Poliovirus-induced changes in cellular membranes throughout infection

Jackson, William T.

doi:10.1016/j.coviro.2014.09.007

Cited by 43 publications

(32 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These replication complexes are virus-modified lysosomes (53). Studies on poliovirus have indicated that intracellular vesicle acidification, a hallmark of autophagosome maturation, promotes maturation of infectious poliovirus particles (54)(55)(56)(57). In IBDV-infected cells, pVP2, VP3, and dsRNA, which are essential components for IBDV assembly (4), colocalized with LAMP1 in autophagic endosomal pathway.…”

Section: Discussionmentioning

confidence: 99%

Infectious Bursal Disease Virus Subverts Autophagic Vacuoles To Promote Viral Maturation and Release

Wang

Duan

Han

et al. 2017

J Virol

View full text Add to dashboard Cite

Autophagy functions as an intrinsic antiviral defense. However, some viruses can subvert or even enhance host autophagic machinery to increase viral replication and pathogenesis. The role of autophagy during avibirnavirus infection, especially late stage infection, remains unclear. In this study, infectious bursal disease virus (IBDV) was used to investigate the role of autophagy in avibirnavirus replication. We demonstrated IBDV induction of autophagy as a significant increase in puncta of LC3 ϩ autophagosomes, endogenous levels of LC3-II, and ultrastructural characteristics typical of autophagosomes during the late stage of infection. Induction of autophagy enhances IBDV replication, whereas inhibition of autophagy impairs viral replication. We also demonstrated that IBDV infection induced autophagosome-lysosome fusion, but without active degradation of their contents. Moreover, inhibition of fusion or of lysosomal hydrolysis activity significantly reduced viral replication, indicating that virions utilized the low-pH environment of acidic organelles to facilitate viral maturation. Using immuno-transmission electron microscopy (TEM), we observed that a large number of intact IBDV virions were arranged in a lattice surrounded by p62 proteins, some of which lay between virions. Additionally, many virions were encapsulated within the vesicular membranes, with an obvious release stage observed by TEM. The autophagic endosomal pathway facilitates low-pH-mediated maturation of viral proteins and membrane-mediated release of progeny virions.IMPORTANCE IBDV is the most extensively studied virus in terms of molecular characteristics and pathogenesis; however, mechanisms underlying the IBDV life cycle require further exploration. The present study demonstrated that autophagy enhances viral replication at the late stage of infection, and the autophagy pathway facilitates IBDV replication complex function and virus assembly, which is critical to completion of the virus life cycle. Moreover, the virus hijacks the autophagic vacuoles to mature in an acidic environment and release progeny virions in a membrane-mediated cellto-cell manner. This autophagic endosomal pathway is proposed as a new mechanism that facilitates IBDV maturation, release, and reinternalization. This report presents a concordance in exit strategies among some RNA and DNA viruses, which exploit autophagy pathway for their release from cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Infectious Bursal Disease Virus Subverts Autophagic Vacuoles To Promote Viral Maturation and Release

Wang

Duan

Han

et al. 2017

J Virol

View full text Add to dashboard Cite

show abstract

“…CVB clearly utilizes autophagy to replicate, but also simultaneously commandeers host proteins such as GBF1, Arf1, and PI4KIIIβ to construct viral replication organelles. How can studies describing induction of autophagy and the formation of virus replication organelles be unified in order to fully comprehend CVB replication within the host cell (Jackson, 2014)?…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Recent progress in understanding coxsackievirus replication, dissemination, and pathogenesis

et al. 2015

View full text Add to dashboard Cite

Coxsackieviruses (CVs) are relatively common viruses associated with a number of serious human diseases, including myocarditis and meningo-encephalitis. These viruses are considered cytolytic yet can persist for extended periods of time within certain host tissues requiring evasion from the host immune response and a greatly reduced rate of replication. A member of Picornaviridae family, CVs have been historically considered non-enveloped viruses – although recent evidence suggest that CV and other picornaviruses hijack host membranes and acquire an envelope. Acquisition of an envelope might provide distinct benefits to CV virions, such as resistance to neutralizing antibodies and efficient nonlytic viral spread. CV exhibits a unique tropism for progenitor cells in the host which may help to explain the susceptibility of the young host to infection and the establishment of chronic disease in adults. CVs have also been shown to exploit autophagy to maximize viral replication and assist in unconventional release from target cells. In this article, we review recent progress in clarifying virus replication and dissemination within the host cell, identifying determinants of tropism, and defining strategies utilized by the virus to evade the host immune response. Also, we will highlight unanswered questions and provide future perspectives regarding the potential mechanisms of CV pathogenesis.

show abstract

“…Many pathogens are degraded by autophagy, but some sub-vert the process for their own benefit, including several picorna-viruses (Jackson, 2014; Shi and Luo, 2012). Previous work by our group has demonstrated that poliovirus 1 (PV) uses acidic amphisomes to promote virus replication and maturation (Richards and Jackson, 2012).…”

Section: Introductionmentioning

confidence: 99%

Enteroviruses Remodel Autophagic Trafficking through Regulation of Host SNARE Proteins to Promote Virus Replication and Cell Exit

et al. 2018

Self Cite

View full text Add to dashboard Cite

Summary Enterovirus D68 (EV-D68) is a medically important respiratory plus-strand RNA virus of children that has been linked to acute flaccid myelitis. We have determined that EV-D68 induces autophagic signaling and membrane formation. Autophagy, a homeostatic degradative process that breaks down protein aggregates and damaged organelles, promotes replication of multiple plus-strand viruses. Induction of autophagic signals promotes EV-D68 replication, but the virus inhibits the downstream degradative steps of autophagy in multiple ways. EV-D68 proteases cleave a major autophagic cargo adaptor and the autophagic SNARE SNAP29, which reportedly regulates fusion between autophago-some to amphisome/autolysosome. Although the virus inhibits autophagic degradation, SNAP29 promotes virus replication early in infection. An orphan SNARE, SNAP47, is shown to have a previously unknown role in autophagy, and SNAP47 promotes the replication of EV-D68. Our study illuminates a mechanism for subversion of autophagic flux and redirection of the autophagic membranes to benefit EV-D68 replication.

show abstract

Poliovirus-induced changes in cellular membranes throughout infection

Cited by 43 publications

References 65 publications

Infectious Bursal Disease Virus Subverts Autophagic Vacuoles To Promote Viral Maturation and Release

Infectious Bursal Disease Virus Subverts Autophagic Vacuoles To Promote Viral Maturation and Release

Recent progress in understanding coxsackievirus replication, dissemination, and pathogenesis

Enteroviruses Remodel Autophagic Trafficking through Regulation of Host SNARE Proteins to Promote Virus Replication and Cell Exit

Contact Info

Product

Resources

About