Inflammatory biomarkers, disease activity index, and self-reported disability may be predictors of chronic arthritis after chikungunya infection: brief report.

The chikungunya virus (ChikV) is a reemerging mosquito-borne pathogen that causes disabling chronic arthritis. The relationship between clinical evolution and inflammatory biomarkers in patients with ChikV-induced arthritis has not been fully described. We performed a prospective case series to evaluate the association among joint involvement, self-reported disability, and inflammatory biomarkers. Patients with ChikV infection were followed for 1 year. Joint involvement and self-reported disability were evaluated with disease activity index 28 (DAS-28) and World Health Organization Disablement Assessment Schedule II (WHODAS-II). Interleukin-6 (IL-6), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and rheumatoid factor (RF) were used as biomarkers. Ten patients with mean age 48 ±15.04 years were included. Symptoms at diagnosis were fever, arthralgias, myalgias, rash, arthritis, nausea, vomiting, and back pain. Polyarticular involvement was present in seven cases. At diagnosis, measures were as follows: DAS-28, 5.08±1.11; WHODAS-II score, 72.3±10.3 %; CRP, 5.09±7.23 mg/dL; ESR, 33.5±17.5 mm/h; RF, 64±21.7 IU/mL; and IL-6, 17.6±10.3 pg/mL. Six patients developed subacute and chronic symptoms. During follow-up, DAS-28 index, WHODAS-II score, ESR, and IL-6 were statistically different in patients with subacute and chronic symptoms compared to those who resolved in the acute phase (p < 0.05). DAS-28 index, WHODAS-II score, and IL-6 were related to chronicity of articular symptoms and could be used as predictors of ChikV-induced arthritis.

Prevalence of the -308 and -238 tumor necrosis factor alpha (TNF-α) promoter polymorphisms in Mexican chronic hepatitis C patients.

BACKGROUND: Tumor necrosis factor alpha (TNF-α) has been involved in the pathogenesis of chronic hepatitis C virus (HCV) infection. Two polymorphisms at positions -308 and -238 in the TNF-α promoter region influence TNF-α expression and these have been linked to a number of infectious diseases. AIM: To analyze the prevalence of the -308 and -238 TNF-α polymorphisms in a group of Mexican HCV-infected patients and in healthy control subjects not related to the patients. MATERIAL AND METHODS: Both polymorphisms were determined in peripheral blood samples from 48 patients with positive anti-HCV antibodies and discernible HCV-RNA levels. Twenty five patients were women and 23 were men. The control group included 100 healthy subjects. Forty-four were women and 56 were men. The polymorphisms were evaluated by polymerase chain reaction amplification (PCR), followed by the Restriction Fragment Length Polymorphism (RFLP) method. RESULTS: The prevalence of the -308 TNF-α polymorphism was found to be 12% in patients with chronic hepatitis C and 20% in control subjects, (P=0.2616); whereas that of the -238 TNF-α polymorphism was found to be 2% and 12% in patients and control subjects, respectively (P=0.061). The TNF-α genotypes were found to be in Hardy-Weinberg equilibrium. CONCLUSIONS: No association was found between -308 and -238 TNF-α polymorphisms and chronic hepatitis C in the Mexican group studied. Our data suggest that additional studies increasing the sample size and a control group which has been exposed to an equal risk of infection are required to investigate whether these polymorphisms represent genetic susceptibility for chronic HCV infection.

Additive effect of ethanol and HCV subgenomic replicon expression on COX-2 protein levels and activity.

The mechanisms by which alcohol exacerbates liver injury in patients with hepatitis C are unknown. We used the hepatitis C virus (HCV) subgenomic replicon cell system to evaluate the effect of ethanol on HCV replication and viral protein synthesis. Our results demonstrate that alcohol stimulates HCV replicon expression at both HCV-RNA and protein levels. Furthermore, we observed that ethanol treatment showed an additive effect in cyclooxygenase-2 (COX-2) protein expression and activity already induced by HCV viral proteins, and in turn increased HCV viral expression. Our results suggest that COX-2 activity is involved in ethanol-induced HCV-RNA and NS5A protein expression, because acetylsalicylic acid (ASA), a COX-1/2 inhibitor, blocked this induction and downregulated COX-2 protein expression and activity. Therefore, we suggest that ethanol increases HCV replication expression, at least in part, by upregulating a key cellular regulator of oxidative stress pathway known as COX-2 or its products.