Rui Qi

BACKGROUND: Studies about asymptomatic norovirus infections have been frequently reported. We aim to assess the global prevalence of asymptomatic infections. METHOD: We identified publications that included the proportion of asymptomatic norovirus infections by searching in PubMed, Ovid, Scopus, and Web of Science and by screening references from the articles reviewed. The principal summary data were the prevalence of asymptomatic norovirus infection. Random-effect models for meta-analysis were fitted to generate estimates of overall and subgroup prevalence. FINDINGS: Of 81 studies included, asymptomatic norovirus prevalence was estimated at 7% (95% CI: 6%-9%). Africa, Meso America and South America had higher prevalence (15%, 14%, 11%, respectively) while the prevalence in Europe and North America was lower (4%). Prevalence was similar between community and hospital (9%). Prevalence was higher in children (8%) than adults (4%). For food handlers, prevalence was estimated at 3%. In context of outbreaks, prevalence estimated from 15 studies was as high as 18% (95% CI: 10%-30%). INTERPRETATION: This knowledge could have an impact on the development of transmission prevention strategies in the future. The high prevalence indicated asymptomatic individuals must not be overlooked. OUTSTANDING QUESTIONS: The high prevalence indicated asymptomatic individuals must not be overlooked. Asymptomatic individuals may play an important role in norovirus transmission. This knowledge could have an impact on the development of transmission prevention strategies.

Tumorigenesis is a complex multifactorial and multistep process in which tumors can utilize a diverse repertoire of immunosuppressive mechanisms to evade host immune attacks. The degradation of tryptophan into immunosuppressive kynurenine is considered an important immunosuppressive mechanism in the tumor microenvironment. There are three enzymes, namely, tryptophan 2,3-dioxygenase (TDO), indoleamine 2,3-dioxygenase 1 (IDO1), and indoleamine 2,3-dioxygenase 2 (IDO2), involved in the metabolism of tryptophan. IDO1 has a wider distribution and higher activity in catalyzing tryptophan than the other two; therefore, it has been studied most extensively. IDO1 is a cytosolic monomeric, heme-containing enzyme, which is now considered an authentic immune regulator and represents one of the promising drug targets for tumor immunotherapy. Collectively, this review highlights the regulation of IDO1 gene expression and the ambivalent mechanisms of IDO1 on the antitumoral immune response. Further, new therapeutic targets via the regulation of IDO1 are discussed. A comprehensive analysis of the expression and biological function of IDO1 can help us to understand the therapeutic strategies of the inhibitors targeting IDO1 in malignant tumors.

PCR amplification indicated the minimum infection rate of Rickettsia spp. was 0.66% in Haemaphysalis longicornis ticks collected from Shandong Province, China. Phylogenetic analysis based on the rrs, gltA, ompA, and ompB genes indicated that the ticks carried R. japonica, Candidatus Rickettsia longicornii, and a novel Rickettsia species related to R. canadensis.

BACKGROUND: Severe fever with thrombocytopenia syndrome (SFTS) is an emerging viral hemorrhagic fever with a high fatality rate and high frequency of person-to-person transmission and is caused by SFTSV, a tick-borne Phlebovirus. Because SFTS has similar clinical manifestations and epidemic characters (such as spatial and temporal distributions) with hemorrhagic fever with renal syndrome (HFRS) in China, we reason that SFTS patients might be misdiagnosed as HFRS. METHODOLOGY/PRINCIPAL FINDINGS: Acute-phase sera of 128 clinically diagnosed HFRS patients were retrospectively analyzed for Hantavirus IgM antibodies with ELISA. Hantavirus-negative patients' sera were further analyzed for SFTSV IgM antibodies with ELISA. ELISA showed that 73 of 128 (57.0%) of clinically diagnosed HFRS patients were IgM antibody positive to Hantaviruses. Among the 55 Hantavirus-IgM negative patients, four (7.3%) were IgM antibody positive to SFTSV. The results indicated that the four SFTS patients were misdiagnosed as HFRS. The misdiagnosed SFTS patients had clinical manifestations common to HFRS and were unable to be differentiated from HFRS clinically. CONCLUSIONS: Our study showed that SFTS patients could be clinically misdiagnosed as HFRS. The misdiagnosis of SFTS as HFRS causes particular concern because it may increase the risk of death of SFTS patients and person-to-person transmission of SFTSV without proper care for and isolation of SFTS patients.