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Background <p><i>Mycoplasma pneumoniae</i>(<i>M. pneumoniae</i>) is one of the most frequent causes of community acquired pneumonia (CAP) in children, while Epstein-Barr virus(EBV) infection typically presents subclinical manifestations in immunocompetent children. Although single <i>M. pneumoniae</i> infection is common enough, <i>M. pneumoniae</i> and EBV co-infection has received little attention in clinical practice. It is worth noting that there have been reports of children with <i>Mycoplasma pneumoniae</i> pneumonia(MPP) coinfect with EBV often suffering from more severe lung injury and affecting multiple organ systems. However, the underlying shared targets or pathways remain unclear. This study aims to preliminarily explore the shared targets and pathways of EBV co-infection in pediatric patients with MPP by using network analysis methods.</p> Methods <p>Relevant targets of MPP and EBV infection were obtained through database mining. The protein-protein interaction(PPI) network construction, Gene Ontology (GO) enrichment analysis and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were employed to identify the shared core target genes and key signalling pathways.</p> Results <p>A total of 425 MPP-related target genes and 744 EBV infection-related target genes were obtained, respectively. 113 shared targets were involved in co-infection, and 5 core proteins were obtained through screening, including tumor necrosis factor alpha(TNF-α), interleukin-6(IL-6), interleukin-2(IL-2), interleukin-10(IL-10), and interferon gamma(IFN-γ), which were common inflammatory cytokines. The clinical manifestations both inside and outside the lungs of MPP children with EBV co-infection were more severe than those of children with simple <i>M. pneumoniae</i> infection, which is related to the fact that their shared pathways are mainly enriched in immune responses.</p> Conclusions <p>The results indicate that multiple shared inflammatory cytokines and pathways are present between M. pneumoniae and EBV co-infection, confirming that the severe symptoms and poor prognosis of co-infection are related to immune injury. As a network-based bioinformatics analysis, these findings are hypothesis-generating and require further experimental and clinical validation.</p> Clinical trial number <p>Not applicable.</p>

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Network analysis of Mycoplasma pneumoniae pneumonia and Epstein-Barr virus co-infection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月10日

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  • Junya Song,
  • Yin Lv,
  • Xin Pei,
  • Yan Wang,
  • Shengnan Li,
  • Yuehua Yao,
  • Ning Jiang

摘要

Background

Mycoplasma pneumoniae(M. pneumoniae) is one of the most frequent causes of community acquired pneumonia (CAP) in children, while Epstein-Barr virus(EBV) infection typically presents subclinical manifestations in immunocompetent children. Although single M. pneumoniae infection is common enough, M. pneumoniae and EBV co-infection has received little attention in clinical practice. It is worth noting that there have been reports of children with Mycoplasma pneumoniae pneumonia(MPP) coinfect with EBV often suffering from more severe lung injury and affecting multiple organ systems. However, the underlying shared targets or pathways remain unclear. This study aims to preliminarily explore the shared targets and pathways of EBV co-infection in pediatric patients with MPP by using network analysis methods.

Methods

Relevant targets of MPP and EBV infection were obtained through database mining. The protein-protein interaction(PPI) network construction, Gene Ontology (GO) enrichment analysis and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were employed to identify the shared core target genes and key signalling pathways.

Results

A total of 425 MPP-related target genes and 744 EBV infection-related target genes were obtained, respectively. 113 shared targets were involved in co-infection, and 5 core proteins were obtained through screening, including tumor necrosis factor alpha(TNF-α), interleukin-6(IL-6), interleukin-2(IL-2), interleukin-10(IL-10), and interferon gamma(IFN-γ), which were common inflammatory cytokines. The clinical manifestations both inside and outside the lungs of MPP children with EBV co-infection were more severe than those of children with simple M. pneumoniae infection, which is related to the fact that their shared pathways are mainly enriched in immune responses.

Conclusions

The results indicate that multiple shared inflammatory cytokines and pathways are present between M. pneumoniae and EBV co-infection, confirming that the severe symptoms and poor prognosis of co-infection are related to immune injury. As a network-based bioinformatics analysis, these findings are hypothesis-generating and require further experimental and clinical validation.

Clinical trial number

Not applicable.