SFTS virus (SFTSV) is a novel bunyavirus that causes severe fever with thrombocytopenia syndrome (SFTS), an emerging infectious disease that occurred in China in recent years, with an average case fatality rate of 10-12%. Intervention in the early clinical stage is the most effective measure to reduce the mortality rate of disease. To elucidate the natural course of and immune mechanisms associated with the pathogenesis of SFTSV, 59 laboratory-confirmed SFTS patients in the acute phase, who were hospitalized between October 2010 and September 2011, were enrolled in this study, and the patients sera were dynamically collected and tested for SFTSV viral RNA load, 34 cytokines or chemokines and other related laboratory parameters. All clinical diagnostic factors in the acute phase of SFTS were evaluated and assessed. The study showed that the severity of the disease in 11 (18.6%) patients was associated with abdominal pain (p 0.007; OR = 21.95; 95% CI, 2.32-208.11) and gingival bleeding (p 0.001; OR=122.11; 95% CI, 6.41-2328). The IP-10, TNF-α, IL-6, IL-10, granzyme B and HSP70 levels were higher over the 7-8 days in severe cases, accompanied by altered AST, CK and LDH levels. HSP70 (p 0.012; OR=8.29; 95% CI, 1.58-43.40) was independently correlated with the severity of the early acute phase of SFTSV infection. The severity of SFTS can be predicted based on the presence of symptoms such as abdominal pain and gingival bleeding and on the level of HSP70 in the acute phase of the disease.

An emerging infectious disease, severe fever with thrombocytopenia syndrome (SFTS), was identified to be associated with a novel SFTS virus (SFTSV). Transmission of the disease among humans has been described, but clinical impact factors and transmission mechanisms still need further study. An outbreak of person-to-person transmission of SFTS in a cluster of nine patients that occurred in an SFTS endemic area, Penglai County, Shandong province, China, was investigated. We found that the onset date of all eight secondary SFTS patients ranged from 7 to 13 days after exposure to the corpse of the index patient, and clinical incubation time was mostly focused on 9-10 days (n = 6). The two dead patients, including the index patient and one secondary infected patient, presented unusually high levels of viral load (6 × 10(8-9) copies/mL), low levels of platelets count (<55 × 10(9)/L), and significant increase of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and creatine kinase values in the second week, and died on day 10 or 11 after disease onset. Genetic sequencing revealed 100% homology among virus strains isolated from the index patient and five secondary patients. Risk factors assessment of the person-to-person transmission revealed that the major exposure factor was blood contact without personal protection equipment. Information from this study provided solid references of SFTS incubation time, clinical and laboratory parameters related to SFTS severity and outcome, and biosafety issues for preventing person-to-person transmission or nosocomial infection of SFTSV.

A nationwide hepatitis B virus (HBV) vaccination program was implemented in China starting in 1992.To study the change in HBV variant prevalence with massive immunization, large HBV surface protein (LHBs) genes from HBV surface antigen (HBsAg)-positive sera were amplified and sequenced. The prevalences of LHBs mutants were compared between the 1992 and 2005 surveys in child and adult groups. The prevalence of "␣" determinant mutants in the children increased from 6.5% in 1992 to 14.8% in 2005, where the G145R mutant occurred most frequently. In contrast, mutation frequencies showed little difference between 1992 (9.4%) and 2005 (9.9%) in adults. Moreover, compared to the 1992 survey, the child group surface (S) protein mutation frequency specifically increased (P ‫؍‬ 0.005) in the 2005 survey, but the pre-S region mutation frequency did not show a significant difference (P > 0.05). However, the mutation frequency in the adult group increased in both the pre-S and S regions. Furthermore, the frequencies of the disease-related pre-S2 deletion and start codon mutations were significantly higher in the adult groups than in the child groups in both the 1992 and 2005 surveys (P < 0.01). Massive immunization enhances the HBV S protein mutation; the prevalence of LHBs mutants, particularly disease-related mutants, tends to increase with patient age. Hepatitis B virus (HBV) infection is a serious public health problem worldwide and a major cause of hepatitis, cirrhosis, and hepatocellular carcinoma (HCC) (1). An estimated 350 million people are living with chronic hepatitis B worldwide (2). In China, a national serosurvey in 1992 revealed that the prevalence of hepatitis B surface antigen (HBsAg) was 9.8% in the general population (3). The most recent national serosurvey, in 2006, demonstrated that the HBsAg carrier rate is 7.2%, and the number of chronic HBV carriers is estimated to be 9.3 million (3, 4).China began infant vaccine injections in national disease surveillance points (DSP) as early as 1986, and the four provinces in the current study were also to perform infant vaccinations at that time (5). In 1992, China formally recommended routine immunization with the hepatitis B virus vaccine for infants. Since then, the massive vaccination program has effectively decreased the risk of HBV infection, and the rate of HBsAg-positive children has significantly declined. Among children Ͻ5 years of age, the prevalence of HBsAg has dramatically decreased from 9.67% (1992) to 0.96% (2006). It is estimated that 80 million children are free from HBV infection due to the vaccination program (3).While universal infantile HBV vaccination is very efficacious, an increase in the mutant prevalence or "vaccine escape mutation" after immunization posed a potential threat to the long-term success of massive vaccination (6-8). Hsu et al. studied the prevalence of HBV variants in children in Taiwan and demonstrated that universal vaccination had accelerated the accumulation of HBsAg "␣" determinant mutants (9). The ␣ determinant is a co...