Arch Dermatol Res (1984) 276:199-200

Short Communications �9 Springer-Verlag 1984

A Human Papillomavirus Closely Related to HPV 13 Found in a Focal Epithelial Hyperplasia Lesion (Heck Disease)

S. Syrj~inen 1, K. Syrj/inen z, H. Ikenberg 3, L. Gissmann 4, and M. Lamberg 5

Department of Oral Pathology, Institute of Dentistry, University of Kuopio, POB 6, SF-70211Kuopio 21, Finland 2 Department of Pathology, University of Kuopio, POB 6, SF-70211 Kuopio 21, Finland 3 Institute for Virology, Center for Hygiene, University of Freiburg, HerderstraBe 11, D-7800 Freiburg, Federal Republic of Germany 4 German Cancer Research Center, Neuenheimer Feld 280, D-6900 Heidelberg 1, Federal Republic of Germany 5 Department of Oral Surgery, Institute of Dentistry, University of Kuopio, POB 6, SF-70211Kuopio 21, Finland

Key words: Human papillomavirus - Heck disease - DNA-hybridizat ion

Focal epithelial hyperplasia (FEH; morbus Heck) is currently regarded as one of the oral squamous cell lesions caused by a human papillomavirus (HPV) [3, 6, 7]. First HPV 1 D N A [4] and then HPV 13 D N A [5] have been found in F E H lesions using the DNA- hybridization procedure. The majority of cases studied so far seem to contain HPV 13 D N A [5].

The present patient is a 30-year-old Finnish female, who had a solitary smooth-surfaced soft growth at the site of left commisure. She reported a biting t rauma at this site some 2 years before. On light microscopy, the excised lesion showed morphology consistent with F E H [6, 7]. When exposed to staining by the indirect immunoperoxidase technique for HPV structural pro- teins [5, 6], the lesion disclosed a few cells with positive staining that were confined to the nuclei. The D N A was extracted f rom freeze-dried material according to the technique detailed previously [5].

Blot-hybridization of this D N A with different radioactively labelled HPV genomes indicated that the papillomavirus present in the lesion was not related to HPV 1 - 6 , 8 - 1 2 , and 1 4 - 1 8 . Hybridization with 32p-labelled HPV 13 DNA, however, either at non- stringent conditions followed by a stringent wash of the filter [1], or at stringent conditions, resulted in a positive signal. The pattern obtained after BAM-HI cleavage clearly differed from HPV 13 (Fig. 1). Therefore, it is assumed that the papillomavirus present in the F E H lesion is closely related but not identical to HPV 13. Additional experiments are required for further charac- terization of this DNA.

Offprint requests to: Kari Syrjgnen, M.D. (address see above)

The present finding of a so-far unrecognized sub- type of HPV is consistent with the known heterogeneity of HPV [2], of which at least 25 types (and even more subtypes) have been already established. This might explain why some of the F E H lesions previously studied have been negative (lack of appropriate probes). The present finding also substantiates the concept that most of the F E H lesions are probably caused by HPV 13 and viruses closely related to it [5]. Whether HPV 13 and its

"subtypes are responsible for the other HPV lesions of the oral cavity [6, 7] remains to be established.

Fig. 1. Southern blot-hybridization of cellular DNA extracted from the FEH lesion (b) (after cleavage with Bam-HI restriction en- donuclease) with 32p-labelled HPV 13 DNA. Hybridization was done under nonstringent conditions (T,, --40~ The intensity of the specific label in b was not reduced even after washing at high stringency (T,, - 20 ~ C) [1]. Lane a contains HPV 13 DNA as positive control. Two of the three Bam-HI fragments are indicated by arrows

200 S. Syrjfinen et al. : Human Papillomavirus in Heck Disease

References

1. Dfirst M, Gissmann L, Ikenberg H, zur Hausen H (1983) A papillomavirus DNA froma cervical carcinoma and its prevalence in cancer biopsy Samples from different geographic regions. Proc Natl Acad Sci USA 80: 3812-3815

2. Gissmann L, Schwarz E (1984) Cloning ofpapillomavirus DNA. In: Becker Y (ed) Developments in molecular virology, vol 5. Recombinant DNA. Martinus Nijhoff Publishers, Hingham, Massachusetts, USA (in press)

3. Kuhlwein A, Nasemann T, Jfinner M, Schaeg G, Reinel D (1981) Nachweis von Papillomviren bei fokaler epithelialer Hyperplasia Heck und die Differentialdiagnose zum weil3en Schleimhaut- nfivus. Hautarzt 32: 617- 621

4. Petzoldt D, Pfister H (1980) HPV 1 DNA in lesions of focal epithelial hyperplasia Heck. Arch Dermatol Res 268:313--314

5. Pfister H, Hettich I, Runne U, Gissmann L, Chill GN (1983) Characterization of human papillomavirus type 13 from focal epithelial hyperplasia Heck lesions, I. Virology 47: 363-366

6. Syrj/inen KJ, Pyrh6nen S, Syrj/inen SM, Lamberg MA (1983) Immunohistological demonstration of human papilloma virus (HPV) antigens in oral squamous cell lesions. Br J Oral Surg 21 : 147-153

7. Syrj~nen KJ, Syrjfinen SM, Lamberg MA, Pyrh6nen S (1983) Human papillomavirus (HPV) involvement in squamous cell lesions of the oral cavity. Proc Finn Dent Soc 79 :1-8

Received October 28, 1983