ABSTRACT
BACKGROUND: The epidemiological shift of hepatitis A has contributed to a sustained community-wide outbreak in Korea during 2008. OBJECTIVES: To assess the risk factors associated with hepatitis A virus (HAV) propagation, and to analyze the circulating genotype in the sustained community-wide outbreak. STUDY DESIGN: The hospital-based case-control study was conducted in an 850-bed university hospital in Seoul from April to August, 2008. For molecular analysis of HAV isolates, a 488-bp gene fragment of the VP1 region was amplified and sequenced. RESULTS: In the multivariated logistic regression model, the risk factors of HAV infection adjusted by age were contacts with hepatitis A case (OR 3.98, 95% CI: 1.36-11.66), residence with child aged Subject(s)
Community-Acquired Infections/epidemiology
, Hepatitis A virus/genetics
, Hepatitis A/epidemiology
, Adult
, Case-Control Studies
, Community-Acquired Infections/virology
, Disease Outbreaks
, Female
, Food Microbiology
, Hepatitis A/virology
, Hospitals
, Humans
, Korea/epidemiology
, Logistic Models
, Male
, Middle Aged
, Molecular Epidemiology/methods
, Multivariate Analysis
, Phylogeny
, Risk Factors
, Viral Structural Proteins/genetics
, Water Microbiology
ABSTRACT
Methylation events play a critical role in various cellular processes including regulation of gene transcription and proliferation. We observed that methyltransferase activity underwent time-dependent changes in the cytosol of the rat hepatocytes upon partial hepatectomy. However,any change in the methylation of nuclear proteins is not clear during hepatocyte proliferation. The nuclear fraction possesses basal level of methyltransferase to catalyze methylation of several proteins ranging from 7 to 70 kD prior to any hepatecmony. The specific p16 (16 kD)band was transiently and heavily methylated post 1 day hepatectomy, and then became non-detectable, but not in the control liver. Methylation of p16 band was completely inhibited by exogenously added histones, particularly 2AS, 1,2A and 2B subtypes. The methylated p16 protein remains stable in either acid or alkali- induced demethylation conditions, indicating that methylation is not likely to occur on isoaspartyl or C-terminal cysteinyl residues. Exogenous addition of non-hydrolyzable GTP caused a dose-dependent suppression of a p16 methylation suggesting that G-proteins might play a role as an endogenous methylation inhibitor in vivo. Taken together, we have identified the proliferation event associated-methylation of the nuclear p16 protein in the hepatocytes undergoing liver regeneration.
