F the general population [54]. The cause of psoriasis is still under
F the general population [54]. The cause of psoriasis is still under debate, but it is generally accepted to have a genetic hereditary component, and a hyperproliferative epidermal nature driven by activated lymphocytes [55]. Theprevalence of psoriasis in HIV-1-seropositive individuals is similar to that of their seronegative counterparts [56]. However, ��-Amanitin site psoriatic lesions in AIDS patients tend to be more severe, acral, extensive, destructive and recalcitrant [54,57] (Figures 2E and 2F). Of note, the prevalence of psoriatic arthritis is greatly increased in the HIV-1/AIDS population compared with its immunocompetent counterpart [58]. The pathogenesis of psoriasis in the context of HIV-1 infection has been associated with many immunologic events that include a decrease in the number of Langherhan’s cells, but also with a potential epidermal proliferative effect of HIV-1 itself, an altered CD8:CD4 ratio and high synthesis of nitric oxide driven by HIV-1 in macrophages [56]. This association has actually led to an obscure hypothesis involving psoriasis and psoriatic arthritis with a retroviral background [59,60]. PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27663262 In fact, in patients with known risk for HIV-1 exposure, new onset of psoriasis may sometimes be a marker of HIV-1 infection [61]. A full comparative analysis between HIV-1-related and HIV-1-negative psoriasis is depicted in Table 2. Expanding on the pathogenesis of psoriasis, the causative trigger of the lymphocytic activation remains unknown; however, self-antigens may play a significant role in breaking the peripheral tolerance [69]. Recently, there is growing evidence that links certain conditions of autoimmune origin to human endogenous retroviruses (HERVs) [8,70]. HERVs are genomic sequences that use reverse transcriptase and that can move from one chromosomal site to another, belonging to a class of parasitic elements that represent as much as 40 of the mammalian genome [71]. These elements were integrated into our genome million of years ago, when exogenous retroviruses infected germ cells; once integrated, these sequences were transmitted vertically as mutations of essential genes in a mendelian fashion [70]. Retrovirologists often refer to HERVs as defective proviruses with accumulated deletions, frame shift mutations, or with stop codons in gag, pol or env open reading frames, that limit their infectious capacity [8]. The activation of these dormant sequences of the genome has been linked to the pathogenesis of several autoimmune diseases, including most of the chronic arthropathies and systemic lupus erythematosus [72,73]. Several HERVs are expressed in normal peripheral blood lymphocytes [74], keratinocytes [75] and many other tissues [76]. Notably, the hypothesis associating HERVs with psoriasis resulted from the detection of viral-like particles resembling murine C-type retrovirus in psoriatic plaques in 1983 [77]. The microscopic findings were further supported by the detection of p27, a retrovirus-like particle in skin and lymphocytes from psoriatic patients [78,79],Cedeno-Laurent et al. Journal of the International AIDS Society 2011, 14:5 http://www.jiasociety.org/content/14/1/Page 6 ofTable 2 Comparison between HIV-1 seronegative psoriasis and HIV-1 related psoriasisVariable Frequency Severity Clinical features 1-3 Mild-moderate Erythematous plaques usually circumscribed to elbows-knees (psoriasis vulgaris) HIV-1-seronegative psoriasis HIV-1-related psoriasis Similar to HIV-seronegative population Moderate-sever.
