BK virus

Although without any clinical symptoms, footprints of BK virus have been detected in specimens from females affected by spontaneous abortion.

A survey of 400 healthy blood donors was reported as showing that 82% were positive for IgG against BK virus.

[6] In some renal transplant patients, the necessary use of immunosuppressive drugs has the side-effect of allowing the virus to replicate within the graft, a disease called BK nephropathy.

[citation needed] BK viremia load > 185 000 copies/ml at the time of first positive BKV diagnosis – to be the strongest predictor for BKVAN (97% specificity and 75% sensitivity).

In addition the BKV peak viral loads in blood reaching 223 000 copies/ml at any time was found to be predictive for BKVAN (91% specificity and 88% sensitivity) .

A recent surge in BKVAN correlates with use of potent immunosuppressant drugs, such as tacrolimus and mycophenolate mofetil (MMF).

[citation needed] In a study conducted by Teschner et al. in 2009, 12/13 patients who had their MMF exchanged with leflunomide cleared the virus by 109 days.

Both of these viruses can be identified and differentiated from each other by carrying out serological tests using specific antibodies or by using a PCR-based genotyping approach.

Transcription from ORI site produces mRNA coding the early, functional proteins, known as small and large T antigens, (sTAg and LTAg).

The most common and transmissible (wild-type) form based on NCCR region is called Archetype and has five sequence blocks (O-P-Q-R-S).

Rearranged virus can have deletions, insertions or other types of mutations that lead to variation in the P-Q-R-S blocks.

[16] Based on DNA sequence variation, BKV is categorized into four genotypes (I, II, III, IV) which are further divided into subtypes (Ia, Ib1, Ib2, Ic, and IVa1, IVa2, IVb1, IVb2, IVc1, IVc2).

The capsid proteins VP1-3 are produced in the cytoplasm and later recruited to the nucleus in order to assemble new virus particles.

The virus can transfer viral components or even infectious particles between cells using cellular secretory system by utilizing extracellular vesicles.

Another mechanism on how the virus can be self-limiting is by using microRNA and targeting the DNA sequence of the functional protein Large T antigen.

This miRNA is transcribed during the late viral phase and is believed to effectively limit the archetype virus form.

Small T antigen can interact with a cellular enzyme protein phosphatase 2A which interferes with cell cycle progression.

Micrograph showing a polyomavirus infected cell – large (blue) cell below-center-left. Urine cytology specimen.
Different viral forms based on NCCR sequence variant (archetype or rearranged). The NCCR contains O,P,Q,R,S blocks and their variations.