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Novel polymerase chain reaction method for detecting cutaneous human papillomavirus DNA
Author(s) -
Sasagawa Toshiyuki,
Mitsuishi Tsuyoshi
Publication year - 2012
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.22195
Subject(s) - genotyping , virology , polymerase chain reaction , genotype , human papillomavirus , common warts , papillomaviridae , biology , hpv infection , restriction fragment length polymorphism , genital warts , microbiology and biotechnology , medicine , genetics , cervical cancer , gene , cancer , human immunodeficiency virus (hiv) , syphilis
There is no simple test to identify the human papillomavirus (HPV) genotypes that cause cutaneous warts. A new polymerase chain reaction (PCR) method, called SK‐PCR, was developed for this purpose. This PCR amplifies 210–238 base pairs of L1 DNA of 17 HPV types (HPV‐1a, ‐2a, ‐3, ‐4, ‐7, ‐10, ‐27, ‐28, ‐29, ‐40, ‐57, ‐60, ‐63, ‐65, ‐77, ‐91, and ‐94), which are thought to cause various cutaneous warts, including common, flat, butcher's, punctate, and pigmented warts. The method is novel because the location of these primers is completely different from that of any previous PCR method for HPV. The target sequences are specific to alpha‐, gamma‐, and mu‐papillomaviruses (PVs), but not to beta‐PVs. Furthermore, direct sequencing and restriction fragment length polymorphism (RFLP) were used to determine the HPV genotypes. Fifty of samples of plantar warts were examined, and HPV‐27 was identified in 22 warts, HPV‐57 in 15 warts, and HPV‐2a in 9 warts. These PVs, which are alpha species 4, were the most common. HPV‐4 and ‐65 (gamma‐PVs) and HPV‐1a and ‐63 (mu‐PVs) were detected in one case each. A single HPV type was identified in all of these warts. This method appears to be useful for genotyping the HPVs causing skin warts, and for distinguishing between HPV‐induced warts and warty lesions unrelated to HPV infection. J. Med. Virol. 84:138–144, 2011. © 2011 Wiley Periodicals, Inc.