Autophagy-inducing peptides from mammalian VSV and fish VHSV rhabdoviral G glycoproteins (G) as models for the development of new therapeutic molecules

García-Valtanen, Pablo; Ortega-Villaizán, María del Mar; Martínez‐López, Alicia; Medina-Gali, Regla María; Pérez, Luis; Mackenzie, Simon; Figueras, António; Coll, Julio; Estepa, A.

doi:10.4161/auto.29557

Cited by 64 publications

(55 citation statements)

References 65 publications

(82 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Rhabdoviruses vesicular stomatitis virus (VSV), VHSV and spring viremia carp virus (SVCV) glycoproteins induced autophagy in zebrafish in vivo and in vitro ZF4 cells transfected with either VSV or VHSV glycoprotein resulting in reduced yields of both VHSV and SVCV in infected cells (García‐Valtanen et al . ). In Drosophila , VSV glycoprotein‐induced autophagy led to reduced virus replication and conversely, inhibiting autophagy increased virus replication (Shelly et al .…”

Section: Discussionmentioning

confidence: 97%

“…Autophagy is a cellular survival mechanism that functions to self-degrade protein and organelles during times of nutrient starvation and is also a mechanism to combat intracellular viruses (Kudchodkar & Levine 2009;Glick, Barth & Macleod 2010). Rhabdoviruses vesicular stomatitis virus (VSV), VHSV and spring viremia carp virus (SVCV) glycoproteins induced autophagy in zebrafish in vivo and in vitro ZF4 cells transfected with either VSV or VHSV glycoprotein resulting in reduced yields of both VHSV and SVCV in infected cells (Garc ıa-Valtanen et al 2014). In Drosophila, VSV glycoprotein-induced autophagy led to reduced virus replication and conversely, inhibiting autophagy increased virus replication (Shelly et al 2009).…”

Section: The Effects Of Heat-killed Vhsv On Infection Of Rtgill-w1 Bymentioning

confidence: 99%

See 1 more Smart Citation

Temporary protection of rainbow trout gill epithelial cells from infection with viral haemorrhagic septicaemia virus IVb

Al-Hussinee

Pham

Russell

et al. 2016

Journal of Fish Diseases

View full text Add to dashboard Cite

The branchial epithelium is not only a primary route of entry for viral pathogens, but is also a site of viral replication and subsequent shedding may also occur from the gill epithelium. This study investigated the potential of agents known to stimulate innate immunity to protect rainbow trout epithelial cells (RTgill-W1) from infection with VHSV IVb. RTgill-W1 cells were pretreated with poly I:C, FuGENE(®) HD + poly I:C, lipopolysaccharide (LPS), LPS + poly I:C or heat-killed VHSV IVb and then infected with VHSV IVb 4 days later. Cytopathic effect (CPE) was determined at 2, 3, 4, 7 and 11 days post-infection. Virus in cells and supernatant was detected using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). All of the treatments delayed the onset of CPE (per cent of monolayer destruction), compared with untreated controls; however, killed VHSV or poly I:C combined with LPS was the most effective. Similarly, the detection of viral RNA in the supernatant was delayed, and the quantity was significantly (P < 0.05) reduced by all treatments with the exception of LPS alone (4 days). Unlike many of the other treatments, pretreatment of RTgill-W1 with heat-killed VHSV did not upregulate interferon 1, 2 or MX 1 gene expression.

show abstract

Section: Discussionmentioning

confidence: 97%

Section: The Effects Of Heat-killed Vhsv On Infection Of Rtgill-w1 Bymentioning

confidence: 99%

Temporary protection of rainbow trout gill epithelial cells from infection with viral haemorrhagic septicaemia virus IVb

Al-Hussinee

Pham

Russell

et al. 2016

Journal of Fish Diseases

View full text Add to dashboard Cite

show abstract

“…A latest study has shown that two fish rhabdoviruses (viral haemorrhagic septicaemia virus, VHSV and SVCV) induce autophagy in the model vertebrate species zebrafish and have implicated autophagy as a negative regulator of viruses replication (Garcia‐Valtanen et al ., ). However, our study with EPC cells indicates that autophagy positively regulates SVCV replication and promotes viral yields.…”

