Mechanistic insights into the kidney injury in chickens induced by hypervirulent fowl adenovirus serotype 4
Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has become globally prevalent since 2015 as a predominant pathogen on poultry farms, leading to substantial economic losses for the poultry industry. However, the molecular mechanisms underlying kidney injury induced by FAdV-4 infection remain unclea...
Saved in:
| Published in | Microbiology spectrum Vol. 13; no. 5; p. e0005825 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Society for Microbiology
25.03.2025
|
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has become globally prevalent since 2015 as a predominant pathogen on poultry farms, leading to substantial economic losses for the poultry industry. However, the molecular mechanisms underlying kidney injury induced by FAdV-4 infection remain unclear. In this study, we primarily elucidated the mechanisms of kidney injury induced by FAdV-4 infection in chickens, utilizing both in vitro and in vivo models. Our results demonstrate that FAdV-4 infection in chickens causes degeneration and necrosis of kidney epithelial cells, glomerular injury, and expansion of the endoplasmic reticulum, while also triggering a robust inflammatory response in kidney cells. Notably, we observed the cell-to-cell transmission of virus particles delivered by autophagosome-like vesicles, and the viral infection-induced cellular autophagy facilitated viral replication in the kidney cells. These findings offer a novel perspective to understand the molecular mechanisms of FAdV-4-induced kidney injury and establish a basis for further investigation into the molecular pathogenesis of hypervirulent FAdV-4. |
|---|---|
| AbstractList | Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has become globally prevalent since 2015 as a predominant pathogen on poultry farms, leading to substantial economic losses for the poultry industry. However, the molecular mechanisms underlying kidney injury induced by FAdV-4 infection remain unclear. In this study, we primarily elucidated the mechanisms of kidney injury induced by FAdV-4 infection in chickens, utilizing both in vitro and in vivo models. Our results demonstrate that FAdV-4 infection in chickens causes degeneration and necrosis of kidney epithelial cells, glomerular injury, and expansion of the endoplasmic reticulum, while also triggering a robust inflammatory response in kidney cells. Notably, we observed the cell-to-cell transmission of virus particles delivered by autophagosome-like vesicles, and the viral infection-induced cellular autophagy facilitated viral replication in the kidney cells. These findings offer a novel perspective to understand the molecular mechanisms of FAdV-4-induced kidney injury and establish a basis for further investigation into the molecular pathogenesis of hypervirulent FAdV-4. Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has emerged as a significant poultry pathogen since 2015, exhibiting clinical multi-organ and multi-tissue tropism post-infection, resulting in substantial economic losses in the poultry industry. However, the molecular mechanism underlying kidney injury caused by FAdV-4 infection remains unclear. Our results indicated that FAdV-4 infection in chickens induces damage to kidney tissues, characterized by the degeneration and necrosis of kidney epithelial cells, glomerular injury, endoplasmic reticulum stress, and the activation of a robust inflammatory response in the kidney cells. Notably, autophagosome-like vesicles enclosed clusters of viral particles that were transmitted between kidney cells post-infection. There might be a novel mechanism of vesicle-mediated cell-to-cell transmission of hypervirulent FAdV-4 that hijacks autophagosome-like vesicles. We also investigated cellular autophagy in