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Bovine plasmacytoid dendritic cells are the major source of type I interferon
"... Type I interferons (alpha/beta interferons [IFN-/]) are the main innate cytokines that are able to induce a cellular antiviral state, thereby limiting viral replication and disease pathology. Plasmacytoid dendritic cells (pDCs) play a crucial role in the control of viral infections, especially in re ..."
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Type I interferons (alpha/beta interferons [IFN-/]) are the main innate cytokines that are able to induce a cellular antiviral state, thereby limiting viral replication and disease pathology. Plasmacytoid dendritic cells (pDCs) play a crucial role in the control of viral infections, especially in response to viruses that have evolved mechanisms to block the type I IFN signal transduction pathway. Using density gradient separation and cell sorting, we have highly enriched a population of bovine cells capable of producing high levels of biologically active type I IFN. These cells represented less than 0.1 % of the total lymphocyte population in blood, pseudoafferent lymph, and lymph nodes. Phenotypic analysis identified these cells as bovine pDCs (CD3 CD14 CD21 CD11c NK TCR CD4 MHC II CD45RB CD172a CD32). High levels of type I IFN were generated by these cells in vitro in response to Toll-like receptor 9 (TLR-9) agonist CpG and foot-and-mouth disease virus (FMDV) immune complexes. In contrast, immune complexes formed with UV-inactivated FMDV or FMDV empty capsids failed to elicit a type I IFN response. Depletion of CD4 cells in vivo resulted in levels of type I IFN in serum early during FMDV infection that were significantly lower than those for control animals. In conclusion, pDCs interacting with immune-complexed virus are the major source of type I interferon production during acute FMDV infection in cattle. Foot-and-mouth disease virus (FMDV) is the etiological
Guinea Pig-Adapted Foot-and-Mouth Disease Virus with Altered Receptor Recognition Can Productively Infect a Natural Host �
, 2007
"... These include: This article cites 75 articles, 38 of which can be accessed free at: ..."
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These include: This article cites 75 articles, 38 of which can be accessed free at:
Valosin-containing protein (VCP/ p97) is required for poliovirus replication and is involved in cellular protein secretion pathway in poliovirus infection
- J. Virol
"... Poliovirus (PV) modifies membrane-trafficking machinery in host cells for its viral RNA replication. To date, ARF1, ACBD3, BIG1/BIG2, GBF1, RTN3, and PI4KB have been identified as host factors of enterovirus (EV), including PV, involved in mem-brane traffic. In this study, we performed small interfe ..."
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Poliovirus (PV) modifies membrane-trafficking machinery in host cells for its viral RNA replication. To date, ARF1, ACBD3, BIG1/BIG2, GBF1, RTN3, and PI4KB have been identified as host factors of enterovirus (EV), including PV, involved in mem-brane traffic. In this study, we performed small interfering RNA (siRNA) screening targeting membrane-trafficking genes for host factors required for PV replication. We identified valosin-containing protein (VCP/p97) as a host factor of PV replication required after viral protein synthesis, and its ATPase activity was essential for PV replication. VCP colocalized with viral pro-teins 2BC/2C and 3AB/3B in PV-infected cells and showed an interaction with 2BC and 3AB but not with 2C and 3A. Knockdown of VCP did not suppress the replication of coxsackievirus B3 or Aichi virus. A VCP-knockdown-resistant PVmutant had an A4881G (a mutation of E253G in 2C) mutation, which is known as a determinant of a secretion inhibition-negative phenotype. However, knockdown of VCP did not affect the inhibition of cellular protein secretion caused by overexpression of each individ-ual viral protein. These results suggested that VCP is a host factor required for viral RNA replication of PV amongmembrane-trafficking proteins and provides a novel link between cellular protein secretion and viral RNA replication. Poliovirus (PV) is a small nonenveloped virus with a single-strand positive genomic RNA of about 7,500 nucleotides (nt) belonging to Human enterovirus C in the genus Enterovirus, the family Picornaviridae. PV is the causative agent of poliomyelitis, which is caused by the destruction of motor neurons by the direct
The Correspondence
, 1994
"... This paper addresses a current debate in the bioethics community between principlists, who consider that principles are at the heart of moral life, and narrativists, who see communication at its core. Using a case study entitled ‘‘The forgetful mourner’ ’ to introduce the tensions between each of th ..."
