Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infection caused by a novel Bunyavirus. Analysis on the dynamic changes of clinical, laboratory, and immunological abnormalities associated with SFTS in a concurrent study is lacking. Thirty-three SFTS patients were admitted to Jiangsu People's Hospital, Nanjing, China, and diagnosis was made based on the clinical symptoms and positive viral RNA detected by RT-PCR. Four patients deceased and twenty-nine survived. Blood samples were collected every other day between Day 5 and Day 15 from the onset of fever. Samples from healthy volunteers were used as normal controls. Peak viral RNA load, serum enzymes, IL-6, and IL-10 were significantly higher in deceased patients compared to survivors. Viral load, serum enzymes, and cytokines declined in survivors within 2 weeks from onset of fever. CD69+ T cells were elevated early after infection while HLA-DR+ and CTLA4+ T cells were elevated during the recovery phase of those who survived. High level SFTSV viral load was concurrently observed with reduced PLT, elevated serum enzymes, elevated pro-inflammatory and anti-inflammatory cytokines, and activation of CD69+ T cells. The degree and pattern of changes in these parameters may indicate the clinical outcome in SFTSV-infected patients.

Severe fever with thrombocytopenia syndrome (SFTS) associated with severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging infectious disease. 12 patients with severe fever with thrombocytopenia syndrome in our study were presented mainly with fever and severe malaise. The clinical manifestations typically became worse on the 6th or 7th day. The average fever time is 9.11 ± 1.54 days. Most of them had multiorgan dysfunction, and part of them had hemophagocytic lymphohistiocytosis histiocytosis (HLH). The characteristic laboratory findings in the early stage were the drop of white blood cells (WBC), platelets (PLT) and serum Ca++, while increase of aspartate amino transferase (AST), creatine kinase (CK), and lactate dehydrogenase (LDH). CD3+CD4+ were significantly decreased, while CD3-CD56+ were significantly increased, whereas CD3+CD8+ were constantly elevated throughout the disease course. Ten to 14 days after illness onset, symptoms were improved, accompanied by resolution of laboratory abnormalities. These results indicate that severe fever with thrombocytopenia syndrome has an acute onset and self-limited course. It is a systemic infection. The host immune response caused tissues and organs injury. The improvement of symptoms and laboratory tests is consistent with the elimination of the virus and recover of immune response. Further investigation should be done in order to better understand this disease and guide the clinical treatment.

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pSW3891/HBc vaccination elicits specific anti-HBc response and induces HBc-specific CTL response in immunized Balb/c mice.

Infection with hepatitis B virus (HBV) remains a worldwide health problem, and DNA-based vaccines against HBV have been tested for therapeutic applications. HBV possesses three envelope lipoproteins that are translated from a single reading-frame: large, middle, and small HBV surface antigens. Among these envelope proteins, the middle HBV surface antigen (MHBs) contains a constitutive N-linked glycosylation site at position 4 (Asn4) in the amino-terminal portion (MQWNSTTFHQ) of pre-S2 domain. Asn4 (shown in bold) is essential for secretion of viral particles and conserved among all serotypes of HBV, but its influence on the immunogenicity of MHBs remains unknown. Here, we constructed four MHBs genes carrying mutations, underlined, in the amino-terminal portion of pre-S2 domain. One mutant protein contains Q at position 4 (MQWQSTTFHQ). In addition, each of three mutant MHBs proteins contains a N-linked glycosylation site (N-X-S/T), relocated to position 5 (MQWQNTTFHQ), 6 (MQWQSNTSHQ) or 7 (MQWQSTNFTQ) in pre-S2 domain. The expression and immunogenic properties of mutant DNA vaccines were examined in 293T human renal epithelial cells and in BALB/c mice, respectively. We showed that Asn4 was critical for secretion and immunogenicity of MHBs. Moreover, the MHBs protein that carries a N-linked glycosylation site at position 5 or 7 retained the properties similar to wild-type MHBs. In contrast, the secretion-defective mutant protein carrying Asn at position 6 induced only marginal humoral and cellular immune responses in mice, despite the N-linked glycosylation. In conclusion, N-linked glycosylation at an appropriate position in pre-S2 domain is an essential requirement for DNA vaccine expressing MHBs.

This study provides the first evidence that CD25 is a novel marker of bile canaliculus. Characteristics of CD25 expression may shed light on immunohistochemistry and immunofluorescence analysis of bile canaliculus in both basic and clinical hepatic investigations.