Scholarlink

Background <p><i>Alphanecrovirus tessellati</i> and <i>Alphanecrovirus oleae</i> are closely related alphanecroviruses, sharing over 74% genomic identity and frequently co-infecting plants under natural conditions. Despite their frequent coexistence, the molecular consequences of single versus mixed infections, particularly concerning host RNA silencing responses, remain poorly understood. Here, we investigated the antiviral defense responses of <i>Nicotiana benthamiana</i> to single and mixed infections with both viruses, focusing on symptom development, viral accumulation, <i>Dicer-like</i> (<i>DCL</i>) gene expression, and virus-derived small interfering RNA (vsiRNA) profiles.</p> Results <p>Single infections resulted in contrasting disease phenotypes: <i>A. oleae</i> induced severe systemic necrosis and high viral accumulation, whereas <i>A. tessellati</i> caused transient infections with mild symptoms. In mixed infections, <i>A. tessellati</i> accumulated to significantly higher levels and was associated with enhanced disease severity, indicating that the interaction between the two viruses altered infection dynamics and favored <i>A. tessellati</i> accumulation. In contrast, <i>A. oleae</i> showed reduced relative genomic RNA accumulation in mixed infections despite the persistence of disease symptoms. Gene expression analyses showed consistent upregulation of <i>DCL4</i> and <i>DCL2</i> during mixed infection, supporting their involvement in antiviral RNA silencing under co-infection conditions. Small RNA profiling revealed infection-dependent differences in vsiRNA accumulation patterns. Notably, mixed infection was associated with a change in the predominant vsiRNA size class for <i>A. oleae,</i> alongside a shift in vsiRNAs genomic targeting from the RdRp gene during single infection to the suppressor-associated p6 gene during mixed infection, indicating a reprogramming of host silencing responses.</p> Conclusions <p>Our results demonstrate that closely related viruses can differentially modulate host RNA silencing responses depending on the infection context. These findings highlight the plasticity of antiviral RNA silencing during viral co-infections and provide new insights into how mixed infections reshape host-virus interactions at the molecular level.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Mixed viral infections uncover multifaceted RNA silencing strategies in plant antiviral defense

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月7日

查看全文
  • Patrick Materatski,
  • Joana Amaro Ribeiro,
  • Cristiana Marques,
  • André Albuquerque,
  • Maria do Rosário Félix,
  • Carla Varanda

摘要

Background

Alphanecrovirus tessellati and Alphanecrovirus oleae are closely related alphanecroviruses, sharing over 74% genomic identity and frequently co-infecting plants under natural conditions. Despite their frequent coexistence, the molecular consequences of single versus mixed infections, particularly concerning host RNA silencing responses, remain poorly understood. Here, we investigated the antiviral defense responses of Nicotiana benthamiana to single and mixed infections with both viruses, focusing on symptom development, viral accumulation, Dicer-like (DCL) gene expression, and virus-derived small interfering RNA (vsiRNA) profiles.

Results

Single infections resulted in contrasting disease phenotypes: A. oleae induced severe systemic necrosis and high viral accumulation, whereas A. tessellati caused transient infections with mild symptoms. In mixed infections, A. tessellati accumulated to significantly higher levels and was associated with enhanced disease severity, indicating that the interaction between the two viruses altered infection dynamics and favored A. tessellati accumulation. In contrast, A. oleae showed reduced relative genomic RNA accumulation in mixed infections despite the persistence of disease symptoms. Gene expression analyses showed consistent upregulation of DCL4 and DCL2 during mixed infection, supporting their involvement in antiviral RNA silencing under co-infection conditions. Small RNA profiling revealed infection-dependent differences in vsiRNA accumulation patterns. Notably, mixed infection was associated with a change in the predominant vsiRNA size class for A. oleae, alongside a shift in vsiRNAs genomic targeting from the RdRp gene during single infection to the suppressor-associated p6 gene during mixed infection, indicating a reprogramming of host silencing responses.

Conclusions

Our results demonstrate that closely related viruses can differentially modulate host RNA silencing responses depending on the infection context. These findings highlight the plasticity of antiviral RNA silencing during viral co-infections and provide new insights into how mixed infections reshape host-virus interactions at the molecular level.