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To the Editor: Before 2007, two human polyomaviruses were known to infect humans: BK virus and JC virus (1,2). Recently, 2 novel polyomaviruses, KI polyomavirus (KIPyV) and WU polyomavirus (WUPyV), [...]

Aim: Analysis of the prevalence of serum 1gM antibodies directed against the HCV-core antigen (HCV-lgM) in patients with Porphyria cutanea tarda (PCT), taking into account the hepatic histological picture, liver biochemical markers and the PT biochemical indices. Background: Hepatic damage, especially that due to HCV infection, has been previously reported as a PCT trigger. HCV-IgM reactivity, a marker of chronic HCV hepatitis. suggested to be related to active virus replication could also he related to the PCT clinical course. Methods: Blood samples of 97 patients, previously analyzed for a panel of clinical, histological and laboratory variables, followed in our Centre for Porphyria! stored at - 80°C, were available to be retrospectively assayed for anti-HCV-core 1gM (HCV-IgM, ELISA). Results: 61% HCV-IgM positivity was found, with no apparent significant relationship with the respective histological hepatitis classification, PCT remission phase, and PCT familiarity, when evaluated on overall patients. The levels of HCV-IgM presented a peculiar behaviour when correlated to the serum AST values. In fact, there was a significant positive correlation in those with HCV-IgM <4 and a not significant, inverse correlation in the remaining group. These two groups showed other differences: the HCV-IgM levels were correlated to histology, PCT remission and to the markers of liver disease (such as AST and ALT) only in the first group. Conclusion: a relationship between IgM response. PCT activity and the underlying liver disease is suggested. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented about a study of patients with HIV-1 to detect KI and WU polyomaviruses in Italy.

Bacteria and mammalian cells have developed sophisticated sensing mechanisms to detect and eliminate foreign genetic material or to restrict its expression and replication. Progress has been made in the understanding of these mechanisms, which keep foreign or unwanted nucleic acids in check. The complex of mechanisms involved in RNA and DNA sensing is part of a system which is now appreciated as "immune sensing of nucleic acids" or better "nucleic acid immunity." Nucleic acids, which are critical components for inheriting genetic information in all species, including pathogens, are key structures recognized by the innate immune system. However, while nucleic acid recognition is required for host defense against pathogens, there is a potential risk of self-nucleic acids recognition. In fact, besides its essential contribution to antiviral or microbial defense and restriction of endogenous retro elements, deregulation of nucleic acid immunity can also lead to human diseases due to erroneous detection and response to self-nucleic acids, causing sterile inflammation and autoimmunity. In this review we will discuss the roles of nucleic acid receptors in guarding against pathogen invasion, and how the microbial environment could interfere or influence immune sensing in discriminating between self and non-self and how this may contribute to autoimmunity or inflammatory diseases., (© 2019 Elsevier Inc. All rights reserved.)

Tumor necrosis factor-alpha (TNF-alpha) plays a central role in sustaining the inflammatory process in the skin as well as in the joints of patients with psoriasis and psoriatic arthritis. In fact, biological therapies based on monoclonal antibodies against TNF-alpha have been proven to be effective on both the arthropathy and the cutaneous symptoms of the disease. Among the several effects produced by TNF-alpha on keratinocytes there is the induction of expression of MMP-9, a matrix metalloproteinase (MMP) produced mainly by monocytes and macrophages. In this article we refer to the results of a study on the behavior of MMP-9 in the sera and in the lesional skin in association with effective therapy with infliximab. Measurements of TNF-alpha, MMP-2, vascular endothelial growth factor (VEGF), and E-selectin were also performed in the same samples. Eleven psoriatic patients included in a therapeutic protocol based on the administration of infliximab monotherapy were collected before treatment and after 6 and 12 weeks of therapy. Significant decrease of MMP-9 and MMP-2 levels in the sera was associated with clinical improvement and with the decrease of TNF-alpha, VEGF, and E-selectin, angiogenic molecules already known to be implicated in the clinical expression of psoriasis. The clinical amelioration of the cutaneous expression of psoriasis was significantly associated with the decrease of MMP-9, TNF-alpha, and E-selectin levels, spontaneously released by lesional biopsy samples before and after therapy, measured in the culture supernatants by immunoenzymatic assays. In addition, significant correlations were found between the clinical score and TNF-alpha, MMP-9, and E-selectin lesional production. MMP-9 levels were significantly correlated with those of TNF-alpha. Our findings show the existence of a direct relationship between MMP-9 and TNF-alpha production, strongly suggesting that MMP-9 may play a key role in the skin inflammatory process in psoriasis, while a different role may be attributed to MMP-2.

Background: Inflammation represents an early and key event in the development of both the cutaneous psoriasis and psoriatic arthritis. Compelling evidences indicate that the production of TNF-alpha plays a central role in psoriasis by sustaining the inflammatory process in the skin as well as in the joints. Among the multiple effects produced by TNF-alpha on keratinocytes, the induction of matrix metalloproteinase-9 (MMP-9), a collagenase implicated in joint inflammatory arthritis which acts as an angiogenesis promoting factor, might represent a key mechanism in the pathogenesis of the disease. Aims of the present study were to investigate a) the role of MMP-9 in the development of psoriasis by assessing the presence of MMP-9 in lesional skin and in sera of psoriatic patients; b) the association of MMP-9 with the activity of the disease; c) the relationship between MMP-9 and TNF-alpha production., Methods: Eleven psoriatic patients, clinically presenting joint symptoms associated to the cutaneous disease, were included in a therapeutic protocol based on the administration of anti-TNF-alpha monoclonal antibody (Infliximab). Sera and skin biopsies were collected before treatment and after 6 weeks of therapy. Tissues were kept in short term cultures and production soluble mediators such as TNF-alpha, MMP-9, MMP-2, VEGF and E-Selectin, which include angiogenic molecules associated to the development of plaque psoriasis, were measured in the culture supernatants by immunoenzymatic assays (ng/ml or pg/ml per mg of tissue). MMP-9 concentrations were also measured in the sera. The cutaneous activity of disease was evaluated by the Psoriasis Area and Severity Index (PASI)., Results: Clinical and laboratory assessment indicated that all but one patients had a significant improvement of the PASI score after three months of therapy. The clinical amelioration was associated to a significant decrease of MMP-9 (P = 0.017), TNF-alpha (P = 0.005) and E-selectin (P = 0.018) levels, spontaneously released by lesional biopsies before and after therapy. In addition, significant correlations were found between the PASI measurements and TNF-alpha (r2 = 0.33, P = 0.005), MMP-9 (r2 = 0.25, P = 0.017), E-selectin (r2 = 0.24, P = 0.018) production. MMP-9 levels were significantly correlated with those of TNF-alpha (r2 = 0.30, P = 0.008). A significant decrease of MMP-9 in the sera, associated to the clinical improvement was also found., Conclusion: Our findings show the existence of a direct relationship between MMP-9 and TNF-alpha production strongly suggesting that MMP-9 may play a key role in the skin inflammatory process in psoriasis.