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<p>Mamestra brassicae multiple nucleopolyhedrovirus (MbMNPV) has been widely used as a biocontrol agent against <i>Helicoverpa armigera</i> in China. To understand the relationship between the metabolic response in <i>H. armigera</i> and MbMNPV infection, we analyzed the overall metabolic changes occurring in <i>H. armigera</i> fat bodies during MbMNPV infection. The metabolomic data identified 135 differentially expressed metabolites (DEMs) in the MbMNPV-infected group. Based on the metabolomic data, the changes in phosphatidylcholine levels during the entire infection period and its effect on virus replication were determined. The results showed that virus infection led to a significant upregulation of phosphatidylcholine in <i>H. armigera</i>. Phosphatidylcholine supplementation shortened the median lethal time (LT<sub>50</sub>) and reduced the weight of MbMNPV-infected <i>H. armigera</i>. To further explore the relationship between virus infection and phosphatidylcholine synthesis, we measured the expression of genes related to phosphatidylcholine metabolism and knocked down the significantly upregulated gene <i>LPCAT5</i> using RNA interference. <i>LPCAT5</i> knockdown reduced MbMNPV replication by impairing the biosynthesis of phosphatidylcholine. In addition, MbMNPV infection also affected the central carbon metabolic pathway, which is indirectly related to phosphatidylcholine synthesis. This study shows that MbMNPV infection can promote its own infection process by upregulating the synthesis of phosphatidylcholine, providing new insight into the interactions between MbMNPV and <i>H. armigera</i>.</p>

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Metabolic profiling of baculovirus infection in Helicoverpa armigera fat body shows that Mamestra brassicae multiple nucleopolyhedrovirus promotes self-replication by increasing the synthesis of phosphatidylcholine

  • 期刊论文

  • 发表日期：

    2025年12月15日

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  • Hanwen Cao,
  • Zhenpu Liang,
  • Guozhi Zhang,
  • Xinping Yang,
  • Xiaoxia Zhang

摘要

Mamestra brassicae multiple nucleopolyhedrovirus (MbMNPV) has been widely used as a biocontrol agent against Helicoverpa armigera in China. To understand the relationship between the metabolic response in H. armigera and MbMNPV infection, we analyzed the overall metabolic changes occurring in H. armigera fat bodies during MbMNPV infection. The metabolomic data identified 135 differentially expressed metabolites (DEMs) in the MbMNPV-infected group. Based on the metabolomic data, the changes in phosphatidylcholine levels during the entire infection period and its effect on virus replication were determined. The results showed that virus infection led to a significant upregulation of phosphatidylcholine in H. armigera. Phosphatidylcholine supplementation shortened the median lethal time (LT50) and reduced the weight of MbMNPV-infected H. armigera. To further explore the relationship between virus infection and phosphatidylcholine synthesis, we measured the expression of genes related to phosphatidylcholine metabolism and knocked down the significantly upregulated gene LPCAT5 using RNA interference. LPCAT5 knockdown reduced MbMNPV replication by impairing the biosynthesis of phosphatidylcholine. In addition, MbMNPV infection also affected the central carbon metabolic pathway, which is indirectly related to phosphatidylcholine synthesis. This study shows that MbMNPV infection can promote its own infection process by upregulating the synthesis of phosphatidylcholine, providing new insight into the interactions between MbMNPV and H. armigera.