Section: Discussionmentioning

confidence: 97%

Spring viraemia of carp virus induces autophagy for necessary viral replication

Liu

Zhu

et al. 2014

Cell Microbiol

View full text Add to dashboard Cite

SummaryOutbreaks of spring viraemia of carp virus (SVCV) in several carp species and other cultivated fish can cause significant mortality and jeopardize the billion-dollar worldwide fish industry. Spring viraemia of carp virus, also known as Rhabdovirus carpio, is a bullet-shaped RNA virus that enters and amplifies in gill epithelium and later spreads to internal organs. Young fish under stressed conditions (spring cold water, etc.) are more vulnerable to SVCV-induced lethality because of their lack of a mature immune system. Currently, the host response of SVCV remains largely unknown. Here, we observed that autophagy is activated in SVCVinfected epithelioma papulosum cyprini (EPC) cells. We demonstrated that the SVCV glycoprotein, rather than viral replication, activates the autophagy pathway. In addition, SVCV utilized the autophagy pathway to facilitate its own genomic RNA replication and to enhance its titres in the supernatants. Autophagy promoted the survival of SVCV-infected cells by eliminating damaged mitochondrial DNA generated during viral infection. We further showed that SVCV induces autophagy in EPC cells through the ERK/mTOR signalling pathway. Our results reveal a connection between autophagy and SVCV replication and propose autophagy suppression as a novel means to restrict SVCV viral replication.

show abstract

“…24,35,36 A recent study reports that vesicular stomatitis virus, viral hemorrhagic septicemia virus and spring viremia carp virus, members of the Rhabdoviridae family, can trigger autophagy. 37 However, to date there has been no report about RABV inducing autophagy. To answer this question, we focused on 2 RABV strains, the virulent RABV strain GD-SH-01 and the attenuated rabies virus strain HEP-Flury.…”

Section: Discussionmentioning

confidence: 99%

Wild-type rabies virus induces autophagy in human and mouse neuroblastoma cell lines

Peng

Sheng-He

et al. 2016

Autophagy

View full text Add to dashboard Cite

Different rabies virus (RABV) strains have their own biological characteristics, but little is known about their respective impact on autophagy. Therefore, we evaluated whether attenuated RABV HEP-Flury and wildtype RABV GD-SH-01 strains triggered autophagy. We found that GD-SH-01 infection significantly increased the number of autophagy-like vesicles, the accumulation of enhanced green fluorescent protein (EGFP)-LC3 fluorescence puncta and the conversion of LC3-I to LC3-II, while HEP-Flury was not able to induce this phenomenon. When evaluating autophagic flux, we found that GD-SH-01 infection triggers a complete autophagic response in the human neuroblastoma cell line (SK), while autophagosome fusion with lysosomes was inhibited in a mouse neuroblastoma cell line (NA). In these cells, GD-SH-01 led to apoptosis and mitochondrial dysfunction while triggering autophagy, and apoptosis could be decreased by enhancing autophagy. To further identify the virus constituent causing autophagy, 5 chimeric recombinant viruses carrying single genes of HEP-Flury instead of those of GD-SH-01 were rescued. While the HEP-Flury virus carrying the wild-type matrix protein (M) gene of RABV triggered LC3-I to LC3-II conversion in SK and NA cells, replacement of genes of nucleoprotein (N), phosphoprotein (P) and glycoprotein (G) produced only minor autophagy. But no one single structural protein of GD-SH-01 induced autophagy. Moreover, the AMPK signaling pathway was activated by GD-SH-01 in SK. Therefore, our data provide strong evidence that autophagy is induced by GD-SH-01 and can decrease apoptosis in vitro. Furthermore, the M gene of GD-SH-01 may cooperatively induce autophagy.

show abstract

Autophagy-inducing peptides from mammalian VSV and fish VHSV rhabdoviral G glycoproteins (G) as models for the development of new therapeutic molecules

Cited by 64 publications

References 65 publications

Temporary protection of rainbow trout gill epithelial cells from infection with viral haemorrhagic septicaemia virus IVb

Temporary protection of rainbow trout gill epithelial cells from infection with viral haemorrhagic septicaemia virus IVb

Spring viraemia of carp virus induces autophagy for necessary viral replication

Wild-type rabies virus induces autophagy in human and mouse neuroblastoma cell lines

Contact Info

Product

Resources

About