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Peer-reviewedCC BY 4.0Frontiers in Endocrinology

HIV viral protein expression disrupts bone tissue homeostasis in mice

  • Joan Villarroya1,2
  • Natalia Artigas3
  • Tania Quesada-López1,2
  • Rubén Cereijo1,2
  • Pere Domingo4
  • Francesc Villarroya1,2
  • Francesc Ventura3
  • Marta Giralt1,2
4 affiliations
  1. 1Department of Biochemistry and Molecular Biomedicine and Institute of Biomedicine (IBUB), University of Barcelona
  2. 2CIBER “Fisiopatología de la Obesidad y Nutrición” (CIBEROBN), Instituto de Salud Carlos III
  3. 3Department of Physiological Sciences, University of Barcelona, and IDIBELL
  4. 4Infectious Diseases Unit, Hospital de la Santa Creu i Sant Pau
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Abstract

HIV infection is associated with metabolic and skeletal comorbidities that persist despite effective antiretroviral therapy. However, the direct contribution of viral proteins to these alterations remains incompletely understood. Here, we investigated the impact of HIV transgene expression on adipose tissue content, inflammatory status, and bone tissue homeostasis in mice. HIV transgenic mice Tg26 exhibited lipoatrophy in both young and aged animals, accompanied by only mild changes in systemic inflammatory parameters. In parallel, HIV transgene expression was associated with early-onset bone loss, affecting both cortical and trabecular compartments. Molecular analyses of calvarial bone revealed dysregulation of key regulators of bone remodeling, indicating an imbalance in osteoblast and osteoclast activity. Consistently, circulating bone turnover markers were elevated in HIV transgenic mice, supporting a state of increased, coupled high-turnover bone remodeling. Collectively, these findings suggest that HIV viral protein expression is sufficient to induce persistent alterations in skeletal homeostasis, highlighting a role of viral factors in the pathogenesis of HIV-associated metabolic and bone disease.

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Cite

BibTeXRIS
BibTeX
@article{villarroya2026viral,
  title = {{HIV viral protein expression disrupts bone tissue homeostasis in mice}},
  author = {Joan Villarroya and Natalia Artigas and Tania Quesada-López and Rubén Cereijo and Pere Domingo and Francesc Villarroya and Francesc Ventura and Marta Giralt},
  journal = {Frontiers in Endocrinology},
  year = {2026},
  month = oct,
  doi = {10.3389/fendo.2026.1920538},
  url = {https://www.frontiersin.org/articles/10.3389/fendo.2026.1920538/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - HIV viral protein expression disrupts bone tissue homeostasis in mice
AU  - Joan Villarroya
AU  - Natalia Artigas
AU  - Tania Quesada-López
AU  - Rubén Cereijo
AU  - Pere Domingo
AU  - Francesc Villarroya
AU  - Francesc Ventura
AU  - Marta Giralt
PY  - 2026
DA  - 2026/10/20
JO  - Frontiers in Endocrinology
DO  - 10.3389/fendo.2026.1920538
UR  - https://www.frontiersin.org/articles/10.3389/fendo.2026.1920538/full
AB  - HIV infection is associated with metabolic and skeletal comorbidities that persist despite effective antiretroviral therapy. However, the direct contribution of viral proteins to these alterations remains incompletely understood. Here, we investigated the impact of HIV transgene expression on adipose tissue content, inflammatory status, and bone tissue homeostasis in mice. HIV transgenic mice Tg26 exhibited lipoatrophy in both young and aged animals, accompanied by only mild changes in systemic inflammatory parameters. In parallel, HIV transgene expression was associated with early-onset bone loss, affecting both cortical and trabecular compartments. Molecular analyses of calvarial bone revealed dysregulation of key regulators of bone remodeling, indicating an imbalance in osteoblast and osteoclast activity. Consistently, circulating bone turnover markers were elevated in HIV transgenic mice, supporting a state of increased, coupled high-turnover bone remodeling. Collectively, these findings suggest that HIV viral protein expression is sufficient to induce persistent alterations in skeletal homeostasis, highlighting a role of viral factors in the pathogenesis of HIV-associated metabolic and bone disease.
SN  - 1664-2392
ER  -