ORCID Profile
0000-0001-5027-9423
Current Organisation
Huashan Hospital Fudan University
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Publisher: Elsevier BV
Date: 08-2015
DOI: 10.1016/J.JCV.2015.05.013
Abstract: The clinical features of avian-origin influenza virus A (H7N9) virus infection have been extensively characterized, but viral RNA detection in extra-pulmonary s les has seldom been studied. To study shedding of viral RNA in extra pulmonary s les in patients with avian influenza H7N9 infections. A retrospective study of throat swabs, urine, fecal s les and sera collected sequentially from 18 hospitalized patients with H7N9 infections in Shanghai, China, between April and July in 2013 was conducted. Viral RNA could be detected in urine s les from 17 patients, in fecal s les from 15 and in sera from 14 with a real-time reverse transcription polymerase chain reaction. The median duration of shedding of viral RNA was 19.7 days in throat swabs, 22 days in feces, 21.1 days in urines and 16.2 days in sera, indicating prolonged shedding of viral RNA in feces and urine compared with that in throat swabs. Prolonged duration of viral RNA detection in throat swabs and urine s les was observed in more severe patients. Moreover, in previously reported oseltamivir resistant patients, the NA gene with a 292K mutation could also be detected in their extra-pulmonary as well as in their respiratory s les. Our data indicated a high frequency of viral RNA detection in feces, urine and sera in H7N9-infected patients and pointed out the potential risk of transmission.
Publisher: Springer Science and Business Media LLC
Date: 26-02-0021
DOI: 10.1038/S41467-018-03243-7
Abstract: Severe influenza A virus (IAV) infection is associated with immune dysfunction. Here, we show circulating CD8 + T-cell profiles from patients hospitalized with avian H7N9, seasonal IAV, and influenza vaccinees. Patient survival reflects an early, transient prevalence of highly activated CD38 + HLA-DR + PD-1 + CD8 + T cells, whereas the prolonged persistence of this set is found in ultimately fatal cases. Single-cell T cell receptor (TCR)-αβ analyses of activated CD38 + HLA-DR + CD8 + T cells show similar TCRαβ ersity but differential clonal expansion kinetics in surviving and fatal H7N9 patients. Delayed clonal expansion associated with an early dichotomy at a transcriptome level (as detected by single-cell RNAseq) is found in CD38 + HLA-DR + CD8 + T cells from patients who succumbed to the disease, suggesting a ergent differentiation pathway of CD38 + HLA-DR + CD8 + T cells from the outset during fatal disease. Our study proposes that effective expansion of cross-reactive influenza-specific TCRαβ clonotypes with appropriate transcriptome signatures is needed for early protection against severe influenza disease.
Publisher: Springer Science and Business Media LLC
Date: 19-08-2021
DOI: 10.1038/S41590-021-00996-0
Abstract: Follicular helper T (T
Publisher: American Society for Clinical Investigation
Date: 06-07-2017
Publisher: Proceedings of the National Academy of Sciences
Date: 23-12-2013
Abstract: A unique avian-origin H7N9 influenza virus caused 134 human infections with 44 deaths. The host factors contributing to moderate vs. severe disease are not clear. Here, we show that H7N9 severity was associated with a higher level of cytokines/chemokines. We demonstrate that the cytokines in the infected lung were 100- to 1,000-fold higher than those in the plasma. Furthermore, we found that the IFN-induced transmembrane protein-3 (IFITM3) C/C genotype was associated with severe clinical outcome, as reflected by reduced time in seeking medical aid more rapid progression to acute respiratory distress syndrome and higher viral load, cytokine/chemokine levels, and mortality rate. Overall, our data suggest that the IFITM3 genotype is a primary driver of the observed differences in clinical outcome after H7N9 infection.
