What is BK virus (BKV) Infection?

BK Virus (BKV) Infection also known as polyomavirus is a member of the human polyomavirus family. BKV resides dormant in uroepithelial cells as it is mostly acquired in childhood and is not known to cause tissue damage in immunocompetent individuals. The virus can become reactivated in case of immunodeficiency (e.g., secondary to HIV infection or immunosuppressive medications), and result in cellular damage and organ dysfunction.

The kidney, lung, eye, liver, and brain are sites of BK virus-associated disease, both primary and reactivated. BK virus infection in the kidney manifests as hemorrhagic cystitis, ureteric stenosis, nephritis and others. Pulmonary diseases that involve BK virus include pneumonitis and acute nonspecific upper respiratory tract infection.

In transplant recipients, however, BKV reactivation is common and can lead to distinctive pathological entities in different patient groups such as in renal transplant (RT) recipients, it is associated with nephropathy (BKVN) and ureteral stenosis, and in hematopoietic stem cell transplant (HSCT) recipients with hemorrhagic cystitis (HC).

The symptoms of the infection include changes in vision and color of your urine (urine that is brown or red in color), pain while urinating, increase in urination frequency, cough, cold or trouble breathing, fever, muscle pain or weakness, seizures.

Unfortunately, there are no marketed drugs for this infection and the mainstay of managing reactivation is by immunosuppression, which is achieved by discontinuation of an agent, decreasing an agent, switching immunosuppressant within the same or another class, and steroid avoidance.

Nephropathy (PVAN) occurs most often in renal transplantation patients within 1 year of transplantation. The risk of BK virus reactivation after 1 year is greatly reduced. Late onset BK reactivation in patients more than 1 year from transplant is associated with changes in immunosuppression such as steroid pulse to treat chronic rejection.

Factors associated with increased risk of BK virus reactivation include prior exposure to BK virus, older age of the host, and high anti-BK virus IgG levels prior to transplantation.

BKV infections generally occur in patients, which undergo transplantation or surgical procedures. Viral infections after renal transplantation have emerged as an important cause of allograft loss. It affects about 15% of renal transplant recipients in the first post-transplant year and lack an effective prophylaxis strategy.

The diagnosis methodologies and incremental healthcare spending across the world. The launch of emerging therapies is expected during the forecast period of 2021–2030.Owing to the positive outcomes of the some of the rare candidates during the developmental stage by key players, such

AlloVir (Viralym-M), Amplyx Pharmaceuticals (MAU868) and others have the potential to create a significant positive shift in BK virus infection market size. However, there are few other companies such as Memo Therapeutics and others that are also involved in developing therapeutic interventionsin preclinicalstage of development.

BK polyomavirus causes frequent infections during childhood and establishes persistent infections within renal tubular cells and the uroepithelium, with minimal clinical implications.

The goal in treating BKV replication is to eliminate the virus while preserving the maximal amount of renal function. Treatment options for BKV infections come from studies in the kidney and bone marrow transplant population. As BKV infection involves reactivation of a latent virus in the setting of a suppressed immune system, the most widely accepted intervention is to reduce immunosuppression. The prevention of BKVN by monitoring BK viral load and appropriately decreasing immunosuppression for BKV replication appears to improve graft survival in non-randomized trials in the kidney transplant population.

Reduction of immunosuppression is the mainstay of BKVN treatment. Management approaches differ and can include discontinuation of the anti-metabolite, dose reduction of the calcineurin inhibitor (CNI) by 25–50% targeting significantly lower levels (tacrolimus 3–4 ng/mL and cyclosporine 50–100 ng/mL, or even less) or switching from tacrolimus to cyclosporine. Despite reduction in immunosuppression, renal allograft losses have been reported and this has led to the use of antiviral agents in addition to reduction in immunosuppression.

The use of anti-viral therapy such as leflunomide or cidofovir has also decreased immunosuppression in some cases. Leflunomide is an immunosuppressant medication developed for use in treatment of rheumatoid arthritis. Moreover, Cidofovir, a nucleoside analogue is also used in the treatment of cytomegalovirus retinitis, has shown activity against BKV. The drug has also showed conjunction with lowering immunosuppression.

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