Novel Nonstructural Protein 4 Genetic Group in Rotavirus of Porcine Origin

Novel Genetic Group in Rotaviru

Developing persulfate-activator soft solid (PASS) as slow release oxidant to remediate phenol-contaminated groundwater

The research objective was to develop a persulfate-activator soft solid (PASS) as a biodegradable slow-release oxidant to treat phenol-contaminated groundwater. PASS was prepared by graft copolymerization of acrylic acid (AA) and acrylamide (AM) onto 1% (w/v) sodium alginate mixed with 500 mg L−1 sodium persulfate and 5 mg L−1 ferrous sulfate. The physical and chemical properties of PASS were characterized using scanning electron microscopy, Fourier transform infrared spectroscopy, thermogravimetric analysis, differential scanning calorimetry, the water content and swelling ratio. Various variables, including the ratio of AA/AM, pH, temperature and the type of groundwater cations affecting PS release, were investigated. The maximum PS release in DI water was 98% in the ratio of PASS 1 (AA/AM, 75/25), 96% at pH 3, 83% at 25 °C, and 80% with Na+. The major factors controlling PS release were the AA/AM ratio and pH. PASS 1 can be stable in size and shape for 6–8 days and completely degraded within 34 days. The degradation rates of 10 mgL−1 phenol using PASS produced the highest kobs values for each variable at a ratio of PASS 1 (k = 0.1408 h−1), pH 7 (k = 0.1338 h−1), 25 °C (k = 0.1939 h−1), and Ca2+ (k = 0.1336 h−1). The temperature of the groundwater was key to driving the reaction between PS and phenol. PASS 1 was applied in simulated phenol-contaminated groundwater via horizontal tanks containing Ottawa sand. The results indicated 93.2% phenol removal within 72 h in a narrow horizontal flow tank and 41.7% phenol removal in a wide horizontal flow tank with aeration

Possible occurrence of a genetic bottleneck in dengue serotype 2 viruses between the 1980 and 1987 epidemic seasons in Bangkok Thailand

Cocirculation of two genetic subtypes of denguc serotype 2 viruses was first observed in the 1980 epidemic season in Thailand. To further delineate the evolutionary history and the contribution of these subtypes to subsequent epidemics, we determined the envelope glycoprotcin gene sequence of 20 dengue serotype 2 viruses isolated from infected patients during 1987 and compared them with those derived from earlier years. Subtype ifia strains represented the majority (18 of 19) of dengue type 2 viruses derived from Bangkok metropolitan area, whereas all three strains from a province in the northeastern region belonged to subtype Ilib, indicating uneven local distni bution of dengue subtypes within the same year. Three types of sequence variation were identified in both subtypes: substitutions that were unique to individual strains; substitutions that were shared among all subtype HIa on Ilib viruses of both the 1980 and 1987 epidemics; and those that were shared only among all subtypes lila or IIlb viruses of the 1987 epidemic, but were absent from the corresponding subtypes of 1980. While the first and second types of substitution were indicative of the most recent random mutations and previous mutations that had been fixed in virus populations, respectively, the third type suggested possible occurrence of a genetic bottleneck and subsequent expan sion of one or a limited number of subtype lila strains in Bangkok between 1980 and 1987. Immunobbot analysis of intracellular NS1 antigen with anti-NS1 monocbonal antibodies also revealed antigenic heterogeneity of the NSl protein that correlated with the subdivision based on envelope protein variation

HCV induces transforming growth factor β1 through activation of endoplasmic reticulum stress and the unfolded protein response

HCV replication disrupts normal endoplasmic reticulum (ER) function and activates a signaling network called the unfolded protein response (UPR). UPR is directed by three ER transmembrane proteins including ATF6, IRE1, and PERK. HCV increases TGF-β1 and oxidative stress, which play important roles in liver fibrogenesis. HCV has been shown to induce TGF-β1 through the generation of reactive oxygen species (ROS) and p38 MAPK, JNK, ERK1/2, and NFκB-dependent pathways. However, the relationship between HCV-induced ER stress and UPR activation with TGF-β1 production has not been fully characterized. In this study, we found that ROS and JNK inhibitors block HCV up-regulation of ER stress and UPR activation. ROS, JNK and IRE1 inhibitors blocked HCV-activated NFκB and TGF-β1 expression. ROS, ER stress, NFκB, and TGF-β1 signaling were blocked by JNK specific siRNA. Knockdown IRE1 inhibited JFH1-activated NFκB and TGF-β1 activity. Knockdown of JNK and IRE1 blunted JFH1 HCV up-regulation of NFκB and TGF-β1 activation. We conclude that HCV activates NFκB and TGF-β1 through ROS production and induction of JNK and the IRE1 pathway. HCV infection induces ER stress and the UPR in a JNK-dependent manner. ER stress and UPR activation partially contribute to HCV-induced NF-κB activation and enhancement of TGF-β1

First Report from the Asian Rotavirus Surveillance Network

Rotavirus remains the most common cause of severe, dehydrating diarrhea among children worldwide. Several rotavirus vaccines are under development. Decisions about new vaccine introduction will require reliable data on disease impact. The Asian Rotavirus Surveillance Network, begun in 2000 to facilitate collection of these data, is a regional collaboration of 36 hospitals in nine countries or areas that conduct surveillance for rotavirus hospitalizations using a uniform World Health Organization protocol. We summarize the Network's organization and experience from August 2001 through July 2002. During this period, 45% of acute diarrheal hospitalizations among children 0–5 years were attributable to rotavirus, higher than previous estimates. Rotavirus was detected in all sites year-round. This network is a novel, regional approach to surveillance for vaccine-preventable diseases. Such a network should provide increased visibility and advocacy, enable more efficient data collection, facilitate training, and serve as the paradigm for rotavirus surveillance activities in other regions

MECHANISMS OF VIRUS-INDUCED IMMUNOSUPPRESSION AND MODULATION OF VIRUS MULTIPLICATION BY LYMPHOKINES.

MECHANISMS OF VIRUS-INDUCED IMMUNOSUPPRESSION AND MODULATION OF VIRUS MULTIPLICATION BY LYMPHOKINES

Enteric and non-enteric adenoviruses associated with acute gastroenteritis in pediatric patients in Thailand, 2011 to 2017.

Human adenovirus (HAdV) is known to be a common cause of diarrhea in children worldwide. Infection with adenovirus is responsible for 2-10% of diarrheic cases. To increase a better understanding of the prevalence and epidemiology of HAdV infection, a large scale and long-term study was needed. We implemented a multi-year molecular detection and characterization study of HAdV in association with acute gastroenteritis in Chiang Mai, Thailand from 2011 to 2017. Out of 2,312 patients, HAdV was detected in 165 cases (7.2%). The positive rate for HAdV infection was highest in children of 1 and 2 years of age compared to other age groups. HAdV subgroup C (40.6%) was the most prevalent, followed by subgroups F (28.5%), B (20.6%), A and D (4.8% each), and E (0.6%). Of these, HAdV-F41 (22.4%), HAdV-C2 (18.2%), HAdV-B3 (15.2%), and HAdV-C1 (13.3%) were the most common genotypes detected. HAdV infection occurred throughout the year with a higher detection rate between May and July. In conclusion, our study demonstrated the infection rate, seasonal distribution and genotype diversity of HAdV infection in children with diarrhea in Chiang Mai, Thailand over a period of 7 year. Not only enteric adenovirus (F40 and F41) but also non-enteric adenovirus (B3, C1, C2) may play an important role in gastroenteritis in this area. The information will be beneficial for the prevention and control of HAdV outbreaks in the future