Yang Yang1, Gary Wong2, Liuqing Yang3, Shuguang Tan4, Jianming Li3, Bing Bai5, Zhixiang Xu3, Hong Li6, Wen Xu6, Xiaonan Zhao6, Chuansong Quan7, Haixia Zheng3, William J Liu7, Wenjun Liu4, Lei Liu3, Yingxia Liu8, Yuhai Bi9, George F Gao10. 1. Shenzhen Key Laboratory of Pathogen and Immunity, Guangdong Key Laboratory for Diagnosis and Treatment of Emerging Infectious Diseases, State Key Discipline of Infectious Disease, Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen Third People's Hospital, Shenzhen 518112, China; CAS Key Laboratory of Pathogenic Microbiology and Immunology, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease, Institute of Microbiology, Center for Influenza Research and Early-Warning (CASCIRE), Chinese Academy of Sciences, Beijing 100101, China. 2. Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai 200031, China; Département de microbiologie-infectiologie et d'immunologie, Université Laval, Québec City G1V 0A6, Canada. 3. Shenzhen Key Laboratory of Pathogen and Immunity, Guangdong Key Laboratory for Diagnosis and Treatment of Emerging Infectious Diseases, State Key Discipline of Infectious Disease, Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen Third People's Hospital, Shenzhen 518112, China. 4. CAS Key Laboratory of Pathogenic Microbiology and Immunology, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease, Institute of Microbiology, Center for Influenza Research and Early-Warning (CASCIRE), Chinese Academy of Sciences, Beijing 100101, China. 5. Department of Infectious Diseases and Shenzhen Key Lab for Endogenous Infection, Shenzhen Nanshan Hospital of Shenzhen University, Shenzhen 518000, China. 6. Yunnan Center for Disease Control and Prevention, Kunming 650022, China. 7. National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention (China CDC), Beijing 102206, China. 8. Shenzhen Key Laboratory of Pathogen and Immunity, Guangdong Key Laboratory for Diagnosis and Treatment of Emerging Infectious Diseases, State Key Discipline of Infectious Disease, Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen Third People's Hospital, Shenzhen 518112, China; University of Chinese Academy of Sciences Medical School, Chinese Academy of Sciences, Beijing 101408, China. Electronic address: yingxialiu@hotmail.com. 9. Shenzhen Key Laboratory of Pathogen and Immunity, Guangdong Key Laboratory for Diagnosis and Treatment of Emerging Infectious Diseases, State Key Discipline of Infectious Disease, Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen Third People's Hospital, Shenzhen 518112, China; CAS Key Laboratory of Pathogenic Microbiology and Immunology, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease, Institute of Microbiology, Center for Influenza Research and Early-Warning (CASCIRE), Chinese Academy of Sciences, Beijing 100101, China. Electronic address: beeyh@im.ac.cn. 10. Shenzhen Key Laboratory of Pathogen and Immunity, Guangdong Key Laboratory for Diagnosis and Treatment of Emerging Infectious Diseases, State Key Discipline of Infectious Disease, Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen Third People's Hospital, Shenzhen 518112, China; CAS Key Laboratory of Pathogenic Microbiology and Immunology, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Disease, Institute of Microbiology, Center for Influenza Research and Early-Warning (CASCIRE), Chinese Academy of Sciences, Beijing 100101, China; National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention (China CDC), Beijing 102206, China; University of Chinese Academy of Sciences Medical School, Chinese Academy of Sciences, Beijing 101408, China. Electronic address: gaof@im.ac.cn.
Abstract
OBJECTIVE: The newly emerged highly pathogenic (HP) H7N9 avian influenza virus during Wave Five has caused 28 human infections, while differences in disease severity between low pathogenic (LP)- and HP-H7N9 human infections remain unclear. METHODS: Clinical data, concentrations of serum cytokines, dynamics of virus shedding and PaO2/FiO2 from patients infected with LP-H7N9 (n = 7, LP group) and HP-H7N9 (n = 5, HP group) viruses during Wave Five were compared. In addition, critical mutations associated with H7N9 virulence in mammal/human were analyzed. RESULTS: Lymphopenia, elevated aspartate aminotransferase, alanine aminotransferase, C-reactive protein and lactate dehydrogenase were common features, with higher incidences of leukopenia and thrombocytopenia in the LP group. The acute phase of both groups was accompanied with elevated cytokines associated with disease severity, including MIF, MCP-1 and IP-10. Diffuse exudation of the lungs and consolidation were observed from all patients. The dynamics of virus shedding and PaO2/FiO2 were similar between both groups. Notably, a higher prevalence of neuraminidase inhibitors (NAIs) resistance in the HP-H7N9 virus was found. CONCLUSIONS: Our results indicate that this newly emerged HP-H7N9 virus caused similar disease severity in humans compared with LP-H7N9 virus, while higher case fatality rate and prevalence of NAI-resistance in human HP-H7N9 infections were of great concern.
OBJECTIVE: The newly emerged highly pathogenic (HP) H7N9avian influenza virus during Wave Five has caused 28 humaninfections, while differences in disease severity between low pathogenic (LP)- and HP-H7N9 human infections remain unclear. METHODS: Clinical data, concentrations of serum cytokines, dynamics of virus shedding and PaO2/FiO2 from patients infected with LP-H7N9 (n = 7, LP group) and HP-H7N9 (n = 5, HP group) viruses during Wave Five were compared. In addition, critical mutations associated with H7N9 virulence in mammal/human were analyzed. RESULTS:Lymphopenia, elevated aspartate aminotransferase, alanine aminotransferase, C-reactive protein and lactate dehydrogenase were common features, with higher incidences of leukopenia and thrombocytopenia in the LP group. The acute phase of both groups was accompanied with elevated cytokines associated with disease severity, including MIF, MCP-1 and IP-10. Diffuse exudation of the lungs and consolidation were observed from all patients. The dynamics of virus shedding and PaO2/FiO2 were similar between both groups. Notably, a higher prevalence of neuraminidase inhibitors (NAIs) resistance in the HP-H7N9 virus was found. CONCLUSIONS: Our results indicate that this newly emerged HP-H7N9 virus caused similar disease severity in humans compared with LP-H7N9 virus, while higher case fatality rate and prevalence of NAI-resistance in humanHP-H7N9 infections were of great concern.
Authors: William J Liu; Haixia Xiao; Lianpan Dai; Di Liu; Jianjun Chen; Xiaopeng Qi; Yuhai Bi; Yi Shi; George F Gao; Yingxia Liu Journal: Front Med Date: 2021-04-16 Impact factor: 4.592
Authors: Sahar Motallebi; Rex C Y Cheung; Babak Mohit; Shahram Shahabi; Amir Alishahi Tabriz; Syamak Moattari Journal: Am J Prev Med Date: 2021-11-11 Impact factor: 5.043