Psoriasis vulgaris, the most common form of psoriasis, is a chronic inflammatory skin disease that affects 2-3% of the worldwide population. It has been reported in patients with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) suggesting the percutaneous transmission of this infection which may cause the exacerbation of psoriasis. Interestingly, elevated expression of ACE2 receptor on differentiating keratinocytes and basal cell layer of the epidermis of patients with psoriasis and COVID-19 involving pro inflammatory cytokines such as IFN-γ and IL-17, has been reported; however little is known about the participation of other receptors expressed on the surface of psoriatic keratinocytes, in the SARS-CoV-2 infection. Here we hypothesize that, in the skin of patients with psoriasis who have been diagnosed with COVID-19, the interaction of the SARS-CoV-2 S glycoprotein with the HSPGs Synd-1 and CD44 through their HS side chains and N-linked glycan, and Gal-3 and Gal-8 through the N- glycans located on the ACE2, integrin-β1, CD147, IFN-γR and IL-17A-R, would generate a Gal-glycan lattice at the surface of SARS-CoV-2 virus and psoriatic keratinocyte. Such Gal-glycan lattice in addition to influence keratinocyte proliferation and terminal differentiation, might induce conformational changes in the SARS-CoV-2 S glycoprotein facilitating the attachment and virus entry. We consider that future work will be required to understand the mechanisms regulating Gal-glycan lattice assembly during psoriatic keratinocyte and SARS-CoV-2 interaction as well as for the development of new inhibitors of virus attachment and internalization.

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