Publisher: Springer Science and Business Media LLC
Date: 04-10-2021
Publisher: Wiley
Date: 2021
DOI: 10.1002/CTI2.1251
Publisher: American Society for Microbiology
Date: 06-2018
DOI: 10.1128/JVI.00110-18
Abstract: Two lineages of influenza D virus (IDV) have been found to infect cattle and promote bovine respiratory disease complex, one of the most commonly diagnosed causes of morbidity and mortality within the cattle industry. Furthermore, IDV can infect other economically important domestic livestock, including pigs, and has the potential to infect humans, which necessitates the need for an efficacious vaccine. In this study, we designed a DNA vaccine expressing consensus hemagglutinin-esterase fusion (HEF) protein (FluD-Vax) and tested its protective efficacy against two lineages of IDV (D/OK and D/660) in guinea pigs. Animals that received FluD-Vax ( n = 12) developed appreciable titers of neutralizing antibodies against IDV lineage representatives, D/OK and D/660. Importantly, vaccinated animals were protected against intranasal challenge with IDV [3 × 10 5 50% tissue culture infective dose(s) (TCID 50 )] D/OK ( n = 6) or D/600 ( n = 6), based on the absence of viral RNA in necropsied tissues (5 and 7 days postchallenge) using quantitative reverse transcription-PCR and in situ hybridization. In contrast, animals that received a sham DNA vaccine ( n = 12) had no detectable neutralizing antibodies against IDV, and viral RNA was readily detectable in respiratory tract tissues after intranasal challenge (3 × 10 5 TCID 50 ) with IDV D/OK ( n = 6) or D/660 ( n = 6). Using a TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay, we found that IDV D/OK and D/600 infections induced apoptosis in epithelial cells lining alveoli and bronchioles, as well as nonepithelial cells in lung tissues. Our results demonstrate for the first time that the consensus IDV HEF DNA vaccine can elicit complete protection against infection from two lineages of IDV in the guinea pig model. IMPORTANCE Influenza D virus (IDV) infection has been associated with bovine respiratory disease complex, one of the most devastating diseases of the cattle population. Moreover, with broad host range and high environmental stability, IDV has the potential to further gain virulence or even infect humans. An efficacious vaccine is needed to prevent infection and stop potential cross-species transmission. In this study, we designed a DNA vaccine encoding the consensus hemagglutinin-esterase fusion (HEF) protein of two lineages of IDV (D/OK and D/660) and tested its efficacy in a guinea pig model. Our results showed that the consensus DNA vaccine elicited high-titer neutralizing antibodies and achieved sterilizing protection against two lineage-representative IDV intranasal infections. To our knowledge, this is the first study showing that a DNA vaccine expressing consensus HEF is efficacious in preventing different lineages of IDV infections.
Publisher: Springer Science and Business Media LLC
Date: 13-05-2015
DOI: 10.1038/NCOMMS7833
Abstract: The avian origin A/H7N9 influenza virus causes high admission rates ( %) and mortality ( %), with ultimately favourable outcomes ranging from rapid recovery to prolonged hospitalization. Using a multicolour assay for monitoring adaptive and innate immunity, here we dissect the kinetic emergence of different effector mechanisms across the spectrum of H7N9 disease and recovery. We find that a ersity of response mechanisms contribute to resolution and survival. Patients discharged within 2–3 weeks have early prominent H7N9-specific CD8 + T-cell responses, while in iduals with prolonged hospital stays have late recruitment of CD8 + /CD4 + T cells and antibodies simultaneously (recovery by week 4), augmented even later by prominent NK cell responses (recovery days). In contrast, those who succumbed have minimal influenza-specific immunity and little evidence of T-cell activation. Our study illustrates the importance of robust CD8 + T-cell memory for protection against severe influenza disease caused by newly emerging influenza A viruses.
Publisher: Informa UK Limited
Date: 2014
DOI: 10.1038/EMI.2014.80
Publisher: American Association for the Advancement of Science (AAAS)
Date: 29-09-2023
No related grants have been discovered for Yanmin Wan.