Rabies virus matrix protein targets host actin cytoskeleton: a protein–protein interaction analysis

Zandi, Fatemeh; Khalaj, Vahid; Goshadrou, Fatemeh; Meyfour, Anna; Gholami, Alireza; Enayati, Somayeh; Mehranfar, Mahsa; Rahmati, Saman; Kheiri, Elmira Vadaye; Badie, Hamid Gholamipour; Vaziri, Behrouz

doi:10.1093/femspd/ftaa075

Cited by 11 publications

(7 citation statements)

References 54 publications

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“…Two-dimensional far-western blotting confirmed that the M protein of RABV also interacts with six different proteins in rat brain stem including the actin cytoplasmic-1 that was verified in co-immunoprecipitation. All these proteins regulate vital cellular processes as described earlier and the findings were also verified in mouse neuro-N2a cells ( 60 ).…”

Section: Resultssupporting

confidence: 66%

Rabies Virus Exploits Cytoskeleton Network to Cause Early Disease Progression and Cellular Dysfunction

Nawaz

Guo

et al. 2022

Front. Vet. Sci.

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Rabies virus (RABV) is a cunning neurotropic pathogen and causes top priority neglected tropical diseases in the developing world. The genome of RABV consists of nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G), and RNA polymerase L protein (L), respectively. The virus causes neuronal dysfunction instead of neuronal cell death by deregulating the polymerization of the actin and microtubule cytoskeleton and subverts the associated binding and motor proteins for efficient viral progression. These binding proteins mainly maintain neuronal structure, morphology, synaptic integrity, and complex neurophysiological pathways. However, much of the exact mechanism of the viral-cytoskeleton interaction is yet unclear because several binding proteins of the actin-microtubule cytoskeleton are involved in multifaceted pathways to influence the retrograde and anterograde axonal transport of RABV. In this review, all the available scientific results regarding cytoskeleton elements and their possible interactions with RABV have been collected through systematic methodology, and thereby interpreted to explain sneaky features of RABV. The aim is to envisage the pathogenesis of RABV to understand further steps of RABV progression inside the cells. RABV interacts in a number of ways with the cell cytoskeleton to produce degenerative changes in the biochemical and neuropathological trails of neurons and other cell types. Briefly, RABV changes the gene expression of essential cytoskeleton related proteins, depolymerizes actin and microtubules, coordinates the synthesis of inclusion bodies, manipulates microtubules and associated motors proteins, and uses actin for clathrin-mediated entry in different cells. Most importantly, the P is the most intricate protein of RABV that performs complex functions. It artfully operates the dynein motor protein along the tracks of microtubules to assist the replication, transcription, and transport of RABV until its egress from the cell. New remedial insights at subcellular levels are needed to counteract the destabilization of the cytoskeleton under RABV infection to stop its life cycle.

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Section: Resultssupporting

confidence: 66%

Rabies Virus Exploits Cytoskeleton Network to Cause Early Disease Progression and Cellular Dysfunction

Nawaz

Guo

et al. 2022

Front. Vet. Sci.

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“…First, the internalization and uptake of RABV requires an intact actin network, and the depolymerization of actin filaments inhibits the virus infection. Next, RABV utilizes the microtubules and the motor protein dynein/kinesin for intracellular transport [ 18 , 19 , 20 , 29 , 30 ]. During this stage, the M protein enhances the expression of cellular histone deacetylase 6 (HDAC6) to depolymerize the microtubules and facilitate viral RNA synthesis [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

“…As the major structural components of IFs in skeletal, cardiac, and some smooth muscle cells, desmin is important for the maintenance and integrity of the cytoskeleton [ 17 ]. Our identification of desmin as a novel host interactor with RABV-M is particularly intriguing since RABV exploits the cytoskeleton network to facilitate different stages of its lifecycle and the development of pathological processes [ 18 , 19 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

Host Desmin Interacts with RABV Matrix Protein and Facilitates Virus Propagation

Wen

Liu

et al. 2023

Viruses

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Microfilaments and microtubules, two crucial structures of cytoskeletal networks, are usurped by various viruses for their entry, egress, and/or intracellular trafficking, including the Rabies virus (RABV). Intermediate filaments (IFs) are the third major component of cytoskeletal filaments; however, little is known about the role of IFs during the RABV infection. Here, we identified the IF protein desmin as a novel host interactor with the RABV matrix protein, and we show that this physical interaction has a functional impact on the virus lifecycle. We found that the overexpression of desmin facilitates the RABV infection by increasing the progeny virus yield, and the suppression of endogenous desmin inhibits virus replication. Furthermore, we used confocal microscopy to observe that the RABV-M co-localizes with desmin in IF bundles in the BHK-21 cells. Lastly, we found that mice challenged with RABV displayed an enhanced expression of desmin in the brains of infected animals. These findings reveal a desmin/RABV-M interaction that positively regulates the virus infection and suggests that the RABV may utilize cellular IFs as tracks for the intracellular transport of viral components and efficient budding.

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“…Some researchers have also found that the actin filament system provides the driving force required for viral assembly, budding, and release after infection, thereby participating in the regulation of the viral life cycle [2]. Clinically, studies have demonstrated the important role of the actin filament system in viral infection-related diseases [5][6][7].…”

Section: Actin Filamentsmentioning

confidence: 99%

The regulation of host cytoskeleton during SARS-CoV-2 infection in the nervous system

Zhang

Jiu

2023

Brain Science Advances

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The global economy and public health are currently under enormous pressure since the outbreak of COVID-19. Apart from respiratory discomfort, a subpopulation of COVID-19 patients exhibits neurological symptoms such as headache, myalgia, and loss of smell. Some have even shown encephalitis and necrotizing hemorrhagic encephalopathy. The cytoskeleton of nerve cells changes drastically in these pathologies, indicating that the cytoskeleton and its related proteins are closely related to the pathogenesis of nervous system diseases. In this review, we present the up-to-date association between host cytoskeleton and coronavirus infection in the context of the nervous system. We systematically summarize cytoskeleton-related pathogen-host interactions in both the peripheral and central nervous systems, hoping to contribute to the development of clinical treatment in COVID-19 patients.

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Rabies virus matrix protein targets host actin cytoskeleton: a protein–protein interaction analysis

Cited by 11 publications

References 54 publications

Rabies Virus Exploits Cytoskeleton Network to Cause Early Disease Progression and Cellular Dysfunction

Rabies Virus Exploits Cytoskeleton Network to Cause Early Disease Progression and Cellular Dysfunction

Host Desmin Interacts with RABV Matrix Protein and Facilitates Virus Propagation

The regulation of host cytoskeleton during SARS-CoV-2 infection in the nervous system

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