Cell-to-cell spread of poliovirus in the spinal cord of bonnet monkeys (Macaca radiata).

Ponnuraj, Esther M.; John, T. Jacob; Levin, Myron J.; Simoes, E. A. F.

doi:10.1099/0022-1317-79-10-2393

Cited by 19 publications

(24 citation statements)

References 41 publications

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“…However, nonlytic spread could play a role in viral transport through the CNS. A study in 1998 on the cell-to-cell spread of poliovirus in the spinal cord of Bonnet monkeys hints at a possible role for nonlytic spread in the CNS (29). The authors infected monkeys with poliovirus in the ulnar nerve and tracked viral spread at different times post-infection.…”

Section: What Is the Purpose Of Nonlytic Spread?mentioning

confidence: 99%

Escape of non-enveloped virus from intact cells

Bird

Kirkegaard

2015

Virology

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How do viruses spread from cell to cell? Enveloped viruses acquire their surrounding membranes by budding. If a newly enveloped virus has budded through the plasma membrane, it finds itself outside the cell immediately. If it has budded through the bounding membrane of an internal compartment such as the ER, the virus finds itself in the lumen, from which it can exit the cell via the conventional secretion pathway. Thus, although some enveloped viruses destroy the cells they infect, there is no topological need to do so. On the other hand, naked viruses such as poliovirus lack an external membrane. They are protein-nucleic acid complexes within the cytoplasm or nucleus of the infected cell, like a ribosome, a spliceosome or an aggregate of Huntingtin protein. The simplest way for such a particle to pass through the single lipid bilayer that separates it from the outside of the cell would be to violate the integrity of that bilayer. Thus, it is not surprising that the primary mode of exit for non-enveloped viruses is cell lysis. However, more complex exit strategies are possible, such as the creation of new compartments whose complex topologies allow the exit of cytoplasm and its contents without violating the integrity of the cell. Here we will discuss the non-lytic spread of poliovirus and recent observations of such compartments during viral infection with several different picornaviruses.

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Section: What Is the Purpose Of Nonlytic Spread?mentioning

confidence: 99%

Escape of non-enveloped virus from intact cells

Bird

Kirkegaard

2015

Virology

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“…It has been shown that LC3 silencing with a siRNA leads to a decrease of viral cell-to-cell spread whereas autophagy induction favors this non-lytic release in both cultured cells and mice (Bird et al, 2014). The release of viral particles via a non-lytic process was also previously suggested by a study in the spinal cords of bonnet monkeys (Ponnuraj et al, 1998). In a recent publication it was also shown the release of enwrapped virus via autophagosomallike vesicles, enriched in phosphatidylserine, which were highly efficient in infection (Chen et al, 2015).…”

Section: Poliovirus: Double-membrane Autophagosomal-like Vesicles Ermentioning

confidence: 67%

A Novel Mechanism Underlying the Innate Immune Response Induction upon Viral-Dependent Replication of Host Cell mRNA: A Mistake of +sRNA Viruses' Replicases

Delgui

Colombo

2017

Front. Cell. Infect. Microbiol.

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Viruses are lifeless particles designed for setting virus-host interactome assuring a new generation of virions for dissemination. This interactome generates a pressure on host organisms evolving mechanisms to neutralize viral infection, which places the pressure back onto virus, a process known as virus-host cell co-evolution. Positive-single stranded RNA (+sRNA) viruses are an important group of viral agents illustrating this interesting phenomenon. During replication, their genomic +sRNA is employed as template for translation of viral proteins; among them the RNA-dependent RNA polymerase (RdRp) is responsible of viral genome replication originating double-strand RNA molecules (dsRNA) as intermediates, which accumulate representing a potent threat for cellular dsRNA receptors to initiate an antiviral response. A common feature shared by these viruses is their ability to rearrange cellular membranes to serve as platforms for genome replication and assembly of new virions, supporting replication efficiency increase by concentrating critical factors and protecting the viral genome from host anti-viral systems. This review summarizes current knowledge regarding cellular dsRNA receptors and describes prototype viruses developing replication niches inside rearranged membranes. However, for several viral agents it's been observed both, a complex rearrangement of cellular membranes and a strong innate immune antiviral response induction. So, we have included recent data explaining the mechanism by, even though viruses have evolved elegant hideouts, host cells are still able to develop dsRNA receptors-dependent antiviral response.

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“…Although the exact process(es) involved remain unclear, some studies have suggested that CVB1 induction of apoptosis in neighbouring cells is not exclusively caused by the lytic escape of enteroviruses [30,31]. In addition, earlier studies have postulated a direct cell-cell spread of the poliovirus in the central nervous system [32], and a recent study has also described a non-lytic viral mechanism of cell-cell transmission that involves CVB3 induction of cellular protrusions [33]. Whereas enveloped viruses are released through budding from infected cells, non-enveloped viruses use cell lysis for release.…”

Section: Mechanisms Of Viral Entry Into Cellsmentioning

confidence: 99%

Coxsackievirus B transmission and possible new roles for extracellular vesicles

Inal

Jorfi

2013

Biochemical Society Transactions

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Coxsackievirus B1, a member of the Picornaviridae family is a non-enveloped single-stranded RNA virus associated with human diseases including myocarditis and pancreatitis. Infection of the intestinal mucosa, lined by polarized epithelial cells, requires interaction of coxsackievirus with apically located DAF (decay-accelerating factor) before transport to the basolaterally located CAR (coxsackie and adenovirus receptor), where entry is mediated by endocytosis. As with many other non-enveloped viruses, coxsackievirus has to induce lysis of host cells in order to perpetuate infection. However, recent evidence indicates that virus spread to secondary sites is not only achieved by a lytic mechanism and a non-lytic cell-cell strategy has been suggested for coxsackievirus B3. A physical interaction between infected and non-infected cells has been shown to be an efficient mechanism for retroviral transmission and one type of extracellular vesicle, the exosome, has been implicated in HIV-1 transmission. HIV-1 also takes advantage of depolymerization of actin for spread between T-cells. Calpain-mediated depolymerization of the actin cytoskeleton, as a result of increases in intracellular calcium concentration during coxsackievirus infection, would result in a release of host cell-derived microvesicles. If so, we speculate that maybe such microvesicles, increasingly recognized as major vehicles mediating intercellular communication, could play a role in the intercellular transmission of non-enveloped viruses.

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Cell-to-cell spread of poliovirus in the spinal cord of bonnet monkeys (Macaca radiata).

Cited by 19 publications

References 41 publications

Escape of non-enveloped virus from intact cells

Escape of non-enveloped virus from intact cells

A Novel Mechanism Underlying the Innate Immune Response Induction upon Viral-Dependent Replication of Host Cell mRNA: A Mistake of +sRNA Viruses' Replicases

Coxsackievirus B transmission and possible new roles for extracellular vesicles

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