kidney cells in vivo and in vitro during early FAdV-4 infection. The autophagy-related marker proteins LC3B, ATG5, and BECN1 were upregulated post-infection, whereas SQSTM1 was downregulated, indicating that FAdV-4 infection enhances autophagic flux and induces complete autophagy. The viral structural protein Fiber 2 was also observed to colocalize with the autophagy-related marker protein LC3B and the exosome-specific marker protein CD63 in the kidney cells at 24 hpi, suggesting that FAdV-4-induced cellular autophagy promotes viral replication in kidney cells and that autophagosome-like vesicles are involved in early FAdV-4 replication in vivo in chickens. Our results offer novel insights into the pathogenesis of hypervirulent FAdV-4 from the perspective of kidney injury post-infection.Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has emerged as a significant poultry pathogen since 2015, exhibiting clinical multi-organ and multi-tissue tropism post-infection, resulting in substantial economic losses in the poultry industry. However, the molecular mechanism underlying kidney injury caused by FAdV-4 infection remains unclear. Our results indicated that FAdV-4 infection in chickens induces damage to kidney tissues, characterized by the degeneration and necrosis of kidney epithelial cells, glomerular injury, endoplasmic reticulum stress, and the activation of a robust inflammatory response in the kidney cells. Notably, autophagosome-like vesicles enclosed clusters of viral particles that were transmitted between kidney cells post-infection. There might be a novel mechanism of vesicle-mediated cell-to-cell transmission of hypervirulent FAdV-4 that hijacks autophagosome-like vesicles. We also investigated cellular autophagy in kidney cells in vivo and in vitro during early FAdV-4 infection. The autophagy-related marker proteins LC3B, ATG5, and BECN1 were upregulated post-infection, whereas SQSTM1 was downregulated, indicating that FAdV-4 infection enhances autophagic flux and induces complete autophagy. The viral structural protein Fiber 2 was also observed to colocalize with the autophagy-related marker protein LC3B and the exosome-specific marker protein CD63 in the kidney cells at 24 hpi, suggesting that FAdV-4-induced cellular autophagy promotes viral replication in kidney cells and that autophagosome-like vesicles are involved in early FAdV-4 replication in vivo in chickens. Our results offer novel insights into the pathogenesis of hypervirulent FAdV-4 from the perspective of kidney injury post-infection.Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has become globally prevalent since 2015 as a predominant pathogen on poultry farms, leading to substantial economic losses for the poultry industry. However, the molecular mechanisms underlying kidney injury induced by FAdV-4 infection remain unclear. In this study, we primarily elucidated the mechanisms of kidney injury induced by FAdV-4 infection in chickens, utilizing both in vitro and in vivo models. Our results demonstrate that FAdV-4 infection in chickens causes degeneration and necrosis of kidney epithelial cells, glomerular injury, and expansion of the endoplasmic reticulum, while also triggering a robust inflammatory response in kidney cells. Notably, we observed the cell-to-cell transmission of virus particles delivered by autophagosome-like vesicles, and the viral infection-induced cellular autophagy facilitated viral replication in the kidney cells. These findings offer a novel perspective to understand the molecular mechanisms of FAdV-4-induced kidney injury and establish a basis for further investigation into the molecular pathogenesis of hypervirulent FAdV-4.IMPORTANCEHypervirulent fowl adenovirus serotype 4 (FAdV-4) has become globally prevalent since 2015 as a predominant pathogen on poultry farms, leading to substantial