What are the key principles of preventing viruses – polyomaviruses (John Cunningham and BK)?
The main polyomaviruses causing disease in humans are the BK, MK (Merkel cell virus), SV40 (simian vacuolating virus), and JC (John Cunningham) viruses.
The precise route of transmission is not known, but the fecal-oral route, respiratory secretions, sexual transmission, and transmission via blood transfusions have all been implicated. Recently, transplacental transmission of infection has also been demonstrated. Primary infection is usually asymptomatic or may present with flu-like symptoms. The viruses remain latent in multiple organ systems, particularly the genitourinary system and the central nervous system.
Clinical disease is seen in patients with immunosuppression, such as those with HIV/AIDS, and particularly in patients with bone marrow or solid organ transplantation (kidney, kidney-pancreas). There is viral reactivation with subsequent viruria and viremia.
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JC virus causes progressive multifocal leukoencephalopathy (PML) in patients with HIV/AIDS. PML has also been diagnosed in patients on immune suppressive monoclonal antibodies such as natalizumab, rituximab, and efalizumab.
BK virus can cause hemorrhagic cystitis in patients with bone marrow transplants (up to 25-60%). BK virus nephropathy is seen in patients with renal transplantation and can cause worsening renal function, tubulointerstitial nephritis, ureteric stenosis, and eventual graft loss. Despite frequent reactivation of BK virus in AIDS patients, clinical manifestations are extremely rare.
MK virus has been implicated in the rare Merkel cell carcinoma, seen in the elderly and the immunosuppressed.
What are the key conclusions for available clinical trials and meta-analyses that inform control of viruses – polyomaviruses (John Cunningham and BK)?
Sixty five to ninety two percent of the population test seropositive for JC virus (major), and about 75-90% of adults are seropositive for BK virus. As primary infection occurs in childhood, and the mode of transmission has not been firmly established, there is no standard infection control practice for polyomaviruses.
What is the role of and impact of viruses – polyomaviruses (John Cunningham and BK) or infections and the need for control relative to infections at other sites or other specific pathogens?
JC virus causes PML in patients with HIV/AIDS and those on monoclonal antibodies such as natalizumab. Treatment here consists of stopping the inciting agent (e.g., natalizumab) or treatment of AIDS.
BK viremia, viruria, and nephritis are seen in 30, 13, and 8% of renal transplant patients, respectively. Polyomavirus-associated nephropathy can lead to graft loss. Some centers now perform pre-emptive monthly screening of blood for BK virus by polymerase chain reaction. This helps in the early identification of viremia, with the appropriate decrease in immunosuppression, and initiation of the appropriate antiviral drug.
Unfortunately, there is no known infection control practice to prevent the acquisition of polyomaviruses.
What national and international guidelines exist related to viruses – polyomaviruses (John Cunningham and BK)?
No guidelines on the infection control of polyomaviruses exist at this time.
What other consensus group statements exist and what do key leaders advise?
Currently, the management of polyomaviruses is dependent on early identification and diagnosis of disease, and early initiation of treatment. For BK virus nephropathy, cidofovir, and leflunomide are effective antiviral drugs, with both BK virus and JC virus responding to the reduction of immunosuppression, and, in the case of HIV/AIDS, initiation of anti-retroviral therapy.
References
Boothpur, R, Brennan, DC. “Human polyoma viruses and disease with emphasis on clinical BK and JC”. Journal of Clinical Virology. vol. 47. pp. 306-312.
Boldorini, R, Allegrini, S, Miglio, U, Paganotti, A, Cocca, N, Zaffaroni, M. “Serological evidence of vertical transmission of JC and BK polyomaviruses in humans”. Journal of General Virology. vol. 92. pp. 1044-1050.
Hirsch, HH, Steiger, J, Polyomavirus, BK. The Lancet Infectious Diseases. vol. Vol 3. October 2003.
Carson, KR, Focosi, D, Major, EO, Petrini, M, Richey, EA, West, DP. “Monoclonal antibody-associated progressive multifocal leucoencephalopathy in patients treated with rituximab, natalizumab, and efalizumab: a Review from the Research on Adverse Drug Events and Reports (RADAR) Project”. The Lancet Oncology. vol. 10. 2009. pp. 816-824.
Feng, H, Shuda, M, Chang, Y, Moore, PS. “Clonal Integration of a Polyomavirus in Human Merkel Cell Carcinoma.”. Science. vol. 319. 2008 February 22. pp. 1096-1100.
Major, EO, Amemiya, K, Tornatore, CS, Houff, SA, Berger, JR. “Pathogenesis and Molecular Biology of Progressive Multifocal Leukoencephalopathy, the JC Virus-Induced Demyelinating Disease of the Human Brain”. Clinical Microbiology Reviews. Jan 1992. pp. 49-73.
Hariharan, S. “BK virus nephritis after renal transplantation”. Kidney International. vol. 69. pp. 655-662.
Petrov, R, Elbahloul, O, Gallichio, MH, Stellrecht, K, Conti, DJ. “Monthly Screening for Polyoma Virus Eliminates BK Nephropathy and Preserves Renal function”. Surgical Infections. vol. Volume: 10. March 19, 2009.
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