Exosomes-mediated transmission of foot-and-mouth disease virus in vivo and in vitro

Zhang, Keshan; Xu, Shiqiang; Shi, Xijuan; Xu, Guangyu; Shen, Chao; Liu, Xiangtao; Zheng, Haixue

doi:10.1016/j.vetmic.2019.04.030

Cited by 29 publications

(15 citation statements)

References 56 publications

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“…The results showed that the SVV-exo group had a higher copy number on non-susceptible cells than the SVV control group, indicating that SVV-exo mediated the proliferation of SVV. Henceforth, the results suggest that exosomes can serve as delivery vectors for pathogen-associated molecules [ 23 ]. In addition, their role in viral infections is attracting more and more attention [ 24 , 25 ].…”

Section: Discussionmentioning

confidence: 99%

Intercellular transmission of Seneca Valley virus mediated by exosomes

Shi

et al. 2020

Vet Res

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Seneca Valley virus (SVV) is a non-encapsulated single-stranded positive-strand RNA virus whose transmission routes have not yet been fully elucidated. Exosomes have been implicated in the intercellular transport of a variety of materials, such as proteins, RNA, and liposomes. However, whether exosomes can mediate SVV intercellular transmission remains unknown. In this study, we extracted exosomes from SVV-infected IBRS-2 cells to investigate intercellular transmission. Our results suggest that the intercellular transmission of SVV is mediated by exosomes. The results of co-localization and RT-qPCR studies showed that exosomes harbor SVV and enable the virus to proliferate in both susceptible and non-susceptible cells. Furthermore, the replication of SVV was inhibited when IBRS-2 cells were treated with interfering RNA Rab27a and exosome inhibitor GW4869. Finally, neutralization experiments were performed to further verify whether the virus was encapsulated by the exosomes that mediated transmission between cells. It was found that exosome-mediated intercellular transmission was not blocked by SVV-specific neutralizing antibodies. This study reveals a new transmission route of SVV and provides clear evidence regarding the pathogenesis of SVV, information which can also be useful for identifying therapeutic interventions.

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Section: Discussionmentioning

confidence: 99%

Intercellular transmission of Seneca Valley virus mediated by exosomes

Shi

et al. 2020

Vet Res

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“…It was also shown that ZIKV is able to induce the amplification of EV production through increased expression and activity of SMPD3 and that EVs containing viral RNAs and proteins promote viral transmission (Zhou W. et al, 2019). FMDV (foot and mouth disease virus) can also be transmitted through host EVs that carry genomic RNAs and some viral proteins, and FMDV replication is not fully blocked by neutralizing antibodies, suggesting an immune evasion mechanism (Zhang et al, 2019). For SFTS (a tick-borne bunyavirus associated with hemorrhagic fever), exosomes from infected cells contained viable virions that were able to infect cells by an alternative route independent of classical receptors (Silvas et al, 2016).…”

Section: Vesicles or Viral Particles? Overlap Between Viral Budding Amentioning

confidence: 99%

“…EVs facilitate viral transmission HSV-1 (Bello-Morales and López-Guerrero, 2020), KSHV (Chen et al, 2020)., NDV (Zhou C. et al, 2019), PRRSV (Wang et al, 2017), enterovirus 71 (Gu et al, 2020), HCV (Bukong et al, 2014), HIV (Kadiu et al, 2012), SFTS (Silvas et al, 2016) Viral RNAs/proteins inside EVs Coronavirus (Maeda et al, 1999), EBV (Keryer-Bibens et al, 2006), HCV (Kouwaki et al, 2017)., HTLV-1, (Jaworski et al, 2014), RVFV (Ahsan et al, 2016), ZIKV (Zhou W. et al, 2019;Martıńez-Rojas et al, 2020) Infectious virus-like particles/cloaked virions inside EVs DENV (Reyes-Ruiz et al, 2019), enterovirus 71 (Gu et al, 2020), HCV (Bartosch et al, 2003;Timpe et al, 2008) Transfer of infective RNA through EVs withouth complete viral particles HCV (Longatti et al, 2015), FMDV (Zhang et al, 2019), EVs turn cells more permissive to infection, membrane/receptor modulation HIV (Arenaccio et al, 2014;Dubrovsky et al, 2020), Rhinovirus (Miura, 2019) Host molecules in EVs facilitate viral stability and replication in recipient cells HBV , HCV (Bukong et al, 2014;Altan-Bonnet, 2016), HIV (Arenaccio et al, 2014;Ranjit et al, 2020) Amplification of EV production ZIKV (Zhou W. et al, 2019) EVs from uninfected cells can activate latent viruses HIV (Barclay et al, 2020) EVS RELATED TO IMMUNE RESPONSES…”

