Heat Shock Protein 90 and Heat Shock Protein 70 Are Components of Dengue Virus Receptor Complex in Human Cells

Valle, Jorge Reyes-del; Chávez-Salinas, Salvador; Medina, Fernando; Ángel, Rosa M. del

doi:10.1128/jvi.79.8.4557-4567.2005

Cited by 321 publications

(197 citation statements)

References 50 publications

(39 reference statements)

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“…HSC70 exhibits a chaperone function: it can bind to newly synthesized polypeptides to form correct conformations (37) and to hydrolyze ATP for degrading clathrin coated on vesicles during endocytosis (38). HSC70 has been reported to participate in the viral entry step of rotavirus, dengue virus, Japanese encephalitis virus, polyomavirus, and hepatitis C virus (HCV) (26,(38)(39)(40)(41)(42). Previous studies on fish HSC70 have all focused on the expression level under heat shock or stress (43)(44)(45).…”

Section: Discussionmentioning

confidence: 99%

GHSC70 Is Involved in the Cellular Entry of Nervous Necrosis Virus

Chang

Chi

2015

J Virol

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Nervous necrosis virus (NNV) is a devastating pathogen of cultured marine fish and has affected more than 40 fish species. NNV belongs to the betanodaviruses of Nodaviridae and is a nonenveloped icosahedral particle with 2 single-stranded positive-sense RNAs. To date, knowledge regarding NNV entry into the host cell remains limited, and no NNV-specific receptor protein has been published. Using grouper fin cell line GF-1 and purified NNV capsid protein in a virus overlay protein binding assay (VOPBA), grouper heat shock cognate protein 70 (GHSC70) and grouper voltage-dependent anion selective channel protein 2 (GVDAC2) were investigated as NNV receptor protein candidates. We cloned and sequenced the genes for GHSC70 and GVDAC2 and expressed them in Escherichia coli for antiserum preparation. Knockdown of the expression of GHSC70 and GVDAC2 genes with specific short interfering RNAs (siRNAs) significantly downregulated viral RNA expression in NNV-infected GF-1 cells. By performing an immunoprecipitation assay, we confirmed that GHSC70 interacted with NNV capsid protein, while VDAC2 did not. Immunofluorescence staining and flow cytometry analysis revealed the presence of the GHSC70 protein on the cell surface. After a blocking assay, we detected the NNV RNA2 levels after 1 h of adsorption to GF-1 cells; the level was significantly lower in the cells pretreated with the GHSC70 antiserum than in nontreated cells. Therefore, we suggest that GHSC70 participates in the NNV entry of GF-1 cells, likely functioning as an NNV receptor or coreceptor protein. IMPORTANCEFish nodavirus has caused mass mortality of more than 40 fish species worldwide and resulted in huge economic losses in the past 20 years. Among the four genotypes of fish nodaviruses, the red-spotted grouper nervous necrosis virus (RGNNV) genotype exhibits the widest host range. In our previous study, we developed monoclonal antibodies with high neutralizing efficiency against grouper NNV in GF-1 cells, indicating that NNV-specific receptor(s) may exist on the GF-1 cell membrane. However, no NNV receptor protein has been published. In this study, we found GHSC70 to be an NNV receptor (or coreceptor) candidate through VOBPA and provided several lines of evidence demonstrating that GHSC70 protein has a role in the NNV entry step of GF-1 cells. To the best of our knowledge, this is the first report identifying grouper HSC70 and its role in NNV entry into GF-1 cells.

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Section: Discussionmentioning

confidence: 99%

GHSC70 Is Involved in the Cellular Entry of Nervous Necrosis Virus

Chang

Chi

2015

J Virol

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“…CRL-2266, ATCC), que son fenotípicamente neuronales y se han aislado a partir de la metás-tasis ósea de un neuroblastoma humano. Esta sublínea celular proviene de las células SK-N-SH y SK-SH5Y, ambas reportadas previamente como sensibles a la infección por dengue (18,19). Los experimentos se realizaron durante los pasajes 6 a 15.…”

Section: Células Y Cultivo Celularunclassified

La infección con el virus del dengue induce apoptosis en células del neuroblastoma humano SH-SY5Y

