Microtubules and viral infection

Silva, Eveline Santos da; Naghavi, Mojgan H.

doi:10.1016/bs.aivir.2023.02.003

Cited by 5 publications

(1 citation statement)

References 225 publications

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“…Viruses are obligate intracellular parasites that depend strictly on the host cell machinery to perform their successful replication [ 52 , 75 , 76 , 77 ]. Specifically, the cytoskeleton provides a scaffold for viral entry, sub-cellular trafficking through the dense cytosol, replication, assembly, and egression [ 78 ].…”

Section: The Cellular Cytoskeletonmentioning

confidence: 99%

Avian Influenza A Viruses Modulate the Cellular Cytoskeleton during Infection of Mammalian Hosts

De Conto

2024

Pathogens

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Influenza is one of the most prevalent causes of death worldwide. Influenza A viruses (IAVs) naturally infect various avian and mammalian hosts, causing seasonal epidemics and periodic pandemics with high morbidity and mortality. The recent SARS-CoV-2 pandemic showed how an animal virus strain could unpredictably acquire the ability to infect humans with high infection transmissibility. Importantly, highly pathogenic avian influenza A viruses (AIVs) may cause human infections with exceptionally high mortality. Because these latter infections pose a pandemic potential, analyzing the ecology and evolution features of host expansion helps to identify new broad-range therapeutic strategies. Although IAVs are the prototypic example of molecular strategies that capitalize on their coding potential, the outcome of infection depends strictly on the complex interactions between viral and host cell factors. Most of the studies have focused on the influenza virus, while the contribution of host factors remains largely unknown. Therefore, a comprehensive understanding of mammals’ host response to AIV infection is crucial. This review sheds light on the involvement of the cellular cytoskeleton during the highly pathogenic AIV infection of mammalian hosts, allowing a better understanding of its modulatory role, which may be relevant to therapeutic interventions for fatal disease prevention and pandemic management.

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Section: The Cellular Cytoskeletonmentioning

confidence: 99%

Avian Influenza A Viruses Modulate the Cellular Cytoskeleton during Infection of Mammalian Hosts

De Conto

2024

Pathogens

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Poxvirus A51R: A microtubule maestro and virulence virtuoso

McGillivary,

Luxton

2024

Cell Reports

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Zika virus NS3 drives the assembly of a viroplasm-like structure

Sultana,

Zheng,

Morton

et al. 2024

Preprint

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Zika virus (ZIKV) is a mosquito-transmitted flavivirus that caused an epidemic in 2015-2016 in the Americas and raised serious global health concerns due to its association with congenital brain developmental defects in infected pregnancies. Upon infection, ZIKV assembles virus particles in a virus-generated toroidal compartment next to the nucleus called the replication factory, or viroplasm, which forms by remodeling the host cell endoplasmic reticulum (ER). How the viral proteins control viroplasm assembly remains unknown. Here we show that the ZIKV non-structural protein 3 (NS3) is sufficient to drive the assembly of a viroplasm-like structure (VLS) in human cells. NS3 encodes a dual-function protease and RNA helicase. The VLS is similar to the ZIKV viroplasm in its assembly near centrosomes at the nuclear periphery, its deformation of the nuclear membrane, its recruitment of ER, Golgi, and dsRNA, and its association with microtubules at its surface. While sufficient to generate a VLS, NS3 is less efficient in several aspects compared to viroplasm formation upon ZIKV infection. We further show that the helicase domain and not the protease domain is required for optimal VLS assembly and dsRNA recruitment. Overall, this work advances our understanding of the mechanism of viroplasm assembly by ZIKV and likely will extend to other flaviviruses.ImportanceThe Zika virus replicates its genome and assembles virus particles in the cytoplasm within the replication organelle, a large virus-induced compartment also called the viroplasm. It does this in part by remodeling the endoplasmic reticulum. However, how the virus directs the host cell to assemble the viroplasm is mostly unknown. This study shows that Zika virus non-structural protein 3 (NS3) is sufficient to assemble a viroplasm-like structures, and indicates that NS3 has a central role in assembling the viroplasm. Understanding how the virus assembles the viroplasm compartment and NS3’s role in it should significantly advance our understanding of the cellular mechanisms of virus infection. This study aims to gain more understanding of the Zika virus and its viroplasm along with the molecular mechanisms for viroplasm assembly which might be shared by other viruses.

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Microtubules and viral infection

Cited by 5 publications

References 225 publications

Avian Influenza A Viruses Modulate the Cellular Cytoskeleton during Infection of Mammalian Hosts

Avian Influenza A Viruses Modulate the Cellular Cytoskeleton during Infection of Mammalian Hosts

Poxvirus A51R: A microtubule maestro and virulence virtuoso

Zika virus NS3 drives the assembly of a viroplasm-like structure

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