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Purpose To assess the time of exposure to the computer and dry eye disease (DED) in subjects with computer vision syndrome (CVS). Methods A cross-sectional study was conducted in office workers, computer users of both sexes, with an age range of 18–45 years without comorbidities; we included 108 subjects divided into 3 groups according to the time of computer exposure in hours per day (H/D): <4 (n = 23), 4 −7.9 (n = 49), >8 (n = 39). A specific questionnaire was applied to them on the exposure time and the type of visual display terminal (VDT) used, as well as the computer vision symptoms scale (CVSS17). DED was diagnosed with the Ocular Surface Disease Index (OSDI). Ocular surface damage and signs of DED were evaluated with the tear rupture time test (TBUT), the integrity of the ocular surface by ocular surface staining (OSS) and the production of the aqueous basal tear film using the Schirmer test. Results Average computer exposure time, measured differently, was positively correlated with DED development. The computer exposure time measured in hours per year and TBUT showed a significant negative correlation (p <0.001) (rho −0.463). Years of computer exposure and staining of the ocular surface showed a significant positive correlation (p <0 0.001; rho 0.404). The accumulated exposure time was negatively correlated with TBUT (p <0.001; rho −0.376) and positively with OSS (p <0.001; rho 0.433). Schirmer test did not correlate with computer exposure time. Conclusion The prolonged time of exposure to the computer in subjects with CVS was significantly correlated with the DED tests, in the different ways of measuring it; but not with the Schirmer test.

Background: There is a lack of specific antiviral therapy against dengue virus (DENV) in current use. Therefore, a great proportion of dengue cases progress to severe clinical forms due to a complex interplay between virus and host immune response. It has been hypothesized that heterotypic non-neutralizing antibodies enhance DENV infection in phagocytic cells, and this induces an inflammatory response that is involved in the pathogenesis of severe dengue. Purpose: To identify the antiviral and immunomodulatory effects of polyphenols on dengue virus infection. Methods: Human U937-DC-SIGN macrophages were infected with DENV serotypes 2 or 3 in the presence or not of enhancing antibody 4G2. Viral titers and the secretion of tumor necrosis factor-alpha, IL-6, IL-10 and interferon-alpha were analyzed timely. Results: DENV infection alone induced high production of IL-6 and TNF-α, but in the presence of 4G2 antibody, viral titers and TNF-α secretion were potentiated. Based on anti-inflammatory antecedents, the polyphenols curcumin, fisetin, resveratrol, apigenin, quercetin and rutin were tested for antiviral and immunomodulatory properties. Only quercetin and fisetin inhibited DENV-2 and DENV-3 infection in the absence or presence of enhancing antibody (>90%, p <0.001); they also inhibited TNF-α and IL-6 secretion ( p <0.001). Conclusion: Quercetin and fisetin down-regulate the production of proinflammatory cytokines induced by DENV infection enhanced by antibodies a mechanism involved in severe dengue.

BackgroundIn viral disease, infection is controlled at the cellular level by type I interferon (IFN-I), but dengue virus (DENV) has the ability to inhibit this response. Type III interferon, also known as lambda IFN (IFN-III or IFN-λ), is a complementary pathway to the antiviral response by IFN-I. This work analyzed the IFN-λ (IFN-III) mediated antiviral response against DENV serotype 2 (DENV-2) infection.MethodsDengue fever patients were sampled to determine their IFN-λ levels by ELISA. To study the IFN-λ response during DENV infection we selected the epithelial cell line C33-A, and we demonstrated that it is permissive to DENV-2 infection. The effect of IFN-λ on virus replication was determined in these cells, in parallel to the expression of IFN-stimulated genes (ISGs), and Suppressor of Cytokine Signaling (SOCS), genes measured by RT-qPCR.ResultsWe found increased (~1.8 times) serological IFN-λ in dengue fever patients compared to healthy blood donors. IFN-λ inhibited DENV-2 replication in a dose-dependent manner in vitro. The reduction of viral titer corresponded with increased ISG mRNA levels (MX1 and OAS1), with the highest inhibition occurring at ISG’s peak expression. Presence of IFN-negative regulators, SOCS1 and SOCS3, during DENV-2 infection was associated with reduced IFN-λ1 expression.ConclusionsEvidence described here suggests that IFN-λ is a good candidate inhibitor of viral replication in dengue infection. Mechanisms for the cellular and organismal interplay between DENV and IFN- λ need to be further studied as they could provide insights into strategies to treat this disease. Furthermore, we report a novel epithelial model to study dengue infection in vitro.