2016

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Contribución de los autores:Jaime E. Castellanos: ejecución del proyecto, análisis e interpretación de datos José I. Neissa: aplicación de la metodología Sigrid J. Camacho: análisis e interpretación de datos Todos los autores participaron en la redacción del manuscrito. Introducción. El dengue es una enfermedad humana producida por el virus del mismo nombre, que se transmite por la picadura de mosquitos del género Aedes. La infección tiene una amplia gama de presentaciones clínicas que van desde la ausencia de síntomas hasta los casos fatales y afecta principalmente a la población pediátrica. Según la nueva clasificación de la enfermedad, las manifestaciones neurológicas se consideran un criterio para el diagnóstico del dengue grave. Objetivo. Evaluar los posibles mecanismos involucrados en la aparición de los signos neurológicos en una línea celular de neuronas humanas, como modelo de infección con el virus del dengue del serotipo 2 (DENV-2). Materiales y métodos. Se evaluó la sensibilidad y la permisividad de la línea celular SH-SY5Y a la infección por el DENV-2; se encontró que la proporción entre infección y producción viral era similar a las de las células de primates usadas como control positivo de la infección. La infección con el virus del dengue induce apoptosis en células del neuroblastoma humano SH-SY5YResultados. La infección indujo un efecto citopático en la línea celular de neuroblastoma caracterizado por un proceso de muerte apoptótica, con aumento en la proporción de células positivas al emplear los métodos de anexina V y TUNEL. Se encontró una regulación positiva del factor de necrosis tumoral alfa (TNF-α), y el tratamiento con un anticuerpo anti-TNF-α aumentó ligeramente la supervivencia de las células infectadas. La adición de TNF-α exógeno a los cultivos infectados potenció la muerte celular. Conclusión. Estos resultados sugieren, en su conjunto, que la regulación positiva del TNF-α podría hacer parte del proceso que induce daño y muerte celular durante el desarrollo de la encefalitis por dengue.Palabras clave: dengue, apoptosis, factor de necrosis tumoral alfa, supervivencia celular, manifestaciones neurológicas, encefalitis. doi: http://dx.doi.org/10.7705/biomedica.v36i0.2984 Dengue virus induces apoptosis in SH-SY5Y human neuroblastoma cellsIntroduction: Dengue is a human disease caused by a virus with the same name, which is transmitted by the bite of Aedes mosquitoes. The infection has a wide range of clinical presentations ranging from asymptomatic to fatal cases, with the pediatric population being the most susceptible. According to the new classification of the disease, the neurological manifestations are considered a criterion for the diagnosis of severe dengue. Conclusion:These results as a whole suggest that the upregulation of TNF-α could be part of the process that induces cell damage and death in cases of dengue encephalitis.

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“…Hsp90 and Hsp70, heat shock proteins associated with membrane microdomains (or lipid rafts), participate in DENV entry as a receptor complex in human neuroblastoma and monocytic cell lines as well as in human monocytes/macrophages [74], but do not play a role for internalization into liver cells [75]. A related stress protein, the glucose-regulated protein GRP78 or BiP, involved in the unfolded protein response, has been identified as a minor receptor element for DENV-2 internalization into human liver cells [75, 76].…”

Section: The Early Stages Of the Flavivirus Life Cyclementioning

confidence: 99%

Molecular mechanisms involved in the early steps of flavivirus cell entry

Kaufmann

Rossmann

2011

Microbes and Infection

118

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Flaviviruses enter their host cells by receptor-mediated endocytosis, a well-orchestrated process of receptor recognition, penetration and uncoating. Recent findings on these early steps in the life cycle of flaviviruses are the focus of this review. Keywords FLAVIVIRUS; CELL ENTRY; RECEPTOR; ENDOCYTOSIS; ENVELOPE PROTEIN; PH ENVIRONMENT; STRUCTUREThe Flaviviridae are a family of small, enveloped RNA viruses that is comprised of three genera: Flavivirus, Hepacivirus, and Pestivirus. More than 70 viruses have been classified in the genus Flavivirus [1]. The genus includes various noteworthy mosquito-and tick-borne human pathogens, such as Yellow Fever virus (YFV), dengue virus (DENV), Tick-borne Encephalitis Virus (TBEV), and West Nile virus (WNV), that are subclassified into several antigenic complexes and phylogenetic groups [2]. Flaviviruses are typically associated with mild systemic disease, but can also cause severe symptoms such as hemorrhagic fever, encephalitis or death. Many of these viruses are resurgent, are spreading to new environments and are responsible for substantial morbidity and mortality around the globe. Flaviviruses are primarily transmitted through arthropod vectors. Humans and other mammals are not known to commonly develop infectious-level viremias and thus are probably incidental hosts with the exceptions of YFV, DENV and TBEV that are sufficiently well-adapted to a mammalian host. The flavivirus lifecycleThe basic stages of the flavivirus life cycle include attachment to the cell surface, internalization into the host cell, transfer of the viral RNA genome into the cytoplasm, translation of the viral proteins, replication of the genomic RNA, assembly and maturation of the virions, and ultimately the release of progeny viruses from the cell.Flaviviruses are lipid-enveloped viruses (Fig. 1A). After recognition and attachment to specific receptor molecules on the surface of the cell, the virus is internalized into the host * Correspondence should be addressed to M.G.R. (mr@purdue.edu, Tel. 765-494-4911, FAX 765-496-1189).Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. . The polyprotein is subsequently glycosylated by cellular glycosyltransferases and cleaved by a combination of viral and host proteases to release three structural (C, prM, and E) and seven non-structural proteins (NS1, NS2a, NS2b, NS3, NS4a, NS4b, and NS5). NS3 and NS5 are the bestcharacterized non-structural proteins that assemble with several other viral and host proteins to form the replication complex. NS3 combines helicase/NTPase, serine protease, and RNA triphosphatase...

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Heat Shock Protein 90 and Heat Shock Protein 70 Are Components of Dengue Virus Receptor Complex in Human Cells

Cited by 321 publications

References 50 publications

GHSC70 Is Involved in the Cellular Entry of Nervous Necrosis Virus

GHSC70 Is Involved in the Cellular Entry of Nervous Necrosis Virus

La infección con el virus del dengue induce apoptosis en células del neuroblastoma humano SH-SY5Y

Molecular mechanisms involved in the early steps of flavivirus cell entry

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