economic losses for the poultry industry. However, the molecular mechanisms underlying kidney injury induced by FAdV-4 infection remain unclear. In this study, we primarily elucidated the mechanisms of kidney injury induced by FAdV-4 infection in chickens, utilizing both in vitro and in vivo models. Our results demonstrate that FAdV-4 infection in chickens causes degeneration and necrosis of kidney epithelial cells, glomerular injury, and expansion of the endoplasmic reticulum, while also triggering a robust inflammatory response in kidney cells. Notably, we observed the cell-to-cell transmission of virus particles delivered by autophagosome-like vesicles, and the viral infection-induced cellular autophagy facilitated viral replication in the kidney cells. These findings offer a novel perspective to understand the molecular mechanisms of FAdV-4-induced kidney injury and establish a basis for further investigation into the molecular pathogenesis of hypervirulent FAdV-4. Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has emerged as a significant poultry pathogen since 2015, exhibiting clinical multi-organ and multi-tissue tropism post-infection, resulting in substantial economic losses in the poultry industry. However, the molecular mechanism underlying kidney injury caused by FAdV-4 infection remains unclear. Our results indicated that FAdV-4 infection in chickens induces damage to kidney tissues, characterized by the degeneration and necrosis of kidney epithelial cells, glomerular injury, endoplasmic reticulum stress, and the activation of a robust inflammatory response in the kidney cells. Notably, autophagosome-like vesicles enclosed clusters of viral particles that were transmitted between kidney cells post-infection. There might be a novel mechanism of vesicle-mediated cell-to-cell transmission of hypervirulent FAdV-4 that hijacks autophagosome-like vesicles. We also investigated cellular autophagy in kidney cells in vivo and in vitro during early FAdV-4 infection. The autophagy-related marker proteins LC3B, ATG5, and BECN1 were upregulated post-infection, whereas SQSTM1 was downregulated, indicating that FAdV-4 infection enhances autophagic flux and induces complete autophagy. The viral structural protein Fiber 2 was also observed to colocalize with the autophagy-related marker protein LC3B and the exosome-specific marker protein CD63 in the kidney cells at 24 hpi, suggesting that FAdV-4-induced cellular autophagy promotes viral replication in kidney cells and that autophagosome-like vesicles are involved in early FAdV-4 replication in vivo in chickens. Our results offer novel insights into the pathogenesis of hypervirulent FAdV-4 from the perspective of kidney injury post-infection. Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has emerged as a significant poultry pathogen since 2015, exhibiting clinical multi-organ and multi-tissue tropism post-infection, resulting in substantial economic losses in the poultry industry. However, the molecular mechanism underlying kidney injury caused by FAdV-4 infection remains unclear. Our results indicated that FAdV-4 infection in chickens induces damage to kidney tissues, characterized by the degeneration and necrosis of kidney epithelial cells, glomerular injury, endoplasmic reticulum stress, and the activation of a robust inflammatory response in the kidney cells. Notably, autophagosome-like vesicles enclosed clusters of viral particles that were transmitted between kidney cells post-infection. There might be a novel mechanism of vesicle-mediated cell-to-cell transmission of hypervirulent FAdV-4 that hijacks autophagosome-like vesicles. We also investigated cellular autophagy in kidney cells in vivo and in vitro during early FAdV-4 infection. The autophagy-related marker proteins LC3B, ATG5, and BECN1 were upregulated post-infection, whereas