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203,234 studies31 sourcesUpdated 13 min ago
Peer-reviewedCC BYMedComm

Polyomavirus Drives Cerebellar Lesions in AIDS Monkeys With Ataxia.

  • Tian-Zhang Song1
  • Li-Rong Zhang1,2
  • Yun-Mei Wang1
  • Yan Hu1,3
  • Qing Li1
  • Ren-Rong Tian1,4
  • Liu-Meng Yang1
  • Si-Dong Xiong2
  • Dong-Dong Wu1
  • Yong-Tang Zheng1
4 affiliations
  1. 1State Key Laboratory of Genetic Evolution & Animal Models National Resource Center For Non-Human Primates Kunming Institute of Zoology Chinese Academy of Sciences Kunming China.
  2. 2KIZ-SU Joint Laboratory of Animal Model and Drug Development College of Pharmaceutical Sciences Soochow University Suzhou China.
  3. 3University of Chinese Academy of Sciences Beijing China.
  4. 4Yunnan Provincial Key Laboratory of Entomological Biopharmaceutical R&D College of Pharmacy Dali University Dali China.
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Abstract

Cognitive and motor dysfunction occurs in 30%-50% of people with HIV/AIDS. Within this clinical spectrum, HIV-associated ataxia is an uncommon but debilitating disorder with poorly defined neuropathological mechanisms. This study investigated two rhesus macaques with chronic simian immunodeficiency virus (SIV) infection that developed progressive ataxia, characterized by postural imbalance and nystagmus. Comparative neuropathological profiling of cerebellar tissue from ataxic SIV-infected macaques, non-ataxic SIV-infected macaques, and uninfected controls revealed that ataxia was associated with diffuse cerebellar atrophy, disrupted tissue organization, Purkinje cell degeneration, demyelination, glial nodule formation, and prominent microglial neuroinflammation. Cerebellar infection with simian polyomavirus 40 (SV40), a member of the Polyomaviridae family, was identified as the cause of the lesions, with viral tropism primarily involving cerebellar granule neurons. Mechanistically, SV40 infection induced neuronal pyroptosis and inflammatory cytokine release, promoting microglial recruitment and activation, amplifying local neuroinflammation, and culminating in nodular aggregate formation. Collectively, these findings establish SV40 infection as a direct driver of cerebellar pathology in SIV-associated ataxia and define a pathogenic sequence linking granule neuron pyroptosis, microglial activation, and progressive cerebellar injury-a cascade that may parallel polyomavirus-induced ataxia in people living with HIV-1.

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Cite

BibTeXRIS
BibTeX
@article{song2026polyomavirus,
  title = {{Polyomavirus Drives Cerebellar Lesions in AIDS Monkeys With Ataxia.}},
  author = {Tian-Zhang Song and Li-Rong Zhang and Yun-Mei Wang and Yan Hu and Qing Li and Ren-Rong Tian and Liu-Meng Yang and Si-Dong Xiong and Dong-Dong Wu and Yong-Tang Zheng},
  journal = {MedComm},
  year = {2026},
  month = oct,
  doi = {10.1002/mco2.71049},
  url = {https://europepmc.org/article/MED/42898982},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Polyomavirus Drives Cerebellar Lesions in AIDS Monkeys With Ataxia.
AU  - Tian-Zhang Song
AU  - Li-Rong Zhang
AU  - Yun-Mei Wang
AU  - Yan Hu
AU  - Qing Li
AU  - Ren-Rong Tian
AU  - Liu-Meng Yang
AU  - Si-Dong Xiong
AU  - Dong-Dong Wu
AU  - Yong-Tang Zheng
PY  - 2026
DA  - 2026/10/19
JO  - MedComm
DO  - 10.1002/mco2.71049
UR  - https://europepmc.org/article/MED/42898982
AB  - Cognitive and motor dysfunction occurs in 30%-50% of people with HIV/AIDS. Within this clinical spectrum, HIV-associated ataxia is an uncommon but debilitating disorder with poorly defined neuropathological mechanisms. This study investigated two rhesus macaques with chronic simian immunodeficiency virus (SIV) infection that developed progressive ataxia, characterized by postural imbalance and nystagmus. Comparative neuropathological profiling of cerebellar tissue from ataxic SIV-infected macaques, non-ataxic SIV-infected macaques, and uninfected controls revealed that ataxia was associated with diffuse cerebellar atrophy, disrupted tissue organization, Purkinje cell degeneration, demyelination, glial nodule formation, and prominent microglial neuroinflammation. Cerebellar infection with simian polyomavirus 40 (SV40), a member of the Polyomaviridae family, was identified as the cause of the lesions, with viral tropism primarily involving cerebellar granule neurons. Mechanistically, SV40 infection induced neuronal pyroptosis and inflammatory cytokine release, promoting microglial recruitment and activation, amplifying local neuroinflammation, and culminating in nodular aggregate formation. Collectively, these findings establish SV40 infection as a direct driver of cerebellar pathology in SIV-associated ataxia and define a pathogenic sequence linking granule neuron pyroptosis, microglial activation, and progressive cerebellar injury-a cascade that may parallel polyomavirus-induced ataxia in people living with HIV-1.
SN  - 2688-2663
ER  -