Microtubules in Influenza Virus Entry and Egress

Simpson, Caitlin; Yamauchi, Yohei

doi:10.3390/v12010117

Cited by 42 publications

(29 citation statements)

References 178 publications

(262 reference statements)

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“…Dynamin participates in the formation and scission of CCPs or caveolae, playing important roles in both caveolae-mediated and clathrin-mediated endocytosis [ 29 ]. Microtubules serve as tracks for vesicles moving along the membrane system [ 35 , 36 ]. Macropinocytosis is associated with plasma membrane ruffling induced by the activation of actin or microfilaments connected to the plasma membrane [ 37 ].…”

Section: Introductionmentioning

confidence: 99%

Lymphocystis Disease Virus (Iridoviridae) Enters Flounder (Paralichthys olivaceus) Gill Cells via a Caveolae-Mediated Endocytosis Mechanism Facilitated by Viral Receptors

Sheng

Zhong

Zeng

et al. 2020

IJMS

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In previous research, voltage-dependent anion channel protein 2 (VDAC2) and the receptor of activated protein C kinase 1 (RACK1) in flounder (Paralichthys olivaceus) were confirmed as functional receptors for lymphocystis disease virus (LCDV) entry; however, the underlying mechanism of VDAC2- and RACK1-mediated LCDV entry remains unclear. In this study, we elucidated the endocytosis pathway of LCDV entry into flounder gill (FG) cells by treatment with specific inhibitory agents, siRNAs, and co-localization analysis. LCDV entry was significantly inhibited by the disruption of caveolae-mediated endocytosis, dynamin, and microtubules, and the knockdown of caveoline-1 and dynamin expression, but was not inhibited by the disruption of clathrin-mediated endocytosis, micropinocytosis, or low-pH conditions. The disruption of caveolae-mediated and clathrin-mediated endocytosis was verified by the internalization of cholera toxin subunit B (CTB) and transferrin, respectively. Confocal immunofluorescence assay demonstrated that LCDV was co-localized with VDAC2 and RACK1, CTB was co-localized with VDAC2 and RACK1 and partially with LCDV, but transferrin was not co-localized with LCDV, VDAC2, or RACK1, indicating that LCDV utilized the same pathway as CTB, i.e., caveolae-mediated endocytosis. This was different from the pathway of transferrin, which used clathrin-mediated endocytosis. Furthermore, caveolin-1 was co-localized with LCDV, VDAC2, and RACK1, suggesting that caveolin-1 was involved in LCDV entry. These results revealed for the first time that LCDV entered into FG cells via caveolae-mediated endocytosis facilitated by VDAC2 and RACK1 receptors, relying on dynamin and microtubules in a pH-independent manner, which provided new insight into the molecular mechanisms of LCDV entry and potential for the development of antiviral agents, expanding our understanding of iridovirus infection.

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Section: Introductionmentioning

confidence: 99%

Lymphocystis Disease Virus (Iridoviridae) Enters Flounder (Paralichthys olivaceus) Gill Cells via a Caveolae-Mediated Endocytosis Mechanism Facilitated by Viral Receptors

Sheng

Zhong

Zeng

et al. 2020

IJMS

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“…Influenza viruses are respiratory pathogens that represent a significant threat to public health, despite the large-scale implementation of vaccination programs [ 163 ]. IAV is the prototype member of the Orthomyxoviridae that are characterized by segmented negative strand RNA genome and unlike most RNA viruses, IAV replicates in the nucleus [ 164 ].…”

Section: Main Bodymentioning

confidence: 99%

Viral Interactions with Adaptor-Protein Complexes: A Ubiquitous Trait among Viral Species

Geljic

Brlić

Musak

et al. 2021

IJMS

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Numerous viruses hijack cellular protein trafficking pathways to mediate cell entry or to rearrange membrane structures thereby promoting viral replication and antagonizing the immune response. Adaptor protein complexes (AP), which mediate protein sorting in endocytic and secretory transport pathways, are one of the conserved viral targets with many viruses possessing AP-interacting motifs. We present here different mechanisms of viral interference with AP complexes and the functional consequences that allow for efficient viral propagation and evasion of host immune defense. The ubiquity of this phenomenon is evidenced by the fact that there are representatives for AP interference in all major viral families, covered in this review. The best described examples are interactions of human immunodeficiency virus and human herpesviruses with AP complexes. Several other viruses, like Ebola, Nipah, and SARS-CoV-2, are pointed out as high priority disease-causative agents supporting the need for deeper understanding of virus-AP interplay which can be exploited in the design of novel antiviral therapies.

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“…The cytoskeleton components provide a dynamic framework for viral trafficking in the cytoplasm. They are involved in the entire process of the virus in the host, providing efficient elimination, replication, and egress exit [311]. In the first step, the spike protein binds to the cell surface.…”

Section: The Hypothesismentioning

confidence: 99%

A Bioelectromagnetic Proposal Approaching the Complex Challenges of COVID-19

Szász¹

2021

OJBIPHY

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Microtubules in Influenza Virus Entry and Egress

Cited by 42 publications

References 178 publications

Lymphocystis Disease Virus (Iridoviridae) Enters Flounder (Paralichthys olivaceus) Gill Cells via a Caveolae-Mediated Endocytosis Mechanism Facilitated by Viral Receptors

Lymphocystis Disease Virus (Iridoviridae) Enters Flounder (Paralichthys olivaceus) Gill Cells via a Caveolae-Mediated Endocytosis Mechanism Facilitated by Viral Receptors

Viral Interactions with Adaptor-Protein Complexes: A Ubiquitous Trait among Viral Species

A Bioelectromagnetic Proposal Approaching the Complex Challenges of COVID-19

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