We reported previously that patients with psoriasis harbored at a very high
frequency DNA sequences of the oncogenic human papillomavirus type 5 (HPV5
) associated with epidermodysplasia verruciformis. Moreover anti-HPV5 antib
odies were detected in 25% of the cases. Our aim was to find out whether ke
ratinocyte hyperproliferation and/or autoimmunity could be responsible for
HPV5 expression in psoriasis. We found that epidermal repair in patients wi
th extensive second degree burns (n = 19) is frequently associated with the
generation of anti-HPV5 antibodies. In patients with autoimmune bullous di
seases (n = 118), a condition in which keratinocyte proliferation is involv
ed in repair mechanisms, the prevalence of anti-HPV5 antibodies (15%-25%) w
as similar to that reported in psoriasis and significantly higher than that
(5%) observed in individuals with no known history of human papillomavirus
infection (n = 119). A high detection rate (57.9%) of HPV5 DNA was observe
d in patients with bullous diseases. Anti-HPV5 antibodies were found in pat
ients with autoimmune connective tissue disorders with cutaneous involvemen
t (n = 40) as frequently as in patients with bullous diseases. HPV5 DNA was
detected in one of the 10 patients studied. In contrast, the prevalence of
anti-HPV5 antibodies in patients with autoimmune neurological disorders (n
= 47) and in patients with common warts (n = 28) or invasive carcinomas of
the skin (n = 40) was as low as in the general population. It is worth str
essing that a similar prevalence of antibodies against HPV1 was found in al
l groups studied. Our data strongly suggest that extensive keratinocyte pro
liferation is a major factor for the generation of anti-HPV5 antibodies and
that autoimmunity may contribute to this phenomenon. It remains to be dete
rmined whether HPV5 and other human papillomavirus genotypes associated wit
h epidermodysplasia verruciformis contribute to the hyperproliferation of k
eratinocytes occurring in epidermal repair and in psoriasis.