”

Section: Virus Entry In Host Cellsmentioning

confidence: 96%

“…In nectin-1-overexpressing CHO cells, brief Cdc42 activation was accompanied with a more extended RhoA activation and the induction of filopodia-like structures within 30 min of virus attachment [12] (Figure 1). Virus particles associated preferentially with these filopodia, possibly facilitating 'surfing' on the plasma membrane, an actin-myosin-driven transport process that has been described to precede cellular entry of different viruses [23].…”

Section: Virus Entry In Host Cellsmentioning

confidence: 99%

“…Inhibition of actin polymerization in Vero cells has little or no effect on virus entry, indicating that this type of entry does not depend on actin directly [9,10]. However, accumulating evidence suggests alternative pH-dependent and -independent endocytic entry routes for alphaherpesviruses in a variety of cell types, including primary human corneal fibroblasts, human epidermal keratinocytes, C10 murine melanoma cells, Chinese hamster ovary (CHO) cells and HeLa cells [11][12][13][14]. A recent report indicates a role for actin in one of these alternative entry pathways.…”

Section: Virus Entry In Host Cellsmentioning

confidence: 99%

“…A recent report indicates a role for actin in one of these alternative entry pathways. Clement and coworkers found that HSV-1 entry in primary human corneal fibroblasts and nectin-1-overexpressing CHO cells is associated with formation of actin-based filopodia and subsequent uptake of the virus particles through a phagocytosis-like process [12]. In addition, cytochalasin D and latrunculin B, two inhibitors of actin polymerization, blocked uptake of the virus efficiently [12].…”

Section: Virus Entry In Host Cellsmentioning

confidence: 99%

“…Clement and coworkers found that HSV-1 entry in primary human corneal fibroblasts and nectin-1-overexpressing CHO cells is associated with formation of actin-based filopodia and subsequent uptake of the virus particles through a phagocytosis-like process [12]. In addition, cytochalasin D and latrunculin B, two inhibitors of actin polymerization, blocked uptake of the virus efficiently [12]. The dependence of herpesviruses on actin polymerization for successful entry might therefore rely on the entry route taken by the virus in a particular cell type.…”

Section: Virus Entry In Host Cellsmentioning

confidence: 99%

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Actin and Rho GTPases in herpesvirus biology

Favoreel¹,

Enquist²,

Feierbach³

2007

Trends in Microbiology

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Viruses have evolved a variety of interactions with host cells to create an optimal niche for viral replication, persistence and spread. The actin cytoskeleton of the host cell and actin-regulating Rho GTPase signaling pathways can be involved in several of these interactions. This review focuses on recent findings on herpesvirus interactions with actin and Rho GTPases during viral entry, replication in the nucleus and egress. Unraveling these often fascinating interactions might also provide additional insights into sometimes poorly known aspects of actin biology (e.g. its role in the nucleus) and in the development of novel antiviral therapies.Actin filaments and actin-regulating Rho GTPase signaling pathways Filamentous actin is a key structure of the cytoskeleton in every cell. The actin cytoskeleton is involved in many crucial cellular processes, including providing cell integrity, mobility and shape; driving cell division and contraction; and the uptake of extracellular molecules.Actin filaments consist of polarized ATP-bound globular actin monomers. These filamentous actin (F-actin) molecules can associate into bundles or networks through actin cross-linking molecules. The best characterized F-actin bundles and networks are filopodia, lamellipodia and actin stress fibers. Formation of the different actin bundles and networks is regulated by signal transduction pathways that depend on small Rho GTPases [1]. Of the 22 identified mammalian Rho GTPases, the best characterized are RhoA (stress fibers), Rac1 (lamellipodia) and Cdc42 (filopodia). These Rho GTPases act as molecular switches and alternate between their active GTP-bound form and their inactive GDP-bound form. Transition from the active to the inactive form is accompanied by phosphorylation and activation of different downstream effector molecules that initiate signal transduction pathways and subsequent rearrangements in the actin cytoskeleton. These three signal transduction pathways are interwoven and the RhoA pathway generally counteracts the Rac1 and Cdc42 pathways [2]. Details of Rho GTPase signaling networks can be found elsewhere [3].Because of the many cellular functions in which they are involved, it comes as no surprise that many intracellular pathogens interact with actin and actin-regulating signaling pathways. These interactions can occur at several points in the life cycle of the pathogens, including, although not limited to, internalization, intracellular movement and intercellular spread [4,5].There are recent indications that, in particular cell types, herpesviruses also interact with actin and/or Rho GTPases during three major phases of the replication cycle of herpesviruses: entry into the cytoplasm, replication and assembly in the nucleus and maturation and egress. This review presents an overview of these data and points to future directions in research in this new and potentially important field of herpesvirus biology. Special attention is given on the alphaherpesvirus subfamily of herpesviruses, but relevant references to wor...

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Section: Virus Entry In Host Cellsmentioning

confidence: 96%

Section: Virus Entry In Host Cellsmentioning

confidence: 99%

Section: Virus Entry In Host Cellsmentioning

confidence: 99%

Section: Virus Entry In Host Cellsmentioning

confidence: 99%

Section: Virus Entry In Host Cellsmentioning

confidence: 99%

See 3 more Smart Citations

Actin and Rho GTPases in herpesvirus biology

Favoreel¹,

Enquist²,

Feierbach³

2007

Trends in Microbiology

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Actin dynamics in host–pathogen interaction

Stradal

Schelhaas

2018

FEBS Letters

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The actin cytoskeleton and Rho GTPase signaling to actin assembly are prime targets of bacterial and viral pathogens, simply because actin is involved in all motile and membrane remodeling processes, such as phagocytosis, macropinocytosis, endocytosis, exocytosis, vesicular trafficking and membrane fusion events, motility, and last but not least, autophagy. This article aims at providing an overview of the most prominent pathogen‐induced or ‐hijacked actin structures, and an outlook on how future research might uncover additional, equally sophisticated interactions.

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Myosin motors on the pathway of viral infections

2022

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Molecular motors are microscopic machines that use energy from adenosine triphosphate (ATP) hydrolysis to generate movement. While kinesins and dynein are molecular motors associated with microtubule tracks, myosins bind to and move on actin filaments. Mammalian cells express several myosin motors. They power cellular processes such as endo‐ and exocytosis, intracellular trafficking, transcription, migration, and cytokinesis. As viruses navigate through cells, they may take advantage or be hindered by host components and machinery, including the cytoskeleton. This review delves into myosins' cell roles and compares them to their reported functions in viral infections. In most cases, the previously described myosin functions align with their reported role in viral infections, although not in all cases. This opens the possibility that knowledge obtained from studying myosins in viral infections might shed light on new physiological roles for myosins in cells. However, given the high number of myosins expressed and the variety of viruses investigated in the different studies, it is challenging to infer whether the interactions found are specific to a single virus or can be applied to other viruses with the same characteristics. We conclude that the participation of myosins in viral cycles is still a largely unexplored area, especially concerning unconventional myosins.

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A novel role for phagocytosis-like uptake in herpes simplex virus entry

Cited by 47 publications

References 26 publications

Actin and Rho GTPases in herpesvirus biology

Actin and Rho GTPases in herpesvirus biology

Actin dynamics in host–pathogen interaction

Myosin motors on the pathway of viral infections

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