Electron microscopic studies of viral pancreatitis in Coxsackie B4 virus infected mice

Burch, George E.; Harb, Joseph M.

doi:10.1016/0014-4800(79)90004-2

Cited by 9 publications

(9 citation statements)

References 17 publications

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“…By comparison to a ribosome (diameter, ϳ20 nm), the individual components of this lattice were estimated as having a diameter of ϳ8 nm, which is similar to the reported size for enteroviral RNA polymerases (22,24). Virus infection induced additional ultrastructural changes to acinar cells, including the formation of numerous single-membraned electron-lucent vacuoles, disorganized and highly dilated rough ER, and nuclei that appeared to be apoptotic and/or pyknotic (data not shown); these findings are consistent with those of previous ultrastructural analyses of CVB-infected pancreas (5,20,26). Overall, our EM analyses confirm that CVB3 infection triggered the formation of autophagy-like vesicles along with autophagosomes of various sizes.…”

Section: Vol 84 2010 Coxsackievirus Induces Autophagy In the Pancresupporting

confidence: 89%

“…6B and C); these vesicles resembled conventional autophagosomes in that they contained cytoplasmic material, but they were smaller in size (ϳ250 nm). These structures, which resemble the autophagylike vesicles that are induced by poliovirus (35,88), have previously been identified in CVB-infected pancreas and were referred to as compound membrane-vesicle (CMV) complexes (5,26). Autophagosomes of more normal size (500 to 1,500 nm) were also seen in acinar cells from infected pancreas (Fig.…”

Section: Vol 84 2010 Coxsackievirus Induces Autophagy In the Pancrementioning

confidence: 72%

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Coxsackievirus Infection Induces Autophagy-Like Vesicles and Megaphagosomes in Pancreatic Acinar Cells In Vivo

Kemball¹,

Alirezaei²,

Flynn³

et al. 2010

J Virol

145

182

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Autophagy can play an important part in protecting host cells during virus infection, and several viruses have developed strategies by which to evade or even exploit this homeostatic pathway. Tissue culture studies have shown that poliovirus, an enterovirus, modulates autophagy. Herein, we report on in vivo studies that evaluate the effects on autophagy of coxsackievirus B3 (CVB3). We show that in pancreatic acinar cells, CVB3 induces the formation of abundant small autophagy-like vesicles and permits amphisome formation. However, the virus markedly, albeit incompletely, limits the fusion of autophagosomes (and/or amphisomes) with lysosomes, and, perhaps as a result, very large autophagy-related structures are formed within infected cells; we term these structures megaphagosomes. Ultrastructural analyses confirmed that double-membraned autophagy-like vesicles were present in infected pancreatic tissue and that the megaphagosomes were related to the autophagy pathway; they also revealed a highly organized lattice, the individual components of which are of a size consistent with CVB RNA polymerase; we suggest that this may represent a coxsackievirus replication complex. Thus, these in vivo studies demonstrate that CVB3 infection dramatically modifies autophagy in infected pancreatic acinar cells.Macroautophagy-henceforth referred to as autophagy-is an intracellular process that is important for cellular differentiation, homeostasis, and survival. Through autophagy, longlived cytosolic proteins and organelles become encapsulated within double-membraned vesicles, called autophagosomes, which fuse with lysosomes to facilitate degradation of protein and cellular organelles and to promote nutrient recycling/regeneration. Autophagy plays a key role in the host immune response to infection by viruses, bacteria, fungi, and parasites (reviewed in references 10 and 62). Within virus-infected cells, whole virions and/or viral proteins and nucleic acids are captured inside autophagosomes and degraded (following lysosomal fusion) through the process of xenophagy. Moreover, autophagosome fusion with the endosomal/lysosomal pathway facilitates Toll-like receptor recognition of viral materials and delivers endogenous cytosolic viral proteins to the major histocompatibility complex (MHC) class II antigen presentation pathway, which in turn may help to trigger activation of innate immunity (and type I interferon production) and promote antigen presentation to virus-specific CD4 ϩ T cells (reviewed in references 9, 41, 44, 47, 72, and 90). A recent study has shown that autophagy is also involved in the processing and presentation of MHC class I-restricted viral epitopes (13).Given the importance of autophagy in antiviral immunity, it is perhaps not surprising that viruses have evolved mechanisms to evade and/or subvert this pathway (reviewed in references 9, 11, 14, 35, 37, 60, 61, and 77). Several members of the herpesvirus family, most notably herpes simplex virus type 1, inhibit autophagy within an infected cell and encode prote...

