Severe fever with thrombocytopenia syndrome virus (SFTSV) is a highly pathogenic tick-borne bunyavirus that causes lethal infectious disease and severe fever with thrombocytopenia syndrome (SFTS) in humans. The molecular mechanisms and host cellular factors required for SFTSV infection remain uncharacterized. In this issue, Liu et al. used genome-wide CRISPR-based screening to identify the host cellular factors required for SFTSV infection, and the vesicular trafficking protein sorting nexin 11 (SNX11) was identified essential for the establishment of SFTSV infection, particularly for penetration from the endolysosome to the cytoplasm. The cover image shows endolysosomes significantly increased in SNX11-KO cells (bottom red panel) compared with the wild-type cells (upper blue panel). See page 508–520 for details.
Severe fever with thrombocytopenia syndrome phlebovirus (SFTSV) has a wide host range. Not only has it been found in humans, but also in many wild and domesticated animals. The infection of breeding deer on farms is a particularly worrisome public health concern due to the large amount of human contact and the diverse use of deer products, including raw blood. To investigate the prevalence of breeding domesticated deer, we examined the SFTSV infection rate on deer farms in South Korea from 2015 to 2017. Of the 215 collected blood samples, 0.9% (2/215) were found to be positive for viral RNA by PCR, and sequence analysis showed the highest homology with the KADGH human isolate. Both SFTSV specific recombinant N and Gn protein-based ELISAs revealed that 14.0% (30/215) and 7.9% (17/215) of collected blood specimens were positive for SFTSV antibody. These results demonstrate that the breeding farm deer are exposed to SFTSV and could be a potential infection source for humans through direct contact or consumption of byproducts.
Chikungunya fever is a vector-borne viral disease transmitted to humans by chikungunya virus (CHIKV)-infected mosquitoes. There have been many outbreaks of CHIKV infection worldwide, and the virus poses ongoing risks to global health. To prevent and control CHIKV infection, it is important to improve the current CHIKV diagnostic approaches to allow for the detection of low CHIKV concentrations and to correctly distinguish CHIKV infections from those due to other mosquito-transmitted viruses, including dengue virus (DENV), Japanese encephalitis virus (JEV), and Zika virus (ZIKV). Here, we produced monoclonal antibodies (mAbs) against the CHIKV envelope 2 protein (CHIKV-E2) and compared their sensitivity and specificity with commercially available mAbs using enzyme-linked immunosorbent assays (ELISA). Two anti-CHIKV-E2 mAbs, 19-1 and 21-1, showed higher binding affinities to CHIKV-E2 protein than the commercial mAbs did. In particular, the 19-1 mAb had the strongest binding affinity to inactivated CHIKV. Moreover, the 19-1 mAb had very little cross-reactivity with other mosquito-borne viruses, such as ZIKV, JEV, and DENV. These results suggest that the newly produced anti-CHIKV-E2 mAb, 19-1, could be used for CHIKV diagnostic approaches.
季节性流感疫苗几乎每年都需要更新和制备。季节性流感疫苗抗原与流行毒株不相匹配,导致疫苗不能提供有效保护的现象时有发生,因而,迫切需要研发广谱流感疫苗。我们选用流感病毒A/北京/30/95(H3N2)的核蛋白(nucleoprotein,NP)和基质蛋白蛋白2的胞外区(extracellular domain of matrix protein 2,M2e),构建了NP与单拷贝或4个拷贝M2e不同方式组合的4个重组痘苗病毒,并将重组痘苗病毒免疫BALB/C小鼠。随后对小鼠体液和细胞免疫反应进行了检测,并以流感病毒A/波多黎各(Puerto Rico)/8/34(PR8)进行攻毒。结果表明,含全长NP基因的重组痘苗病毒都诱发了NP特异性体液免疫反应,而只有含多拷贝M2e基因的重组痘苗病毒诱发了M2e特异性体液免疫反应。所有重组痘苗病毒都诱发了NP和M2e特异性细胞免疫反应。只有RVJ-4M2eNP诱发了M2e特异的IL-2和IL-10细胞因子反应。此外,20 MLD50 PR8攻毒后RVJ-4M2eNP诱发的交叉保护效果最强。结果提示,重组痘苗病毒RVJ-4M2eNP所含表达基因结构中,4个M2e基因在前、全长NP基因在后,这种基因结构所诱发的交叉保护可能与NP和M2e特异性体液和细胞免疫反应有关。以上结果表明,NP基因和多拷贝M2e基因合理融合对诱发保护性免疫反应具有关键作用,融合抗原4M2eNP可用于广谱流感疫苗的研发。