[Show abstract][Hide abstract] ABSTRACT: The epidemiology of enteroviral infection in South Korea during 1999-2011 chronicles nationwide outbreaks and changing detection and subtyping methods used over the 13-year period. Of 14,657 patients whose samples were tested, 4,762 (32.5%) samples were positive for human enterovirus (human EV); as diagnostic methods improved, the rate of positive results increased. A seasonal trend of outbreaks was documented. Genotypes enterovirus 71, echovirus 30, coxsackievirus B5, enterovirus 6, and coxsackievirus B2 were the most common genotypes identified. Accurate test results correlated clinical syndromes to enterovirus genotypes: aseptic meningitis to echovirus 30, enterovirus 6, and coxsackievirus B5; hand, foot and mouth disease to coxsackievirus A16; and hand, foot and mouth disease with neurologic complications to enterovirus 71. There are currently no treatments specific to human EV infections; surveillance of enterovirus infections such as this study provides may assist with evaluating the need to research and develop treatments for infections caused by virulent human EV genotypes.
[Show abstract][Hide abstract] ABSTRACT: We assessed neurologic sequelae associated with an enterovirus 71 (EV71) outbreak in South Korea during 2009. Four of 94 patients had high signal intensities at brainstem or cerebellum on magnetic resonance imaging. Two patients died of cardiopulmonary collapse; 2 had severe neurologic sequelae. Severity and case-fatality rates may differ by EV71 genotype or subgenotype.
[Show abstract][Hide abstract] ABSTRACT: Human enterovirus 71 (EV 71) has caused large-scale outbreaks of hand-foot-and-mouth disease (HFMD), particularly in the Asian-Pacific region. In this study, we report a major outbreak of EV 71 infection in Korea and describe the clinical differences between EV 71 and non-EV 71 enterovirus infections. We prospectively enrolled patients with suspected viral infections during a recent 2-year period through a nationwide surveillance system. We identified 719 patients with suspected HFMD or herpangina using real-time PCR and genotyping based on VP1 sequence analysis. The major pathogen causing HFMD changed substantially from 2008 to 2009, with EV 71 becoming the most common cause of HFMD in Korea in 2009. We successfully identified the enteroviral genotypes for 218 of the 719 patients. Patients with EV 71 infections tended to be younger than those with non-EV 71 enteroviral infections and presented with HFMD and meningoencephalitis. In addition, the occurrence of fever, headache, and neck stiffness was significantly higher in patients with EV 71 infections. Multivariable analysis showed that for patients presenting with HFMD, fever, or a sore throat, each covariate was independently associated with EV 71 infection; the adjusted odds ratios (with 95% confidence intervals in parentheses) for these variables were 31.86 (10.04 to 101.09), 4.76 (1.71 to 13.25), and 0.18 (0.04 to 0.77), respectively. Our results indicate that EV 71 was a major cause of HFMD in Korea during the study period. In addition, we found that clinical symptoms may be helpful in the early identification of patients with EV 71 infections.
[Show abstract][Hide abstract] ABSTRACT: We investigated the roles and biochemical properties of recombinant murine norovirus-1 (MNV-1) 3D(pol) in RNA synthesis and virus genome-linked protein (VPg) nucleotidylylation. We therefore expressed VPg and 3D(pol) of MNV-1 in Escherichia coli. MNV-1 3D(pol) exhibited RNA-dependent RNA polymerase (RdRp) activity in vitro with poly(A) RNA as a template and MnCl(2) as a cofactor. MNV-1 3D(pol) demonstrated optimum RNA-synthesis activity at pH 7.4 and 37 degrees C in the absence of a primer. Further, VPg was guanylylated by MNV-1 3D(pol) in the presence of MnCl(2) in a template-independent manner. The guanylylation reaction conducted with VPg substitution mutants (Y26F, Y40F, Y45F and Y117F) and a deletion mutant (Delta117-124) indicated that Tyr(117) was the probable target site of guanylylation. Homopolymeric RNAs did not enhance VPg guanylylation, whereas in vitro-transcribed (-) subgenomic (SG) and (+)SG RNA enhanced VPg guanylylation by 9.2 and 3.2 times, respectively. Within (-)SG RNA, the (-)ORF3 region played a critical role in enhancing VPg guanylylation, suggesting that the MNV-1 ORF3 region of negative-strand RNA contains a cis-acting element that stimulates 3D(pol)-mediated VPg guanylylation.
Journal of General Virology 03/2010; 91(Pt 7):1713-22. DOI:10.1099/vir.0.020461-0 · 3.18 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background: Many types of human viruses can infect and replicate in neuronal cells and are closely associated with various diseases, including encephalitis and meningitis. Echovirus 30 (E30), a member of the Picornaviridae family, is a major cause of aseptic meningitis and encephalitis. Human Echovirus 30 which belongs to enterovirus genus can cause encephalitis in neural tissues.
Methods: To characterize the neuronal cellular response to E30 infection, we performed two-dimensional (2-DE) gel electrophoresis and a total of 20 protein spots with a threshold greater than 2-fold were excised from these 2-DE gels and performed in-gel trypsin digestion and subsequent MALDI-TOF and MALDI-TOF/TOF identification.
Results: Two-dimensional proteomic maps have shown differences in expression of 12 proteins. Such as protein disulfide isomerase-related protein 5 (PDI5), tubulin, alpha 1a(TUBA1A), tubulin alpha 6 (TUBA6), uracil DNA glycosylase (UNG), laminin B1 (LMNB1), heterogeneous nuclear ribonucleoprotein K (HNRK), ribosomal protein, large P0 (RPLP0), and ATP-dependent DNA helicase were downregulated in SK-N-SH cells and switch-associated protein 70 (SWAP70), chain A mutant of annexin VI, triple functional domain (TRIO), and blue cone opsin were upregulated in SK-N-SH cells infected with E30.
Conclusion: The implication for human neuronal cellular responses to E30 was analyzed and made more comprehensive characterization of the virus-host interactions in pathogenesis. Further large scale studies are necessary to understand the roles of the differentially expressed cellular proteins in E30 infection.
Infectious Diseases Society of America 2009 Annual Meeting; 10/2009