SQSTM1 was downregulated, indicating that FAdV-4 infection enhances autophagic flux and induces complete autophagy. The viral structural protein Fiber 2 was also observed to colocalize with the autophagy-related marker protein LC3B and the exosome-specific marker protein CD63 in the kidney cells at 24 hpi, suggesting that FAdV-4-induced cellular autophagy promotes viral replication in kidney cells and that autophagosome-like vesicles are involved in early FAdV-4 replication in vivo in chickens. Our results offer novel insights into the pathogenesis of hypervirulent FAdV-4 from the perspective of kidney injury post-infection.IMPORTANCEHypervirulent fowl adenovirus serotype 4 (FAdV-4) has become globally prevalent since 2015 as a predominant pathogen on poultry farms, leading to substantial economic losses for the poultry industry. However, the molecular mechanisms underlying kidney injury induced by FAdV-4 infection remain unclear. In this study, we primarily elucidated the mechanisms of kidney injury induced by FAdV-4 infection in chickens, utilizing both in vitro and in vivo models. Our results demonstrate that FAdV-4 infection in chickens causes degeneration and necrosis of kidney epithelial cells, glomerular injury, and expansion of the endoplasmic reticulum, while also triggering a robust inflammatory response in kidney cells. Notably, we observed the cell-to-cell transmission of virus particles delivered by autophagosome-like vesicles, and the viral infection-induced cellular autophagy facilitated viral replication in the kidney cells. These findings offer a novel perspective to understand the molecular mechanisms of FAdV-4-induced kidney injury and establish a basis for further investigation into the molecular pathogenesis of hypervirulent FAdV-4. Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has emerged as a significant poultry pathogen since 2015, exhibiting clinical multi-organ and multi-tissue tropism post-infection, resulting in substantial economic losses in the poultry industry. However, the molecular mechanism underlying kidney injury caused by FAdV-4 infection remains unclear. Our results indicated that FAdV-4 infection in chickens induces damage to kidney tissues, characterized by the degeneration and necrosis of kidney epithelial cells, glomerular injury, endoplasmic reticulum stress, and the activation of a robust inflammatory response in the kidney cells. Notably, autophagosome-like vesicles enclosed clusters of viral particles that were transmitted between kidney cells post-infection. There might be a novel mechanism of vesicle-mediated cell-to-cell transmission of hypervirulent FAdV-4 that hijacks autophagosome-like vesicles. We also investigated cellular autophagy in kidney cells and during early FAdV-4 infection. The autophagy-related marker proteins LC3B, ATG5, and BECN1 were upregulated post-infection, whereas SQSTM1 was downregulated, indicating that FAdV-4 infection enhances autophagic flux and induces complete autophagy. The viral structural protein Fiber 2 was also observed to colocalize with the autophagy-related marker protein LC3B and the exosome-specific marker protein CD63 in the kidney cells at 24 hpi, suggesting that FAdV-4-induced cellular autophagy promotes viral replication in kidney cells and that autophagosome-like vesicles are involved in early FAdV-4 replication in chickens. Our results offer novel insights into the pathogenesis of hypervirulent FAdV-4 from the perspective of kidney injury post-infection. Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has become globally prevalent since 2015 as a predominant pathogen on poultry farms, leading to substantial economic losses for the poultry industry. However, the molecular mechanisms underlying kidney injury induced by FAdV-4 infection remain unclear. In this study, we primarily elucidated the mechanisms of kidney injury induced by FAdV-4 infection in chickens, utilizing both and models. Our results demonstrate that FAdV-4 infection in chickens causes degeneration and necrosis of kidney epithelial cells, glomerular injury, and expansion of the endoplasmic reticulum, while also triggering a robust inflammatory response in kidney cells. Notably, we observed the cell-to-cell transmission of virus particles delivered by autophagosome-like vesicles, and the viral infection-induced cellular autophagy facilitated viral replication in the kidney cells. These findings offer a novel perspective to understand the molecular mechanisms of FAdV-4-induced kidney injury and establish a basis for further investigation into the molecular pathogenesis of hypervirulent FAdV-4. ABSTRACT Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has emerged as a significant poultry pathogen since 2015, exhibiting clinical multi-organ and multi-tissue tropism post-infection, resulting in substantial economic losses in the poultry industry. However, the molecular mechanism underlying kidney injury caused by FAdV-4 infection remains unclear. Our results indicated that FAdV-4 infection in chickens induces damage to kidney tissues, characterized by the degeneration and necrosis of kidney epithelial cells, glomerular injury, endoplasmic reticulum stress, and the activation of a robust inflammatory response in the kidney cells. Notably, autophagosome-like vesicles enclosed clusters of viral particles that were transmitted between kidney cells post-infection. There might be a novel mechanism of vesicle-mediated cell-to-cell transmission of hypervirulent FAdV-4 that hijacks autophagosome-like vesicles. We also investigated cellular autophagy in kidney cells in vivo and in vitro during early FAdV-4 infection. The autophagy-related marker proteins LC3B, ATG5, and BECN1 were upregulated post-infection, whereas SQSTM1 was downregulated, indicating that FAdV-4 infection enhances autophagic flux and induces complete autophagy. The viral structural protein Fiber 2 was also observed to colocalize with the autophagy-related marker protein LC3B and the exosome-specific marker protein CD63 in the kidney cells at 24 hpi, suggesting that FAdV-4-induced cellular autophagy promotes viral replication in kidney cells and that autophagosome-like vesicles are involved in early FAdV-4 replication in vivo in chickens. Our results offer novel insights into the pathogenesis of hypervirulent FAdV-4 from the perspective of kidney injury post-infection.IMPORTANCEHypervirulent fowl adenovirus serotype 4 (FAdV-4) has become globally prevalent since 2015 as a predominant pathogen on poultry farms, leading to substantial economic losses for the poultry industry. However, the molecular mechanisms underlying kidney injury induced by FAdV-4 infection remain unclear. In this study, we primarily elucidated the mechanisms of kidney injury induced by FAdV-4 infection in chickens, utilizing both in vitro and in vivo models. Our results demonstrate that FAdV-4 infection in chickens causes degeneration and necrosis of kidney epithelial cells, glomerular injury, and expansion of the endoplasmic reticulum, while also triggering a robust inflammatory response in kidney cells. Notably, we observed the cell-to-cell transmission of virus particles delivered by autophagosome-like vesicles, and the viral infection-induced cellular autophagy facilitated viral replication in the kidney cells. These findings offer a novel perspective to understand the molecular mechanisms of FAdV-4-induced kidney injury and establish a basis for further investigation into the molecular pathogenesis of hypervirulent FAdV-4. |
| Author | Chen, Cuiteng Wang, Ziyue Liu, Xiaodong Zhou, Jiayu Chen, Zhen Yang, Pei Huang, Yu Wan, Chunhe Zhu, Chunhua Fu, Guanghua |
