In Vitro and In Vivo Models for the Study of Human Polyomavirus Infection

Abstract

Developments of genome amplification techniques have rapidly expanded the family of human polyomaviruses (PyV). Following infection early in life, PyV persist in their hosts and are generally of no clinical consequence. High-level replication of PyV can occur in patients under immunosuppressive or immunomodulatory therapy and causes severe clinical entities, such as progressive multifocal leukoencephalopathy, polyomavirus-associated nephropathy or Merkel cell carcinoma. The characterization of known and newly-discovered human PyV, their relationship to human health, and the mechanisms underlying pathogenesis remain to be elucidated. Here, we summarize the most widely-used in vitro and in vivo models to study the PyV-host interaction, pathogenesis and anti-viral drug screening. We discuss the strengths and limitations of the different models and the lessons learned.

Absence of JC polyomavirus (JCPyV) viremia in early post‐transplant JCPyV nephropathy: A case report

“…Thus far, JCPyVAN has been reported in at least 14 kidney transplant recipients globally . Half of the patients were found to have allograft dysfunction at the time, while others were asymptomatic . Herein, we report a young male patient who underwent living‐related kidney transplantation and developed JCPyVAN much earlier than previous reports and this is the first report from Thailand to our knowledge.…”

“…JCPyV was first discovered from a patient with Hodgkin's disease with the initials J.C., who developed progressive multifocal leukoencephalopathy (PML) in 1971 . JCPyV essentially has a genetic link to BKPyV based on its structure . These two types of polyomaviruses can cause infection in immunocompromised patients, often with allograft dysfunction in kidney transplant patients secondary to BKPyV .…”

Polyomavirus en hospederos inmunocomprometidos: situación en Sudamérica

“…Hasta la fecha, se han descrito otros trece nuevos PyV humanos: KIPyV 7 y WUPyV 8 , que deben su nombre a las instituciones donde fueron descubiertos (Karolinska Institute y Washington University, respectivamente), MCPyV 9 y TSPyV 10 por su hallazgo en el tumor de células de Merkel y muestras de tricodisplasia espinulosa, respectivamente, el sexto (HPyV6) y el séptimo polyomavirus (HPyV7) identificados en piel 11 , el noveno polyomavirus (HPyV9) 12 descrito por primera vez en suero y orina, y en muestras de heces los PyV denominados MWPyV de Malawi, MXPyV de México y STLPyV de Saint Louis.13 El mismo año una variante del MWPyV, denominada HPyV10, fue encontrado en muestras de condiloma 14 . Y más recientemente, se describen los HPyV12 en hígado y el NYPyV en biopsia muscular 13 (Figura 1).…”

“…MWPyV fue identificado por primera vez en muestras de deposiciones de un niño en Malawi y se han determinado seroprevalencias de 42 a 75% 13,48 . Un estudio realizado en niños norteamericanos con diarrea aguda demostró la presencia del virus en 2,3% de los casos 48 .…”

Relevance of Assembly-Activating Protein for Adeno-associated Virus Vector Production and Capsid Protein Stability in Mammalian and Insect Cells

“…The first was Mark Kay's team, who reported AAVDJ, a shuffled hybrid of AAV serotypes 2, 8, and 9 that possesses high efficiency in the liver and other cell types (5). Since then, numerous other laboratories have harnessed this technology to enrich further novel AAV capsids with improved properties in, for instance, muscle, central nervous system (CNS), stem cells, or eye (see, e.g., references [8][9][10][11][12][13][14][15][16].…”