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Failure to detect human papillomavirus in focal cortical dysplasia type II b
Author(s) -
Shapiro Kevin A.,
McGuone Declan,
Deshpande Vikram,
Sadow Peter M.,
StemmerRachamimov Anat,
Staley Kevin J.
Publication year - 2015
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.24422
Subject(s) - cortical dysplasia , pathology , in situ hybridization , dysplasia , pathological , hpv infection , human papillomavirus , medicine , papillomaviridae , pathogenesis , biology , gene , genetics , cancer , magnetic resonance imaging , gene expression , cervical cancer , radiology
Objective Recent studies have reported evidence of human papillomavirus 16 (HPV‐16) in a very high proportion of pathological specimens of focal cortical dysplasia type IIb, but not in control specimens, motivating the proposal that viral infection during fetal development may play a causal role in the pathogenesis of focal cortical dysplasias. However, the significance of the association between HPV infection and focal cortical dysplasia type IIb, and its reproducibility across surgical centers, remain unclear. Here we sought evidence for HPV‐16 in an independent cohort of surgical specimens. Methods We identified 14 specimens of focal cortical dysplasia type IIb from a single surgical center between 1995 and 2013. Multiple methods were used to establish presence or absence of HPV, including DNA polymerase chain reaction, conventional in situ hybridization, chromogenic in situ hybridization, and immunohistochemistry for p16. Results We found no conclusive evidence of HPV in any of the specimens. All but 1 of the cases were negative by >1 method. Interpretation These results raise questions about the prevalence of HPV infection in focal cortical dysplasias and about its potential importance as a causative agent. Ann Neurol 2015;78:63–67