tetano
Editor, Senior Moderator
J Infect Dis. 2019 Apr 18. pii: jiz165. doi: 10.1093/infdis/jiz165. [Epub ahead of print]
[h=1]Risk assessment of the tropism & pathogenesis of the highly pathogenic avian influenza A/H7N9 virus using ex vivo & in vitro cultures of human respiratory tract.[/h] Chan LLY[SUP]1[/SUP], Hui KPY[SUP]1[/SUP], Kuok DIT[SUP]1[/SUP], Bui CHT[SUP]1[/SUP], Ng KC[SUP]1[/SUP], Mok CKP[SUP]2,[/SUP][SUP]3[/SUP], Yang ZF[SUP]3,[/SUP][SUP]4[/SUP], Guan W[SUP]3[/SUP], Poon LLM[SUP]1[/SUP], Zhong N[SUP]3[/SUP], Peiris JSM[SUP]1[/SUP], Nicholls JM[SUP]5[/SUP], Chan MCW[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Highly pathogenic avian influenza (HPAI)-H7N9 virus arising from low pathogenic avian influenza (LPAI)-H7N9 virus with polybasic amino acid substitutions in the haemagglutinin was detected in 2017. We compared the tropism, replication competence and cytokine induction of HPAI-H7N9, LPAI-H7N9 and HPAI-H5N1 in ex vivo human respiratory tract explants and in vitro culture of human alveolar epithelial cells (AECs) and pulmonary microvascular endothelial cells (HMVEC-L). Replication competence of HPAI- and LPAI-H7N9 were comparable in ex vivo cultures of bronchus and lung. HPAI-H7N9 predominantly infected AECs, while limited infection was observed in bronchus. The reduced tropism of HPAI-H7N9 in bronchial epithelium may explain the lack of human-to-human transmission despite a number of mammalian adaptation markers. Apical and basolateral release of virus was observed only in HPAI-H7N9 and H5N1 infected AECs regardless of infection route. HPAI-H7N9, but not LPAI-H7N9 efficiently replicated in HMVEC-L implying that endothelial tropism may involve in pathogenesis of HPAI-H7N9 disease.
? The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.
[h=4]KEYWORDS:[/h] H5N1; H7N9; HPAI; Risk assessment; alveolar epithelial cells; ex vivo; influenza; pathogenesis; pulmonary microvascular endothelial cells; tropism
PMID: 31001638 DOI: 10.1093/infdis/jiz165
[h=1]Risk assessment of the tropism & pathogenesis of the highly pathogenic avian influenza A/H7N9 virus using ex vivo & in vitro cultures of human respiratory tract.[/h] Chan LLY[SUP]1[/SUP], Hui KPY[SUP]1[/SUP], Kuok DIT[SUP]1[/SUP], Bui CHT[SUP]1[/SUP], Ng KC[SUP]1[/SUP], Mok CKP[SUP]2,[/SUP][SUP]3[/SUP], Yang ZF[SUP]3,[/SUP][SUP]4[/SUP], Guan W[SUP]3[/SUP], Poon LLM[SUP]1[/SUP], Zhong N[SUP]3[/SUP], Peiris JSM[SUP]1[/SUP], Nicholls JM[SUP]5[/SUP], Chan MCW[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Highly pathogenic avian influenza (HPAI)-H7N9 virus arising from low pathogenic avian influenza (LPAI)-H7N9 virus with polybasic amino acid substitutions in the haemagglutinin was detected in 2017. We compared the tropism, replication competence and cytokine induction of HPAI-H7N9, LPAI-H7N9 and HPAI-H5N1 in ex vivo human respiratory tract explants and in vitro culture of human alveolar epithelial cells (AECs) and pulmonary microvascular endothelial cells (HMVEC-L). Replication competence of HPAI- and LPAI-H7N9 were comparable in ex vivo cultures of bronchus and lung. HPAI-H7N9 predominantly infected AECs, while limited infection was observed in bronchus. The reduced tropism of HPAI-H7N9 in bronchial epithelium may explain the lack of human-to-human transmission despite a number of mammalian adaptation markers. Apical and basolateral release of virus was observed only in HPAI-H7N9 and H5N1 infected AECs regardless of infection route. HPAI-H7N9, but not LPAI-H7N9 efficiently replicated in HMVEC-L implying that endothelial tropism may involve in pathogenesis of HPAI-H7N9 disease.
? The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.
[h=4]KEYWORDS:[/h] H5N1; H7N9; HPAI; Risk assessment; alveolar epithelial cells; ex vivo; influenza; pathogenesis; pulmonary microvascular endothelial cells; tropism
PMID: 31001638 DOI: 10.1093/infdis/jiz165