Section: Mechanism Virusmentioning

confidence: 99%

Extracellular Vesicles in Viral Infections: Two Sides of the Same Coin?

Martins

Alves

2020

Front. Cell. Infect. Microbiol.

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Extracellular vesicles are small membrane structures containing proteins and nucleic acids that are gaining a lot of attention lately. They are produced by most cells and can be detected in several body fluids, having a huge potential in therapeutic and diagnostic approaches. EVs produced by infected cells usually have a molecular signature that is very distinct from healthy cells. For intracellular pathogens like viruses, EVs can have an even more complex function, since the viral biogenesis pathway can overlap with EV pathways in several ways, generating a continuum of particles, like naked virions, EVs containing infective viral genomes and quasi-enveloped viruses, besides the classical complete viral particles that are secreted to the extracellular space. Those particles can act in recipient cells in different ways. Besides being directly infective, they also can prime neighbor cells rendering them more susceptible to infection, block antiviral responses and deliver isolated viral molecules. On the other hand, they can trigger antiviral responses and cytokine secretion even in uninfected cells near the infection site, helping to fight the infection and protect other cells from the virus. This protective response can also backfire, when a massive inflammation facilitated by those EVs can be responsible for bad clinical outcomes. EVs can help or harm the antiviral response, and sometimes both mechanisms are observed in infections by the same virus. Since those pathways are intrinsically interlinked, understand the role of EVs during viral infections is crucial to comprehend viral mechanisms and respond better to emerging viral diseases.

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“…Another picornavirus, the aphthovirus responsible for foot-and-mouth disease (FMDV) was long ago observed to be released from cells by an exocytic mechanism involving membrane-limited vesicles [ 63 ]. More recently, a mechanism of exosome-mediated transmission of FMDV has been described in vivo and in vitro [ 64 ] and has also been considered as a potential immune evasion mechanism.…”

Section: Evs In Viral Infectionsmentioning

confidence: 99%

Extracellular Vesicles in Viral Spread and Antiviral Response

Bello-Morales

Ripa

Löpez‐Guerrero

2020

Viruses

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Viral spread by both enveloped and non-enveloped viruses may be mediated by extracellular vesicles (EVs), including microvesicles (MVs) and exosomes. These secreted vesicles have been demonstrated to be an efficient mechanism that viruses can use to enter host cells, enhance spread or evade the host immune response. However, the complex interplay between viruses and EVs gives rise to antagonistic biological tasks—to benefit the viruses, enhancing infection and interfering with the immune system or to benefit the host, by mediating anti-viral responses. Exosomes from cells infected with herpes simplex type 1 (HSV-1) may transport viral and host transcripts, proteins and innate immune components. This virus may also use MVs to expand its tropism and evade the host immune response. This review aims to describe the current knowledge about EVs and their participation in viral infection, with a specific focus on the role of exosomes and MVs in herpesvirus infections, particularly that of HSV-1.

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Exosomes-mediated transmission of foot-and-mouth disease virus in vivo and in vitro

Cited by 29 publications

References 56 publications

Intercellular transmission of Seneca Valley virus mediated by exosomes

Intercellular transmission of Seneca Valley virus mediated by exosomes

Extracellular Vesicles in Viral Infections: Two Sides of the Same Coin?

Extracellular Vesicles in Viral Spread and Antiviral Response

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