| Author_xml | – sequence: 1 givenname: Chunhua orcidid: 0000-0001-7148-4311 surname: Zhu fullname: Zhu, Chunhua – sequence: 2 givenname: Jiayu surname: Zhou fullname: Zhou, Jiayu – sequence: 3 givenname: Zhen surname: Chen fullname: Chen, Zhen – sequence: 4 givenname: Cuiteng surname: Chen fullname: Chen, Cuiteng – sequence: 5 givenname: Ziyue surname: Wang fullname: Wang, Ziyue – sequence: 6 givenname: Pei surname: Yang fullname: Yang, Pei – sequence: 7 givenname: Guanghua surname: Fu fullname: Fu, Guanghua – sequence: 8 givenname: Xiaodong orcidid: 0000-0002-9802-4232 surname: Liu fullname: Liu, Xiaodong – sequence: 9 givenname: Yu surname: Huang fullname: Huang, Yu – sequence: 10 givenname: Chunhe orcidid: 0000-0003-2011-5609 surname: Wan fullname: Wan, Chunhe |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40130861$$D View this record in MEDLINE/PubMed |
| BookMark | eNp1kUtv1DAUhS1UREvpD2CDvGSTwc_EWSFU8ahUxAbWlu3cTDyT2IOdtJp_j2emrdoFq3t9_fnoHp-36CzEAAi9p2RFKVOf8g7cnJZpRQiRqmLyFbpgtJYVEW1z9qw_R1c5bwpFKZFMsjfoXBDKiarpBdr-BDeY4PPsHfYh-_Uw59LMEc8D4K3vAuzLebOkQ8Fu8G4L4YB0i4MO2z0e9jtIdz4tI4QZ9_F-xKaDEA-jjDOkOBcCi3fodW_GDFcP9RL9-fb19_WP6vbX95vrL7eVEbKdK15Da5vamppbIxrWcys5MeBkqySX3EkBYDrTAwNiHGe1reumKXZcb6Gp-SW6Oel20Wz0LvnJpL2OxuvjIKa1Nqn4HUGzzikqiGG0MYIo1RIgjAOVjgAHYYvW55PWbrETdK44TGZ8IfryJvhBr-OdpoxIQY_bfHxQSPHvAnnWk88OxtEEiEvWnCrSKtWItqCrE2ryxPQmLimUf9KU6EPi-jFxfUxcM1kefHi-3dNaj_kWgJ4Al2LOCfon5P-i_wBoMr34 |
| Cites_doi | 10.1128/JVI.01592-10 10.1128/jvi.00284-23 10.3389/fcell.2021.738932 10.1128/JVI.00787-15 10.1128/spectrum.01493-22 10.4161/auto.26843 10.1128/JVI.01938-20 10.1146/annurev-physiol-021119-034658 10.1038/emi.2016.50 10.1080/03079457.2021.1872766 10.1016/j.vetmic.2023.109660 10.1016/j.meegid.2022.105277 10.1038/nrm.2017.125 10.4161/auto.23465 10.1016/j.immuni.2022.06.007 10.1016/j.chom.2017.06.005 10.1016/j.molcel.2010.09.023 10.1128/JVI.01850-18 10.1128/JVI.01255-20 10.3382/ps/pez042 10.3389/fmicb.2018.01091 10.1080/15548627.2015.1017184 10.1007/s00705-022-05390-1 10.3390/biom10010100 10.1128/jvi.01957-21 10.1038/cdd.2009.33 10.1186/s13567-021-00907-z 10.1038/nrm2245 10.1038/nature12029 10.1038/s41579-018-0003-6 10.1016/j.ijbiomac.2020.01.015 10.1016/j.psj.2024.103831 10.1128/jvi.00181-24 10.1016/j.vetmic.2018.07.014 10.3390/cells9092101 10.1038/emi.2016.115 10.1016/j.cell.2015.01.032 10.1016/j.vetmic.2022.109617 10.1016/j.psj.2019.12.059 10.1016/j.mib.2016.05.004 10.1016/j.vetmic.2022.109388 10.1177/10406387211019962 10.1371/journal.pone.0077601 10.1371/journal.ppat.1011201 10.1136/vr.128.25.591 |
| ContentType | Journal Article |
| Copyright | Copyright © 2025 Zhu et al. Copyright © 2025 Zhu et al. 2025 Zhu et al. |
| Copyright_xml | – notice: Copyright © 2025 Zhu et al. – notice: Copyright © 2025 Zhu et al. 2025 Zhu et al. |
| DBID | AAYXX CITATION NPM 7X8 5PM DOA |
| DOI | 10.1128/spectrum.00058-25 |
| DatabaseName | CrossRef PubMed MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Open Access Full Text |
| DatabaseTitle | CrossRef PubMed MEDLINE - Academic |
| DatabaseTitleList | CrossRef MEDLINE - Academic PubMed |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 2165-0497 |
| Editor | Rajao, Daniela S. |
| Editor_xml | – sequence: 1 givenname: Daniela S. surname: Rajao fullname: Rajao, Daniela S. |
| ExternalDocumentID | oai_doaj_org_article_2dc8140a217a408890e023e15c0e3e4b PMC12054176 spectrum00058-25 40130861 10_1128_spectrum_00058_25 |
| Genre | Journal Article |
