NDLI: Apoptosis is mediated by FeHV-1 through the intrinsic pathway and interacts with the autophagic process

Content Provider	Springer Nature : BioMed Central
Author	Ferrara, Gianmarco Longobardi, Consiglia Sgadari, Maria Francesca Restucci, Brunella Iovane, Giuseppe Ciarcia, Roberto Pagnini, Ugo Montagnaro, Serena
Abstract	Background Although FeHV-1 is a primary feline pathogen, little is known about its interactions with host cells. Its relationship with several cellular pathways has recently been described, whereas its interplay with the apoptotic process, unlike other herpesviruses, has not yet been clarified. The aim of this work was to evaluate whether FeHV-1 induces apoptosis in its permissive cells, as well as the pathway involved and the effects of induction and inhibition of apoptosis on viral replication. Methods Monolayers of CRFK cells were infected at different times with different viral doses. A cytofluorimetric approach allowed the quantification of cells in early and late apoptosis. All infections and related controls were also subjected to Western blot analysis to assess the expression of apoptotic markers (caspase 3-8-9, Bcl-2, Bcl-xL, NF-κB). An inhibitor (Z-VAD-FMK) and an inducer (ionomycin) were used to evaluate the role of apoptosis in viral replication. Finally, the expression of autophagy markers during the apoptosis inhibition/induction and the expression of apoptosis markers during autophagy inhibition/induction were evaluated to highlight any crosstalk between the two pathways. Results FeHV-1 triggered apoptosis in a time- and dose-dependent manner. Caspase 3 cleavage was evident 48 h after infection, indicating the completeness of the process at this stage. While caspase 8 was not involved, caspase 9 cleavage started 24 h post-infection. The expression of other mitochondrial damage markers also changed, suggesting that apoptosis was induced via the intrinsic pathway. NF- κB was up-regulated at 12 h, followed by a gradual decrease in levels up to 72 h. The effects of apoptosis inhibitors and inducers on viral replication and autophagy were also investigated. Inhibition of caspases resulted in an increase in viral glycoprotein expression, higher titers, and enhanced autophagy, whereas induction of apoptosis resulted in a decrease in viral protein expression, lower viral titer, and attenuated autophagy. On the other hand, the induction of autophagy reduced the cleavage of caspase 3. Conclusions In this study, we established how FeHV-1 induces the apoptotic process, contributing to the understanding of the relationship between FeHV-1 and this pathway.
Related Links	https://virologyj.biomedcentral.com/counter/pdf/10.1186/s12985-023-02267-w.pdf
Ending Page	11
Page Count	11
Starting Page	1
File Format	HTM / HTML
DOI	10.1186/s12985-023-02267-w
Journal	Virology Journal
Issue Number	1
Volume Number	20
Language	English
Publisher	BioMed Central
Publisher Date	2023-12-12
Access Restriction	Open
Subject Keyword	Virology Apoptosis Feline herpesvirus Caspases Intrinsic pathway Autophagy
Content Type	Text
Resource Type	Article
Subject	Virology Infectious Diseases
Journal Impact Factor	4/2023
5-Year Journal Impact Factor	3.8/2023

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Sağlıklı Görünüşlü ve Solunum Sistemi Problemli Barınak Kedilerinde Feline Herpesvirus Tip 1 (FeHV-1) Enfeksiyonu

Sağlıklı Görünüşlü ve Solunum Sistemi Problemli Barınak Kedilerinde Feline Herpesvirus Tip 1 (FeHV-1) Enfeksiyonu

Autophagy up-regulation upon FeHV-1 infection on permissive cells.

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Apoptosis is mediated by FeHV-1 through the intrinsic pathway and interacts with the autophagic process

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