JC polyomavirus is the causative agent of progressive multifocal leukoencephalopathy (PML), a demyelinating disease resulting from the lytic infection of oligodendrocytes that may develop in immunosuppressed individuals: HIV1 infected or individuals under immunosuppressive therapies. Understanding the biology of JCPyV is necessary for a proper patient management, the development of diagnostic tests, and risk stratification.
The review covers different areas of expertise including the genomic characterization of JCPyV strains detected in different body compartments (urine, plasma, and cerebrospinal fluid) of PML patients, viral mutations, molecular diagnostics, viral miRNAs, and disease.
The implementation of molecular biology techniques improved our understanding of JCPyV biology. Deep sequencing analysis of viral genomes revealed the presence of viral quasispecies in the cerebrospinal fluid of PML patients characterized by noncoding control region rearrangements and VP1 mutations. These neurotropic JCPyV variants present enhanced replication and an altered cell tropism that contribute to PML development. Monitoring these variants may be relevant for the identification of patients at risk of PML. Multiplex realtime PCR targeting both the LTAg and the archetype NCCR could be used to identify them. Failure to amplify NCCR should indicate the presence of a JCPyV prototype speeding up the diagnostic process.

BACKGROUND: Since it was first described in the early 1980s, psittacine beak and feather disease (PBFD) has become recognised as the dominant viral pathogen of psittacine birds in Australia. Our aim was to evaluate and review the effect of PBFD and its position as a key threatening process to Australian psittacine bird species. We review the origin/evolutionary pathways and potential threat of PBFD to endangered psittacine bird populations and captive-breeding flocks.
CONCLUSIONS: The most recent beak and feather disease virus (BFDV) phylogenetic analyses indicate that all endangered Australian psittacine bird species are susceptible to, and equally likely to be infected by, BFDV genotypes from a range of host psittacine species. Management of the disease in captive-breeding programs has relied on testing and culling, which has proven costly. The risk of PBFD should be considered very carefully by management teams contemplating the establishment of captive-breeding flocks for endangered species. Alternative disease prevention tools, including vaccination, which are increasingly being used in wildlife health, should be considered more seriously for managing and preventing PBFD in captive flocks of critically endangered species.