| GrantInformation_xml | – fundername: Fujian Provincial Department of Science and Technology grantid: 2022R1026005 funderid: http://dx.doi.org/10.13039/501100005270 – fundername: Fujian Academy of Agricultural Sciences grantid: YCZX202412 funderid: http://dx.doi.org/10.13039/501100018914 – fundername: Fujian Academy of Agricultural Sciences grantid: CXTD2021005-1 funderid: http://dx.doi.org/10.13039/501100018914 – fundername: Fujian Academy of Agricultural Sciences grantid: KJZD2025002 funderid: http://dx.doi.org/10.13039/501100018914 – fundername: Fujian Provincial Department of Science and Technology grantid: 2022J01466 funderid: http://dx.doi.org/10.13039/501100005270 – fundername: ; grantid: 2022R1026005 – fundername: ; grantid: YCZX202412 – fundername: ; grantid: CXTD2021005-1 – fundername: ; grantid: KJZD2025002 – fundername: ; grantid: 2022J01466 |
| GroupedDBID | 53G AAGFI AAUOK AAYXX ADBBV AGVNZ ALMA_UNASSIGNED_HOLDINGS CITATION EJD FF~ FRP GROUPED_DOAJ H13 M~E OK1 RPM RSF NPM 7X8 5PM |
| ID | FETCH-LOGICAL-a459t-36e9b76ba63ba472f3b530aec5985353c54eeadafe2e0ac326b6677861cfbe763 |
| IEDL.DBID | AAUOK |
| ISSN | 2165-0497 |
| IngestDate | Wed Aug 27 01:25:49 EDT 2025 Thu Aug 21 18:27:30 EDT 2025 Thu Jul 10 18:12:07 EDT 2025 Wed May 07 06:04:22 EDT 2025 Fri May 09 01:30:26 EDT 2025 Tue Jul 01 05:10:16 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 5 |
| Keywords | autophagosome-like vesicles' delivery kidney injury inflammation hypervirulent fowl adenovirus serotype 4 |
| Language | English |
| License | This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license. https://creativecommons.org/licenses/by/4.0 This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-a459t-36e9b76ba63ba472f3b530aec5985353c54eeadafe2e0ac326b6677861cfbe763 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 The authors declare no conflict of interest. |
| ORCID | 0000-0003-2011-5609 0000-0001-7148-4311 0000-0002-9802-4232 |
| OpenAccessLink | https://journals.asm.org/doi/10.1128/spectrum.00058-25 |
| PMID | 40130861 |
| PQID | 3180988749 |
| PQPubID | 23479 |
| PageCount | 16 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_2dc8140a217a408890e023e15c0e3e4b pubmedcentral_primary_oai_pubmedcentral_nih_gov_12054176 proquest_miscellaneous_3180988749 asm2_journals_10_1128_spectrum_00058_25 pubmed_primary_40130861 crossref_primary_10_1128_spectrum_00058_25 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 20250325 |
| PublicationDateYYYYMMDD | 2025-03-25 |
| PublicationDate_xml | – month: 3 year: 2025 text: 20250325 day: 25 |
| PublicationDecade | 2020 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: 1752 N St., N.W., Washington, DC |
| PublicationTitle | Microbiology spectrum |
| PublicationTitleAbbrev | Spectrum |
| PublicationTitleAlternate | Microbiol Spectr |
| PublicationYear | 2025 |
| Publisher | American Society for Microbiology |
| Publisher_xml | – name: American Society for Microbiology |
| References | e_1_3_3_17_2 e_1_3_3_16_2 e_1_3_3_19_2 e_1_3_3_38_2 e_1_3_3_18_2 e_1_3_3_39_2 e_1_3_3_13_2 e_1_3_3_36_2 e_1_3_3_12_2 e_1_3_3_37_2 e_1_3_3_15_2 e_1_3_3_34_2 e_1_3_3_14_2 e_1_3_3_35_2 e_1_3_3_32_2 e_1_3_3_33_2 e_1_3_3_11_2 e_1_3_3_30_2 e_1_3_3_10_2 e_1_3_3_31_2 e_1_3_3_40_2 e_1_3_3_6_2 e_1_3_3_5_2 e_1_3_3_8_2 e_1_3_3_7_2 e_1_3_3_28_2 e_1_3_3_9_2 e_1_3_3_27_2 e_1_3_3_29_2 e_1_3_3_24_2 e_1_3_3_23_2 e_1_3_3_26_2 e_1_3_3_45_2 e_1_3_3_25_2 e_1_3_3_46_2 e_1_3_3_2_2 e_1_3_3_20_2 e_1_3_3_43_2 e_1_3_3_44_2 e_1_3_3_4_2 e_1_3_3_22_2 e_1_3_3_41_2 e_1_3_3_3_2 e_1_3_3_21_2 e_1_3_3_42_2 Sun, M, Yu, S, Ge, H, Wang, T, Li, Y, Zhou, P, Pan, L, Han, Y, Yang, Y, Sun, Y, Li, S, Li, LF, Qiu, HJ (B32) 2022; 96 Afzal, M, Muneer, R, Stein, G (B1) 1991; 128 Shi, D, Zhou, L, Shi, H, Zhang, J, Zhang, J, Zhang, L, Liu, D, Feng, T, Zeng, M, Chen, J, Zhang, X, Xue, M, Jing, Z, Liu, J, Ji, Z, He, H, Guo, L, Wu, Y, Ma, J, Feng, L (B31) 2023; 19 Li, Y, Hu, B, Ji, G, Zhang, Y, Xu, C, Lei, J, Ding, C, Zhou, J (B34) 2020; 94 Wang, X, Qi, X, Yang, B, Chen, S, Wang, J (B20) 2018; 9 Maier, HJ, Cottam, EM, Stevenson-Leggett, P, Wilkinson, JA, Harte, CJ, Wileman, T, Britton, P (B36) 2013; 9 Zhu, C, Zhou, J, Chen, Z, Chen, C, Yang, P, Wang, Z, Fu, G, Wan, C, Huang, Y (B11) 2024; 103 