"Human polyomavirus 2" also appears to mediate encephalopathy, due to infection of cortical pyramidal neurons (CPN) and astrocytes. Analysis of the JCV CPN variant revealed differences from JCV GCN: no mutations were found in the VP1 coding region; however, a 143–base-pair deletion was identified in the agnogene, coding for a 10–amino-acid truncated peptide, which is believed to mediate CPN tropism. Additionally, analysis of the subcellular localization of JC CPN virions in nuclei, cytoplasm, and axons suggests that the virus may travel through axons to increase infectivity.