BK Virus: Infection, Transmission & Diseases

BK virus is a polyomavirus. These describe a group of naked virus particles with a DNA genome. The virus is found throughout the world and almost everyone has contracted the virus, as it is usually transmitted in childhood and persists throughout life. The virus is the causative agent of polyomavirus nephropathy, or PVN.

What is the BK virus?

BK virus (HPyV-1 for short) is a virus that is found throughout the world. It belongs to the family Polyomaviridae, and to the genus Polyomavirus. Human polyomavirus 1 is a synonym for the BK virus. The pathogen is likely transmitted in childhood and then subsequently enters the kidney or central nervous system (CNS), where it eventually persists throughout life. During its persistence, the virus can replicate. However, this only happens when the human body suffers from a weakness of the immune system, as is the case with AIDS or even pregnancy. This is why the BK virus is also called an opportunistic pathogen. The BK virus is a naked virus particle, which means that it is not surrounded by a lipid envelope. Therefore, the pathogen is much more stable and resistant to various environmental influences than viruses surrounded by a lipid envelope. The genome carried by the virus is a double-stranded DNA. The pathogen was first found in 1971 in the urine of a patient who had a kidney transplant. His initials were B. K., which is why the virus was named after him.

Occurrence, distribution, and characteristics

BK virus is found throughout the world. Approximately 75 percent of the world’s population carries the virus. Apparently, the pathogen is transmitted in childhood via smear infection with urine, droplet infection, or through contaminated drinking water and remains persistent in humans throughout life. If the body is infected, the virus spreads to the kidney or central nervous system. When first infected, infection by the virus passes without symptoms in healthy people. However, if the human immune system is weakened, the pathogen may reactivate and multiply. Viral replication is also frequently observed during therapy with immunosuppressants after kidney transplantation. BK nephropathy occurs in about 5 percent of kidney transplant recipients, approximately 8 to 13 months after transplantation. In case of multiplication, there is also an increased risk of infection, as the pathogen is then increasingly excreted in the urine. The BK virus does not carry a lipid envelope, which makes the virus more resistant to various environmental influences. Disinfection alone, for example, is not sufficient to prevent infection with the virus. Special disinfectants are needed for this purpose. The BK virus has a double-stranded DNA. Only a few viruses are unenveloped DNA viruses. These include the adenoviruses, the human papillomavirus, and the second polyomavirus relevant to human medicine, the JC virus. The DNA can be divided into two sections. One section contains the noncoding portion that regulates the control region, replication, and synthesis of viral particles. The other section contains the coding portion of the DNA. This contains the viral proteins, such as the viral capsid proteins VP1, VP2, VP3 and a so-called agnoprotein. The viral genome is surrounded by an icosahedral capsid. This is a protein envelope that forms the viral shape as well as protects the virus. The capsid is composed of the so-called capsomers, which in turn are composed of the capsid proteins VP1, VP2, or VP3.

Diseases and disorders

The BK virus is mainly responsible for the so-called polyomavirus nephropathy. This is a kidney disease that occurs more frequently after kidney transplantation. The virus is present in almost everyone, with an infection rate of almost 75 percent. It persists in the epithelial cells of the kidney and multiplies when there is a weakening of the immune system. This weakening is primarily caused by therapeutic immunosuppression using tacrolimus or mycophenolic acid, which are typically used for treatment after kidney transplantation. In this process, the epithelial cells are damaged and lost. The pathogen is increasingly excreted in the urine, which can infect other people with the virus.An inflammatory reaction also occurs, which may be accompanied by reduced organ function. Polyoma-associated nephropathy (PVN) thus manifests as tubulointerstitial nephritis, i.e. inflammation of the kidney. At the beginning of PVN, which occurs in 5 percent of patients after kidney transplantation, there are initially no symptoms. However, if the blood is examined, elevated levels of creatinine may be seen, indicating deterioration of kidney function. In some cases, narrowing of the ureter occurs, resulting in urinary retention. Although rare, inflammation of the urinary bladder may still occur. Other non-specific symptoms include fever, rash and joint pain, and flank pain. In the worst case, graft rejection occurs.