A189 NON-ALCOHOLIC FATTY LIVER DISEASE AND SEN-V INFECTION: AN INTERIM ANALYSIS

Abstract

Abstract Background Non-alcoholic fatty liver disease (NAFLD) is a common liver disease in which 10–20% of patients are at risk of progressing to cirrhosis. Several risk factors and genetic variants have been proposed to explain such progression but these fail to explain all cases. SEN-V is a hepatotropic ssDNA virus transmitted by both parenteral and non-parenteral routes. In a previous study we documented serologic evidence of SEN-V infection in 21% of 108 patients with chronic Hepatitis B (HBV), C (HCV) or PBC disease. In a recent Japanese study, HCV patients who were SEN-V positive had higher rates of disease progression than those who were SEN-V negative. Conversely, in an Iranian study, liver enzyme levels were lower in HBV patients co-infected with SEN-V. No study has yet documented the prevalence or impact of SEN-V infection in NAFLD. Aims To determine the prevalence and impact of SEN-V infection in NAFLD. Methods Thirty-three consecutive patients with NAFLD confirmed on liver biopsy had serologic testing for SEN-V DNA using short and long primer target sequences; sequencing was confirmed by BLAST and phylogenetic analysis. Patients with other causes of chronic liver disease were excluded. ALT levels, NAFLD activity scores (NAS), and fibrosis scores on biopsy were compared between the SEN-V positive and negative groups using Mann-Whitney, t-test, and chi squared as appropriate. Results SEN-V serologic testing was positive in 15/33 (45%) NAFLD patients, significantly higher than the 24/108 (21%) reported in non-NAFLD historical controls (p < 0.01). Mean serum ALT levels were similar in the two cohorts (SEN-V positive: 109 +/- 163 versus SEN-V negative: 62 +/- 54 IU/L, p= 0.27). The median NAS scores were identical in both groups (5/8) 95% CI [3,6]. Although the median fibrosis stage in SEN-V positive patients was lower (1.0 95% CI [0,3] vs. 2.5 95% CI [1,4] respectively), the difference did not reach statistical significance (p= 0.27). Conclusions Within the limits of this small interim analysis, serologic evidence of SEN-V infection was more common amongst NAFLD patients than historical controls with non-NAFLD chronic liver diseases. However, there were no significant differences in ALT levels, NAS scores or fibrosis stages between SEN-V positive versus negative NAFLD patients. These results suggest that if SEN-V infection has any impact on NAFLD, it may contribute to the development but not severity of the disease. Funding Agencies None