Abstract
Many humans have antibodies against simian lymphotropic polyomavirus (LPyV), but its DNA has not been found in humans. Identification of human polyomavirus 9 (HPyV9) led us to compare the seroprevalence and cross-reactivity of LPyV and HpyV9. Results could indicate that humans who have antibodies against LPyV are infected by HPyV9.
Highlights
Many humans have antibodies against simian lymphotropic polyomavirus (LPyV), but its DNA has not been found in humans
Interpretation of phylogenetic analysis of viral protein 1 (VP1) sequences predicts that cross-reactivity might occur between Trichodysplasia spinulosaassociated polyomavirus and Bornean orangutan PyV, between Merkel cell polyomavirus (MCPyV) and chimpanzee polyomaviruses, and between human polyomavirus 9 (HPyV9) and simian lymphotropic polyomavirus (LPyV)
To detect antibodies against HPyV9, we set up a virus-like particle (VLP)–based ELISA similar to the assay we developed for MCPyV [9]
Summary
Many humans have antibodies against simian lymphotropic polyomavirus (LPyV), but its DNA has not been found in humans. Interpretation of phylogenetic analysis of viral protein 1 (VP1) sequences predicts that cross-reactivity might occur between Trichodysplasia spinulosaassociated polyomavirus and Bornean orangutan PyV, between MCPyV and chimpanzee polyomaviruses, and between HPyV9 and simian lymphotropic polyomavirus (LPyV). The Study We investigated the seroprevalence of HPyV9, MCPyV, and LPyV in children 1–14 years of age and adults18–85 years of age in the Ferrara region of Italy during December 2010–September 2011, and attempted to determine whether cross-reactivity between LPyV and HPyV9 might explain the latter’s seroprevalence reported among humans.
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