The pathogenicity and multi-organ proteomic profiles of Mpox virus infection in SIVmac239-infected rhesus macaques

Dong Zhang, Jiangfeng Liu, Lin Zhu, Baoying Huang, Zhe Cong, Na Li, Jingjing Zhang, Ting Chen, Jianrong Ma, Jiahan Lu, Yongzhi Hou, Chenbo Yang, Wanjun Peng, Qiang Wei (), Wenjie Tan (), Juntao Yang () and Jing Xue ()
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Dong Zhang: Peking Union Medical College
Jiangfeng Liu: School of Basic Medicine Peking Union Medical College
Lin Zhu: Peking Union Medical College
Baoying Huang: Chinese Center for Disease Control and Prevention
Zhe Cong: Peking Union Medical College
Na Li: Peking Union Medical College
Jingjing Zhang: Peking Union Medical College
Ting Chen: Peking Union Medical College
Jianrong Ma: Peking Union Medical College
Jiahan Lu: Peking Union Medical College
Yongzhi Hou: Peking Union Medical College
Chenbo Yang: Peking Union Medical College
Wanjun Peng: School of Basic Medicine Peking Union Medical College
Qiang Wei: Peking Union Medical College
Wenjie Tan: Chinese Center for Disease Control and Prevention
Juntao Yang: School of Basic Medicine Peking Union Medical College
Jing Xue: Peking Union Medical College

Nature Communications, 2025, vol. 16, issue 1, 1-15

Abstract: Abstract Mpox poses a heightened risk of severe disease and mortality among individuals with HIV, yet the molecular mechanisms and immunopathology underlying multi-organ damage caused by the mpox virus (MPXV), particularly in the context of HIV co-infection, remain poorly understood. Here, we observe increased MPXV replication, more extensive skin lesions, and impaired humoral and cellular immune responses in SIV-MPXV co-infected rhesus macaques compared to those infected with MPXV alone. Multi-organ proteomic and phosphoproteomic analyses reveals upregulation of proteins involved in immune and inflammatory pathways in skin lesions and across multiple organs, especially in immune-related tissues. Abnormal activation of DNA replication and cell cycle signaling pathways, which may contribute to enhanced viral replication, is evident in both MPXV and SIV-MPXV co-infected groups. CDK4/6 may present a potential therapeutic target to suppress MPXV replication. These comprehensive proteomic datasets offer valuable insights into the pathogenesis of MPXV in the context of SIV co-infection and support ongoing efforts to mitigate the impact of mpox.

Date: 2025
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DOI: 10.1038/s41467-025-62919-z

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