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Preview of Review of BK-Virus: Structure, Epidemiology, and Pathogenesis
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Summary

- BK Virus (BKV) Structure: Non-enveloped, 40nm diameter, icosahedral capsid, circular double-stranded DNA genome (~5kb), divided into early (small/large T-antigens), late (VP1, VP2, VP3), and non-coding control regions (NCCR).
- Epidemiology: Prevalent in 75-90% of the general population, seroconversion occurs between ages 5-10. Transmitted via respiratory, uro-oral, faecal-oral, blood-borne, sexual routes, and possibly transplacental. Persists in kidney epithelial cells and reactivates asymptomatically, shedding into urine (5-10% of immunocompetent adults, 25-50% of pregnant women).
- Pathogenesis: T-antigen, an early gene product, has oncogenic potential, interacting with tumor suppressors p53 and pRb. BKV is classified into four genotypes (I-IV), with type I being most prevalent. No clear correlation between subtypes and clinical characteristics.
- Diagnosis & Treatment: Gold standard for BKVAN diagnosis is renal biopsy, but non-invasive methods like urine cytology and quantitative PCR (qPCR) are common. Therapy focuses on reducing immunosuppression and restoring immunity, with cidofovir (nucleotide analogue of cytosine) used cautiously for treatment.

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Structure, Epidemiology, Pathogenesis; Role in Cancer Development

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  • File Format: PDF
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  • Language: EN
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