Heterologous interactions between NS1 proteins from different influenza A virus subtypes/strains

Li, Weizhong; Zhang, Heng; Wang, Gefei; Zhang, Chi; Zeng, Xiangxing; Liu, Hui; Chen, XiaoXuan; Xu, YanXuan; Li, Kangsheng

doi:10.1007/s11427-012-4335-6

Cited by 1 publication

(1 citation statement)

References 34 publications

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“…Given that flu viruses have high mutation rates, the identification of ACE2 as a common regulator of lung injury may also be useful to alleviate ALI/ARDS owing to mutated, newly emerging flu viruses including avian origin influenza virus H7N9 and/or currently unknown lethal lung pathogens [29][30][31][32][33][34] . Importantly, our data identify ACE2 as a potential novel mode of action to alleviate the symptoms of acute lung pathologies in individuals infected with highly lethal avian influenza A H5N1 viruses.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme 2 protects from lethal avian influenza A H5N1 infections

et al. 2014

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The potential for avian influenza H5N1 outbreaks has increased in recent years. Thus, it is paramount to develop novel strategies to alleviate death rates. Here we show that avian influenza A H5N1-infected patients exhibit markedly increased serum levels of angiotensin II. High serum levels of angiotensin II appear to be linked to the severity and lethality of infection, at least in some patients. In experimental mouse models, infection with highly pathogenic avian influenza A H5N1 virus results in downregulation of angiotensin-converting enzyme 2 (ACE2) expression in the lung and increased serum angiotensin II levels. Genetic inactivation of ACE2 causes severe lung injury in H5N1-challenged mice, confirming a role of ACE2 in H5N1-induced lung pathologies. Administration of recombinant human ACE2 ameliorates avian influenza H5N1 virus-induced lung injury in mice. Our data link H5N1 virus-induced acute lung failure to ACE2 and provide a potential treatment strategy to address future flu pandemics.

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