A New Infectious Unit: Extracellular Vesicles Carrying Virus Populations

Kerviel, Adeline; Zhang, Mengyang; Altan‐Bonnet, Nihal

doi:10.1146/annurev-cellbio-040621-032416

Cited by 52 publications

(64 citation statements)

References 178 publications

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“…2a ). Virus packaging in EVs is believed to be an important form of virus release in the early stages of infection, which precedes the massive lysis-mediated release of naked virions during advanced infection 33 – 35 . Therefore, we investigated whether the defect in extracellular virus release for EMCV-L Zn infected cells was indicative of a defect in EV-enclosed virus release.…”

Section: Resultsmentioning

confidence: 99%

The encephalomyocarditis virus Leader promotes the release of virions inside extracellular vesicles via the induction of secretory autophagy

et al. 2022

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Naked viruses can escape host cells before the induction of lysis via release in extracellular vesicles (EVs). These nanosized EVs cloak the secreted virus particles in a host-derived membrane, which alters virus-host interactions that affect infection efficiency and antiviral immunity. Currently, little is known about the viral and host factors regulating this form of virus release. Here, we assessed the role of the encephalomyocarditis virus (EMCV) Leader protein, a ‘viral security protein’ that subverts the host antiviral response. EV release upon infection with wildtype virus or a Leader-deficient mutant was characterized at the single particle level using high-resolution flow cytometry. Inactivation of the Leader abolished EV induction during infection and strongly reduced EV-enclosed virus release. We demonstrate that the Leader promotes the release of virions within EVs by stimulating a secretory arm of autophagy. This newly discovered role of the EMCV Leader adds to the variety of mechanisms via which this protein affects virus-host interactions. Moreover, these data provide first evidence for a crucial role of a non-structural viral protein in the non-lytic release of picornaviruses via packaging in EVs.

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Section: Resultsmentioning

confidence: 99%

The encephalomyocarditis virus Leader promotes the release of virions inside extracellular vesicles via the induction of secretory autophagy

et al. 2022

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“…Rotaviruses and noroviruses egress from cells non-lytically as viral clusters inside vesicles 18 . Compared to free fecal viruses (for example, due to vesicle lysis), vesicle-cloaked viruses are protected from fecal proteases and nucleases, enabling high multiplicities of infection (MOIs) and leading to enhanced infectivity 18 , 34 , 35 . Indeed, only vesicle-cloaked, HuNoV-enriched inocula replicated efficiently in the ductal and acinar salivary cell lines as evidenced by qPCR, immunoblots for viral non-structural proteins (NS7, NS6) and single-molecule fluorescence in situ hybridization (FISH) 34 against the (−) replicative HuNoV RNA strands (Fig.…”

Section: Salivary Cell Lines Replicate Human Norovirusmentioning

confidence: 99%

Enteric viruses replicate in salivary glands and infect through saliva

Ghosh

Kumar

Santiana

et al. 2022

Nature

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Enteric viruses like norovirus, rotavirus and astrovirus have long been accepted as spreading in the population through fecal–oral transmission: viruses are shed into feces from one host and enter the oral cavity of another, bypassing salivary glands (SGs) and reaching the intestines to replicate, be shed in feces and repeat the transmission cycle 1 . Yet there are viruses (for example, rabies) that infect the SGs 2 , 3 , making the oral cavity one site of replication and saliva one conduit of transmission. Here we report that enteric viruses productively and persistently infect SGs, reaching titres comparable to those in the intestines. We demonstrate that enteric viruses get released into the saliva, identifying a second route of viral transmission. This is particularly significant for infected infants, whose saliva directly transmits enteric viruses to their mothers’ mammary glands through backflow during suckling. This sidesteps the conventional gut–mammary axis route 4 and leads to a rapid surge in maternal milk secretory IgA antibodies 5 , 6 . Lastly, we show that SG-derived spheroids 7 and cell lines 8 can replicate and propagate enteric viruses, generating a scalable and manageable system of production. Collectively, our research uncovers a new transmission route for enteric viruses with implications for therapeutics, diagnostics and importantly sanitation measures to prevent spread through saliva.

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“…A schematic representing different routes of EV-mediated viral release is shown in Figure 2A. A recent review has discussed the advantages of EV-mediated en bloc transmission of several infectious viruses along with the known molecular mechanisms of cargo delivery [96].…”

Section: Extracellular Vesicles-mediated Release Of Viral Aggregatesmentioning

confidence: 99%

“…Host immune responses present a significant barrier for viruses. particular, can modulate host responses to enhance their infectivity in different ways [96].…”

Section: Viral Aggregation An An Antiviral Response 446mentioning

confidence: 99%

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Viral Aggregation: The Knowns and Unknowns

Pradhan

Varsani

Leff

et al. 2022

Viruses

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Viral aggregation is a complex and pervasive phenomenon affecting many viral families. An increasing number of studies have indicated that it can modulate critical parameters surrounding viral infections, and yet its role in viral infectivity, pathogenesis, and evolution is just beginning to be appreciated. Aggregation likely promotes viral infection by increasing the cellular multiplicity of infection (MOI), which can help overcome stochastic failures of viral infection and genetic defects and subsequently modulate their fitness, virulence, and host responses. Conversely, aggregation can limit the dispersal of viral particles and hinder the early stages of establishing a successful infection. The cost–benefit of viral aggregation seems to vary not only depending on the viral species and aggregating factors but also on the spatiotemporal context of the viral life cycle. Here, we review the knowns of viral aggregation by focusing on studies with direct observations of viral aggregation and mechanistic studies of the aggregation process. Next, we chart the unknowns and discuss the biological implications of viral aggregation in their infection cycle. We conclude with a perspective on harnessing the therapeutic potential of this phenomenon and highlight several challenging questions that warrant further research for this field to advance.

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A New Infectious Unit: Extracellular Vesicles Carrying Virus Populations

Cited by 52 publications

References 178 publications

The encephalomyocarditis virus Leader promotes the release of virions inside extracellular vesicles via the induction of secretory autophagy

The encephalomyocarditis virus Leader promotes the release of virions inside extracellular vesicles via the induction of secretory autophagy

Enteric viruses replicate in salivary glands and infect through saliva

Viral Aggregation: The Knowns and Unknowns

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