BK polyomavirus (BKV) is associated with urinary apparatus pathogenesis in kidney transplant recipient. Immune suppression triggers BKV reactivation that potentially causes polyomavirus associated nephropathy (PVAN), a major post-transplant problem causes graft rejection. Antiviral immunity plays the key role in limiting the viral replication but selection by the immune system or antivirals may cause the evolvement of escape variants with higher fitness. Mutation in VP1, the major capsid protein can allow BKV to escape neutralizing antibodies. In an attempt to detect co-infection and minor variants, BKV VP1 genomic region was amplified by PCR and analysed by deep sequencing from plasma samples of four kidney transplant recipients. BKV genotype I and IV was identified in patients and each patient was detected with one BKV genotype. Multiple point mutations and subsequent changes in amino acid were detected in majority, three out of four, of the patients.
| Identifer | oai:union.ndltd.org:UPSALLA1/oai:DiVA.org:uu-425227 |
| Date | January 2020 |
| Creators | Khatoon, Safia |
| Publisher | Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi |
| Source Sets | DiVA Archive at Upsalla University |
| Language | English |
| Detected Language | English |
| Type | Student thesis, info:eu-repo/semantics/bachelorThesis, text |
| Format | application/pdf |
| Rights | info:eu-repo/semantics/openAccess |
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