Plant virus manipulates insect vector immunity via C2 factor

A study published in Virology Journal reveals that the virus uses a specific viral protein to suppress the insect’s natural antiviral defenses while simultaneously promoting conditions that favor viral accumulation. This manipulation involves a complex shift in the insect’s lipid signaling pathways, specifically altering the balance between two classes of oxylipins that exert opposing effects on viral infection.

The virus is transmitted through a circulative and replicative pathway, meaning it must survive and multiply within the insect’s body before being passed to a new plant host. To achieve this, the virus must navigate the insect’s immune system, which typically works to eliminate pathogens. The study focused on oxylipins, which are lipid-derived signaling molecules that regulate insect immunity. Among these, eicosanoids are generally known to promote antiviral responses, whereas C18 epoxyoctadecamonoenoic acids, or EpOMEs, act as immune suppressors.

To understand the molecular mechanisms behind this immune manipulation, the researchers employed a multi-faceted experimental approach. Quantitative PCR was used to measure viral accumulation, while liquid chromatography-tandem mass spectrometry allowed for the precise quantification of EpOME levels. The team also utilized RNA interference to silence specific candidate genes involved in lipid biosynthesis and degradation, as well as all six genes of the TYLCV genome, to determine their functional roles in the infection process.

The results demonstrated that TYLCV progressively accumulates in the intestine of B. tabaci and significantly alters fatty acid metabolism. Two distinct oxylipin pathways were found to have antagonistic effects on viral accumulation. Prostaglandin E2, along with its biosynthetic machinery, functioned as an antiviral regulator. In contrast, both isomers of EpOME, specifically 9,10- and 12,13-EpOME, promoted viral accumulation. The virus infection led to a more than two-fold increase in EpOME levels. This shift was achieved transcriptionally by inducing the gene Bt-CYP6, which is associated with EpOME synthesis, while suppressing Bt-sEH2 and Bt-sEH3, which are associated with EpOME degradation.

Pharmacological and genetic analyses confirmed the roles of these genes. Bt-CYP6 was identified as an EpOME-associated synthase, while Bt-sEH2 and Bt-sEH3 were confirmed as degradation-associated genes. The promotion of EpOME signaling by the virus had downstream effects on the insect’s physiology. This included the induction of proviral factors such as defensin and cathepsins, while suppressing selected antiviral factors like PGRP and cathepsin-F. This reshaping of the immune landscape creates a more permissive environment for the virus to replicate.

Among all six genes of the TYLCV genome, only the C2 virulence factor controlled the host’s EpOME machinery. When the C2 gene was silenced, the induction of Bt-CYP6 was abolished, and the expression of Bt-sEH2 and Bt-sEH3 was restored. Furthermore, the addition of exogenous EpOME was able to rescue viral accumulation in the absence of the C2 factor.

The study also compared different strains of TYLCV to assess the relationship between virulence and immune manipulation. The more virulent strain, TYLCV-IL, induced stronger EpOME signaling and apoptosis compared to the less virulent strain, TYLCV-Mld. The ability to shift the host from an antiviral eicosanoid-dominant state to a proviral EpOME-dominant state appears to be a key determinant of successful viral transmission.

These findings provide a detailed molecular mechanism for how a plant virus manipulates its insect vector to enhance its own transmission. By targeting the oxylipin signaling pathways, TYLCV effectively disables the insect’s antiviral defenses and promotes viral accumulation.

Subject of Research: Molecular mechanisms of TYLCV manipulation of Bemisia tabaci oxylipin signaling

Article Title: A plant virus, TYLCV, up-regulates an endocrine oxylipin signal in its insect vector, Bemisia tabaci, via the viral C2 virulence factor for viral transmission

Article References: Shahmohammadi, N., Song, T.-G., Son, M.-C., Jeon, J., Lee, D., Kil, E.-J., & Kim, Y. (2026). A plant virus, TYLCV, up-regulates an endocrine oxylipin signal in its insect vector, Bemisia tabaci, via the viral C2 virulence factor for viral transmission. Virology Journal. https://doi.org/10.1186/s12985-026-03354-4

Image Credits: AI Generated

DOI: 10.1186/s12985-026-03354-4

Keywords: TYLCV, Bemisia tabaci, oxylipins, C2 virulence factor, EpOME, prostaglandin E2, viral transmission, insect immunity, RNA interference, intestinal apoptosis, fatty acid metabolism, viral accumulation, immune suppression, plant virus, whitefly vector, lipid signaling, circulative transmission, Bt-CYP6, Bt-sEH2, viral virulence