Published online Mar 25, 2026. doi: 10.5501/wjv.v15.i1.118225
Revised: January 25, 2026
Accepted: March 5, 2026
Published online: March 25, 2026
Processing time: 76 Days and 19.4 Hours
Chronic viral infections, such as human immunodeficiency virus (HIV), hepatitis B (HBV), and hepatitis C (HCV), negatively impact bone health leading to osteopenia/osteoporosis and increased bone fragility. This narrative review aims to provide a comprehensive overview of the contemporary literature on bone changes in patients with chronic viral infections (HIV, HBV, HCV mono-infection, and coinfections), focusing on their clinical implications and the importance of assessing multiscale bone properties to evaluate bone strength decline in these individuals. Previous studies suggest that skeletal alterations in these subjects may arise from direct viral effects on bone cells and from indirect mechanisms involving systemic inflammation, immune dysregulation, therapy-related effects, and distant organ failure (e.g., liver disease). It has been reported that HBV/HCV co-infection in people living with HIV produces the most severe phenotype through additive inflammatory, hepatic, and metabolic insults. Further, an increased risk of developing osteonecrosis of multiple joints has also been reported among people living with HIV. Given the limited contemporary data, future studies should focus on investigating hierarchical alterations in bone structure to deepen our understanding of the complex skeletal changes in patients with chronic viral infections, thereby providing a solid foundation for advancing clinical management. As the population living with chronic viral infections ages, total joint arthroplasty will increasingly become a standard procedure, requiring a deeper understanding of how various hierarchical bone morpho-structural changes affect implant stability and longevity in these patients.
Core Tip: Chronic viral infections, such as human immunodeficiency virus, hepatitis B and hepatitis C mono- and coinfection, negatively impact bone health leading to osteopenia, osteoporosis, and increased bone fragility at an earlier age. However, many questions remain unanswered, underscoring the need for further research into the etiopathogenetic mechanisms underlying multiscale determinants of bone strength to guide more effective, personalized treatments and preventive modalities for these individuals.
