tetano
Editor, Senior Moderator
J Infect Dis. 2019 Oct 3. pii: jiz506. doi: 10.1093/infdis/jiz506. [Epub ahead of print] [h=1]Host-specific restriction of avian influenza virus caused by differential dynamics of ANP32 family members.[/h]
Park YH[SUP]1[/SUP], Chungu K[SUP]1[/SUP], Lee SB[SUP]1[/SUP], Woo SJ[SUP]1[/SUP], Cho HY[SUP]1[/SUP], Lee HJ[SUP]1[/SUP], Rengaraj D[SUP]1[/SUP], Lee JH[SUP]2[/SUP], Song CS[SUP]2[/SUP], Lim JM[SUP]1[/SUP], Han JY[SUP]1[/SUP].
[h=3]Author information[/h] 1 Department of Agricultural Biotechnology and Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul, Republic of Korea. 2 Avian Diseases Laboratory, College of Veterinary Medicine, Konkuk University, Seoul, Republic of Korea.
[h=3]Abstract[/h] Influenza viruses must utilize host factors to complete their lifecycle. Species-specific differences in host factors between birds and mammals mean that avian influenza viruses (AIVs) replicate well in avian hosts but not in human hosts. Acidic nuclear phosphoprotein 32 family member A (ANP32A) has been identified as the host restriction factor for the viral polymerase (vPol) activity of AIVs. ANP32A belongs to the conserved ANP32 family, the functional roles of which during viral replication remain unclear. Here, we targeted chicken ANP32A using CRISPR/Cas9-mediated genome editing to examine the functional roles of ANP32A and other members of the ANP32 family. We found that each chicken and human ANP32 family member had different effects on vPol activity, suggesting that species-specific vPol activity of AIVs could be caused by the differential functions and overall competency of ANP32 family members.
? 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] ANP32 family; cellular host factor; host restriction; influenza virus
PMID: 31581291 DOI: 10.1093/infdis/jiz506
Park YH[SUP]1[/SUP], Chungu K[SUP]1[/SUP], Lee SB[SUP]1[/SUP], Woo SJ[SUP]1[/SUP], Cho HY[SUP]1[/SUP], Lee HJ[SUP]1[/SUP], Rengaraj D[SUP]1[/SUP], Lee JH[SUP]2[/SUP], Song CS[SUP]2[/SUP], Lim JM[SUP]1[/SUP], Han JY[SUP]1[/SUP].
[h=3]Author information[/h] 1 Department of Agricultural Biotechnology and Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul, Republic of Korea. 2 Avian Diseases Laboratory, College of Veterinary Medicine, Konkuk University, Seoul, Republic of Korea.
[h=3]Abstract[/h] Influenza viruses must utilize host factors to complete their lifecycle. Species-specific differences in host factors between birds and mammals mean that avian influenza viruses (AIVs) replicate well in avian hosts but not in human hosts. Acidic nuclear phosphoprotein 32 family member A (ANP32A) has been identified as the host restriction factor for the viral polymerase (vPol) activity of AIVs. ANP32A belongs to the conserved ANP32 family, the functional roles of which during viral replication remain unclear. Here, we targeted chicken ANP32A using CRISPR/Cas9-mediated genome editing to examine the functional roles of ANP32A and other members of the ANP32 family. We found that each chicken and human ANP32 family member had different effects on vPol activity, suggesting that species-specific vPol activity of AIVs could be caused by the differential functions and overall competency of ANP32 family members.
? 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] ANP32 family; cellular host factor; host restriction; influenza virus
PMID: 31581291 DOI: 10.1093/infdis/jiz506