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This paper addresses a current debate in the bioethics community between principlists, who consider that principles are at the heart of moral life, and narrativists, who see communication at its core. Using a case study entitled ‘‘The forgetful mourner’ ’ to introduce the tensions between each of these positions, I go on to explain the central tenets of both principlism and narrative ethics. Rather than focus on their respective weaknesses, which many theorists do, I emphasise instead, the contribution that each approach can make to understanding moral life and the process of ethical decision making in health care situations. My ultimate aim is to identify the, sometimes overlapping, skills that both principlism and narrative ethics require on the part of health professionals who deploy them. I conclude that a good principlist has narrativist tendencies and a good narrativist is inclined toward principlism.
Correspondence
, 2003
"... The ultrastructure of the developing replication site in foot-and-mouth disease virus-infected BHK-38 cells ..."
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The ultrastructure of the developing replication site in foot-and-mouth disease virus-infected BHK-38 cells
COPI is required for enterovirus 71 replication
- PLoS ONE
, 2012
"... Enterovirus 71 (EV71), a member of the Picornaviridae family, is found in Asian countries where it causes a wide range of human diseases. No effective therapy is available for the treatment of these infections. Picornaviruses undergo RNA replication in association with membranes of infected cells. C ..."
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Enterovirus 71 (EV71), a member of the Picornaviridae family, is found in Asian countries where it causes a wide range of human diseases. No effective therapy is available for the treatment of these infections. Picornaviruses undergo RNA replication in association with membranes of infected cells. COPI and COPII have been shown to be involved in the formation of picornavirus-induced vesicles. Replication of several picornaviruses, including poliovirus and Echovirus 11 (EV11), is dependent on COPI or COPII. Here, we report that COPI, but not COPII, is required for EV71 replication. Replication of EV71 was inhibited by brefeldin A and golgicide A, inhibitors of COPI activity. Furthermore, we found EV71 2C protein interacted with COPI subunits by co-immunoprecipitation and GST pull-down assay, indicating that COPI coatomer might be directed to the viral replication complex through viral 2C protein. Additionally, because the pathway is conserved among different species of enteroviruses, it may represent a novel target for antiviral therapies.
DOI 10.1099/vir.0.016279-0
, 2009
"... Feline calicivirus p32, p39 and p30 proteins localize to the endoplasmic reticulum to initiate replication complex formation ..."
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Feline calicivirus p32, p39 and p30 proteins localize to the endoplasmic reticulum to initiate replication complex formation
www.elsevier.com/locate/yviro Inhibition of cellular protein secretion by picornaviral 3A proteins
"... During poliovirus infection, anterograde traffic between the endoplasmic reticulum and the Golgi is inhibited due to the action of 3A, an 87 amino acid viral protein. The ability of poliovirus protein 3A to inhibit ER-to-Golgi traffic is not required for virus growth. Instead, we have suggested that ..."
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During poliovirus infection, anterograde traffic between the endoplasmic reticulum and the Golgi is inhibited due to the action of 3A, an 87 amino acid viral protein. The ability of poliovirus protein 3A to inhibit ER-to-Golgi traffic is not required for virus growth. Instead, we have suggested that the inhibition of host protein secretion, shown to reduce the secretion of interferon-h, IL-6, and IL-8 and the expression of both newly synthesized MHC class I and TNF receptor in the plasma membrane of infected cells, affects growth in host organisms. To determine whether the ability of poliovirus 3A to inhibit ER-to-Golgi traffic is conserved, the ability of 3A proteins from several picornaviruses, including human rhinovirus 14, foot-and-mouth disease virus, enterovirus 71, hepatitis A, and Theiler’s virus, was tested. Only the 3A proteins from another poliovirus, Sabin 3, and closely related coxsackievirus B3 inhibited ER-to-Golgi traffic as effectively as the 3A protein from poliovirus Mahoney type 1. Site-directed mutagenesis based on these findings and the three-dimensional structure of the amino-terminal domain of poliovirus 3A protein revealed that residues in the unstructured amino terminus of 3A are critical for the inhibition of host protein secretion.
Coxsackievirus B3 Proteins Directionally Complement Each Other To
, 2007
"... These include: This article cites 41 articles, 21 of which can be accessed free at: ..."
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These include: This article cites 41 articles, 21 of which can be accessed free at:
CONTENT ALERTS
, 1990
"... Control of protein phosphatase 2A by simian virus 40 small-t antigen. ..."
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