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ORIGINAL RESEARCH article

Front. Microbiol.

Sec. Virology

Volume 16 - 2025 | doi: 10.3389/fmicb.2025.1658838

The role of glycerophospholipid metabolism in feline parvovirus infected CRFK cells

Provisionally accepted
  • Ludong University, Yantai, China

The final, formatted version of the article will be published soon.

Background: Feline panleukopenia, caused by the highly lethal feline parvovirus (FPV), lacks effective prevention and treatment strategies. This study aimed to elucidate the key metabolic regulatory mechanisms during FPV infection.Methods: CRFK cells were infected with the FPV013 strain. Viral identification was performed via cytopathic effect (CPE) observation, transmission electron microscopy (TEM), PCR, and VP2 protein detection using Western blot and immunofluorescence.Untargeted metabolomics analyzed metabolic changes at 12h, 24h, and 48h postinfection (hpi). Key pathways were validated through enzyme activity inhibition (Meclizine targeting PCYT2) and gene silencing (siRNA targeting PLPP1 and LPIN3). Results: Metabolomics revealed the most significant differences at 48 hpi, identifying six significantly altered glycerophospholipid metabolites. Inhibiting PCYT2 enzyme activity significantly reduced viral load (p < 0.01). Silencing either phospholipid phosphatase 1 (PLPP1) or LPIN3 significantly inhibited FPV replication, with IF staining showing reduced VP2 expression (p < 0.01). In contrast, blocking fatty acid synthesis (TOFA/C75 treatment) had no significant effect. Conclusion: FPV infection promotes replication by reprogramming host cell glycerophospholipid metabolism. The PCYT2-mediated PE/PC synthesis pathway and the PLPP1 or LPIN3 regulated diacylglycerol (DG) generation pathway play central roles. This finding highlights the pivotal role of glycerophospholipid metabolism during FPV infection, offering insights into antiviral strategies targeting this pathway.

Keywords: FPV013, PLPP1, Lpin3, glycerophospholipid metabolism, viral replication

Received: 03 Jul 2025; Accepted: 05 Aug 2025.

Copyright: © 2025 Sun, Zhu, Liu, Zhang, Jiang, Yu and Yu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Xin Yu, Ludong University, Yantai, China
Jiayu Yu, Ludong University, Yantai, China

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