ReviewJournal of personalized medicine2023
Bidirectional Relationship between HIV/HBV Infection and Comorbid Depression and/or Anxiety: A Systematic Review on Shared Biological Mechanisms.
Review in Journal of personalized medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Effects of exercise therapy on anxiety and depression in patients with COVID-19: a systematic review and meta-analysis.Frontiers in public health · 2024Pooled it
- Factors influencing breastfeeding failure in mothers with hepatitis B infection: a qualitative study.Frontiers in nutrition · 2026Article
- CD4Frontiers in psychiatry · 2026Article
- Construction of a depression risk prediction model for hepatitis B patients based on machine learning strategy.PloS one · 2026Article
- Long-term psychological and functional outcomes after hepatitis C eradication with direct-acting antivirals: an 80-month follow-up study.Frontiers in psychiatry · 2026Article
- Psychiatric symptoms and necroinflammatory activity in chronic hepatitis B: a cross-sectional study.BMC infectious diseases · 2025Article
- Psychiatric comorbidities in HIV/AIDS patients and its overlap with neurological disorders.Discover mental health · 2025Review
- Article
- Future Challenges for the Diagnosis and Management of Affective Disorders: From Preclinical Evidence to Clinical Trials.Brain sciences · 2025Article
- HIV-associated depression: a translational framework targeting neuroimmune inflammation and psychosocial stress modulation.Frontiers in immunology · 2025Review
- Is There such a Thing as Post-Viral Depression?: Implications for Precision Medicine.Biomolecules & therapeutics · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMental disorders that are comorbid with chronic infectious diseases may worsen clinical outcomes and patients' quality of life. We hypothesized that depression and/or anxiety syndromes or symptoms comorbid with human immunodeficiency virus (HIV) or hepatitis B virus (HBV) infection might stem from shared biological mechanisms.
methodsWe conducted a systematic review applying the PRISMA statement by searching into the PubMed, APA PsycInfo, and Scopus databases. We examined the literature on HIV/HBV infection comorbid with depression and/or anxiety in adults ≥18 years.
resultsThirty-one studies on HIV and three on HBV were analyzed. The Tat protein contributed to HIV-associated mood disorders due to the protein's ability to cause neurodegeneration and induce hypothalamic-pituitary-adrenal (HPA) axis dysregulation in response to natural stressors. The decreased brain-derived neurotrophic factor (BDNF) levels also emerged as a mechanism involved in HIV neuropathogenesis and the associated mood symptoms. Neuroinflammation was implicated in depression and/or anxiety onset in patients with HIV/HBV infections. Microglial activation and release of cytokines, in particular, appeared as potential pathogenetic mechanisms. Furthermore, an altered balance between quinolinic acid and kynurenic acid production emerged in HIV patients with comorbid depression, indicating a glutamatergic dysfunction. Inflammatory cytokine production and the downregulation of cellular immune responses contributed to persisting inflammation, delayed healing, and functional decline in patients with chronic hepatitis B (CHB) infection. A shift in type 1-type 2 cytokine balance might be implicated in HBV-related immune pathogenesis, and depression and anxiety might be considered immunomodulatory factors. Cytokines also caused HPA axis hyperactivity, frequently observed in HIV/HBV patients with comorbid depression/anxiety.
conclusionsThe present systematic review showed, for the first time, that HIV/HBV and depression and/or anxiety might have several biological mechanisms as common denominators. The longitudinal course of the highlighted biological mechanisms should be explored to establish the causative interrelationship among the involved mechanisms. In addition, future research should investigate the possibility that a patient's clinical outcome might improve using pharmacological treatments acting on the biological mechanisms we described as common denominators of chronic inflammatory infective diseases and depression/anxiety.
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