Monoclonal antibodies and progressive multifocal leukoencephalopathy

Figures & data

Figure 1 Genesis of the neurotropic Strain of JC Virus. (Adapted from Jensen and Major85). The JC virus genome is depicted on the left. The genes coding for its three structural proteins and three regulatory proteins (here) are highly conserved, but not the non-coding control region which dictates whether the virus can bind to a cells NF-1X DNA binding proteins. The archetype virus' non-coding control region is at the top; at the bottom, is the 98 bp tandem repeat sequence seen in the virus isolated from brains with PML. This is the mutation that must occur.

Table 1 Proposed stages of PML development

Initial infection (typically <20 years)

Establishment of latent infection

Alteration in the non-coding regulatory region of JCV in latent sites converting the virus to a neurotropic strain

Failed immunosurveillance in the periphery

Periodic re-expression of JCV in PBMCs

Productive JCV infection of PBMC—dependent on B cell maturity and expression of transcriptional factors

Entry of JCV into brain

Establishment of productive oligodendrocyte infection

Failure of immunosurveillance in the brain

Note: JCV, JC virus; PBMC, peripheral blood mononuclear cells; PML, progressive multifocal leukoencephalopathy.

Jensen PN, Major EO. A classification scheme for human polyomavirus JCV variants based on the nucleotide sequence of the noncoding regulatory region. J Neurovirol 2001; 7:280 - 287

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