Human papillomavirus type 5 in primary keratinocytes from psoriatic skin

Abstract

The role of human papillomaviruses (HPVs) in the pathogenesis of psoriasis is uncertain, and it has been postulated that the virus can act as a putative superantigen or it is activated from a latent status by inflammatory cytokines. To determine the involvement of HPV in the pathogenesis of psoriasis, primary cultures of keratinocytes from psoriatic lesions were analysed for the viral presence and for the production of inflammatory cytokines. Biopsies were taken from psoriatic lesions of 11 patients and from healthy donors undergoing plastic surgery. HPV DNA/RNAs were detected by nested polymerase chain reaction methods. The secretion of interleukin-6 (IL-6), IL-8 and IL-18 was determined in the conditioned medium by commercial enzyme-linked immunosorbent assay kits. Sixty-four per cent of the psoriatic keratinocytes were positive to HPV type 5 (HPV5), whereas no normal samples showed the presence of viral sequences. In the corresponding paraffin-embedded sections, multiple infection by HPV5 and HPV1 was detected. Comparable results in the production of inflammatory cytokines were obtained from HPV-infected vs. non-infected cell cultures. Specific HPV5 mRNAs were detected in the keratinocytes in the absence of cytokine stimulation, indicating that the expression of the viral genome may not be a consequence of the activation of the viral promoter by cytokines. The results are suggestive of an involvement of HPV5 in the psoriasis and reinforce the hypothesis that the replication of this virus in the psoriatic keratinocytes may cause the epidermal hyperproliferation as well as the antigen stimulation, which induces autoimmune phenomena.

LL‐37 regulates the overexpression of vascular endothelial growth factor (VEGF) and c‐IAP‐2 in human keratinocytes

“…In the biopsies of psoriatic patients, the presence of virus has been reported 23–25 . Yuan et al 26 .…”

Psoriasis as an autoimmune disease

“…U chorych w około 90% wykwitów wykryto DNA HPV5 i inne związane z nim genotypy EV-HPV. Dodatkowo locus podatności na zakażenia HPV-EV znajduje się na chromosomie 17q w regionie PSORS 2 [58][59][60]. Badacze sugerują, że na początku w łuszczycy istnieje zjawisko poliklonalnej aktywacji komórek T, najprawdopodobniej wywołanej przez superantygeny lub uraz naskórka (objaw Köbnera), natomiast w późniejszej fazie autoreaktywne limfocyty T rozpoznają autoantygeny (białka kapsydu L1 HPV5) w naskórku, co prowadzi do reakcji autoimmunologicznej [61].…”

“…Niektórzy autorzy postulują jednak, że HPV5 działa bezpośrednio tylko jako superantygen [60]. Przeciwnicy tej teorii spekulują, że IFN-γ lub IL-17 mogą aktywować promotor genu dla EV-HPV i w związku z tym wirus nie bierze aktywnego udziału w patogenezie łuszczycy, ale jest tylko obecny latentnie w keratynocytach [60,62].…”

Pediatric psoriasis: an update

“…Other infections that have been noted in psoriatic disease are presence of staphylococcal superantigens16 and HPV DNA 17…”