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Section: Vol 84 2010 Coxsackievirus Induces Autophagy In the Pancresupporting

confidence: 89%

Section: Vol 84 2010 Coxsackievirus Induces Autophagy In the Pancrementioning

confidence: 72%

Coxsackievirus Infection Induces Autophagy-Like Vesicles and Megaphagosomes in Pancreatic Acinar Cells In Vivo

Kemball¹,

Alirezaei²,

Flynn³

et al. 2010

J Virol

145

182

View full text Add to dashboard Cite

show abstract

“…The authors suggested these resembled “autolytic vesicles,” which “appear to represent a secondary response to infection.” Similar vesicles, termed “compound membrane vesicles,” were later identified in images of Coxsackievirus-infected mouse pancreata, indicating that these structures were present during infection of multiple picornaviruses. (Burch and Harb, 1979; Harb and Burch, 1975)…”

Section: Observation Of Autophagosomes During Infectionmentioning

confidence: 99%

Viruses and the autophagy pathway

2015

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Studies of the cellular autophagy pathway have exploded over the past twenty years. Now appreciated as a constitutive degradative mechanism that promotes cellular homeostasis, autophagy is also required for a variety of developmental processes, cellular stress responses, and immune pathways. Autophagy certainly acts as both an anti-viral and pro-viral pathway, and the roles of autophagy depend on the virus, the cell type, and the cellular environment. The goal of this review is to summarize, in brief, what we know so far about the relationship between autophagy and viruses, particularly for those who are not familiar with the field. With a massive amount of relevant published data, it is simply not possible to be comprehensive, or to provide a complete “parade of viruses”, and apologies are offered to researchers whose work is not described herein. Rather, this review is organized around general themes regarding the relationship between autophagy and animal viruses.

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“…[47,48] Observations of autophagosomes were not limited to PV; by 1972, in mice infected with CVB3, “autophagic vacuoles” are described in pancreatic acinar cells, and images of such vesicles appear throughout the literature. [49,50] Using high-pressure freezing techniques to maximize resolution, the Kirkegaard group was able to identify double-membraned vesicles as early as 4hpi in COS-1 cells. [17,51] These vesicles, which are decorated with the PV 2C and 3A proteins, have apparent cytosolic contents and are in the range of 500nM in diameter.…”

Section: The Autophagy Pathway and Awolmentioning

confidence: 99%

Poliovirus-induced changes in cellular membranes throughout infection

Jackson

2014

Current Opinion in Virology

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The membrane landscape of a cell often changes drastically upon infection by a virus. In the case of the well-studied positive strand RNA virus poliovirus, the short infection cycle induces vesicles and tubular structures early in infection, and double-membraned vesicles late in infection. In this review, the current understanding of membrane changes in a PV-infected cell, the host and viral factors that facilitate these changes, and how these changes may promote virus replication will be discussed. Host factors involved in membrane rearrangement during infection include components of the COPI and COPII secretory pathways, lipid kinases, and the autophagy pathway. The roles of cellular membranes include acting as a scaffold for the RNA replication complex and roles in exit of mature virus. Finally, recent studies suggesting that not all picornaviruses are truly “non-enveloped” are discussed in the context of the field, raising the possibility that cell-derived membranes play a role in delivering poliovirus particles to the extracellular space.

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Electron microscopic studies of viral pancreatitis in Coxsackie B4 virus infected mice

Cited by 9 publications

References 17 publications

Coxsackievirus Infection Induces Autophagy-Like Vesicles and Megaphagosomes in Pancreatic Acinar Cells In Vivo

Coxsackievirus Infection Induces Autophagy-Like Vesicles and Megaphagosomes in Pancreatic Acinar Cells In Vivo

Viruses and the autophagy pathway

Poliovirus-induced changes in cellular membranes throughout infection

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