Brimacombe, CL, Grove, J, Meredith, LW, Hu, K, Syder, AJ, Flores, MV, Timpe, JM, Krieger, SE, Baumert, TF, Tellinghuisen, TL, Wong-Staal, F, Balfe, P, McKeating, JA (B42) 2011; 85 Wang, S, Zhang, K, Yao, Y, Li, J (B25) 2021; 9 Mase, M, Tanaka, Y, Iseki, H, Watanabe, S (B3) 2022; 167 Feng, Z, Hensley, L, McKnight, KL, Hu, F, Madden, V, Ping, L, Jeong, SH, Walker, C, Lanford, RE, Lemon, SM (B40) 2013; 496 Kroemer, G, Mariño, G, Levine, B (B17) 2010; 40 Choi, Y, Bowman, JW, Jung, JU (B19) 2018; 16 Wang, S, Xu, Z, Liu, Y, Yu, M, Zhang, T, Liu, P, Qi, X, Chen, Y, Meng, L, Guo, R, Zhang, L, Fan, W, Gao, L, Duan, Y, Zhang, Y, Cui, H, Gao, Y (B35) 2024; 98 He, Q, Lu, S, Lin, Y, Xu, L, Chen, Z, Wang, Q (B43) 2023; 278 van Niel, G, D’Angelo, G, Raposo, G (B38) 2018; 19 Metz, P, Chiramel, A, Chatel-Chaix, L, Alvisi, G, Bankhead, P, Mora-Rodriguez, R, Long, G, Hamacher-Brady, A, Brady, NR, Bartenschlager, R (B18) 2015; 89 Lin, Y, Zhao, Z, Huang, A, Lu, M (B30) 2020; 9 Niu, D, Feng, J, Duan, B, Shi, Q, Li, Y, Chen, Z, Ma, L, Liu, H, Wang, Y (B9) 2022; 101 Niu, Y, Sun, Q, Zhang, G, Liu, X, Shang, Y, Xiao, Y, Liu, S (B12) 2018; 223 Xian, H, Watari, K, Sanchez-Lopez, E, Offenberger, J, Onyuru, J, Sampath, H, Ying, W, Hoffman, HM, Shadel, GS, Karin, M (B44) 2022; 55 Wang, J, Ba, G, Han, YQ, Ming, SL, Wang, MD, Fu, PF, Zhao, QQ, Zhang, S, Wu, YN, Yang, GY, Chu, BB (B14) 2020; 146 Biering, SB, Choi, J, Halstrom, RA, Brown, HM, Beatty, WL, Lee, S, McCune, BT, Dominici, E, Williams, LE, Orchard, RC, Wilen, CB, Yamamoto, M, Coers, J, Taylor, GA, Hwang, S (B28) 2017; 22 Pei, J, Zhao, M, Ye, Z, Gou, H, Wang, J, Yi, L, Dong, X, Liu, W, Luo, Y, Liao, M, Chen, J (B33) 2014; 10 Grgić, H, Poljak, Z, Sharif, S, Nagy, É (B8) 2013; 8 Xie, Q, Cao, S, Zhang, W, Wang, W, Li, L, Kan, Q, Fu, H, Geng, T, Li, T, Wan, Z, Gao, W, Shao, H, Qin, A, Ye, J (B15) 2021; 52 Klionsky, DJ (B29) 2007; 8 Wang, T, Wang, C, Han, J, Hou, X, Hu, R, Chang, W, Wang, L, Qi, X, Wang, J (B22) 2023; 276 Kaushal, GP, Chandrashekar, K, Juncos, LA, Shah, SV (B26) 2020; 10 Chen, YH, Du, W, Hagemeijer, MC, Takvorian, PM, Pau, C, Cali, A, Brantner, CA, Stempinski, ES, Connelly, PS, Ma, HC, Jiang, P, Wimmer, E, Altan-Bonnet, G, Altan-Bonnet, N (B39) 2015; 160 Mete, A, Armien, AG, Rejmanek, D, Mott, M, Crossley, BM (B6) 2021; 33 Wang, B, Song, C, Yang, P, Song, M, Zhao, S, Qiao, Q, Wang, Z, Zhao, J (B13) 2022; 10 Choi, ME (B27) 2020; 82 Del Valle, FP, Camba, SI, Umali, DV, Sasai, K, Shirota, K, Katoh, H, Tajima, T (B2) 2020; 99 Altan-Bonnet, N (B41) 2016; 32 Yuan, F, Hou, L, Wei, L, Quan, R, Wang, J, Liu, H, Liu, J (B16) 2021; 95 Liu, Y, Wan, W, Gao, D, Li, Y, Yang, X, Liu, H, Yao, H, Chen, L, Wang, C, Zhao, J (B4) 2016; 5 Ye, J, Liang, G, Zhang, J, Wang, W, Song, N, Wang, P, Zheng, W, Xie, Q, Shao, H, Wan, Z, Wang, C, Chen, H, Gao, W, Qin, A (B5) 2016; 5 Hu, B, Zhang, Y, Jia, L, Wu, H, Fan, C, Sun, Y, Ye, C, Liao, M, Zhou, J (B24) 2015; 11 Ma, H, Ding, Y, Du, K, Chang, K, Niu, Y (B21) 2022; 269 Ren, G, Wang, H, Yan, Y, Liu, F, Huang, M, Chen, R (B10) 2019; 98 Li, W, You, G, Haiyilati, A, Wang, H, Jiao, H, Wang, Y, Gao, L, Cao, H, Li, X, Zheng, SJ (B23) 2023; 97 Dogrammatzis, C, Deschamps, T, Kalamvoki, M (B37) 2019; 93 Eisenberg-Lerner, A, Bialik, S, Simon, HU, Kimchi, A (B45) 2009; 16 Lai, VD, Min, K, Lai, HTL, Mo, J (B7) 2021; 50 |
| References_xml | – ident: e_1_3_3_43_2 doi: 10.1128/JVI.01592-10 – ident: e_1_3_3_24_2 doi: 10.1128/jvi.00284-23 – ident: e_1_3_3_26_2 doi: 10.3389/fcell.2021.738932 – ident: e_1_3_3_19_2 doi: 10.1128/JVI.00787-15 – ident: e_1_3_3_14_2 doi: 10.1128/spectrum.01493-22 – ident: e_1_3_3_34_2 doi: 10.4161/auto.26843 – ident: e_1_3_3_17_2 doi: 10.1128/JVI.01938-20 – ident: e_1_3_3_28_2 doi: 10.1146/annurev-physiol-021119-034658 – ident: e_1_3_3_6_2 doi: 10.1038/emi.2016.50 – ident: e_1_3_3_8_2 doi: 10.1080/03079457.2021.1872766 – ident: e_1_3_3_44_2 doi: 10.1016/j.vetmic.2023.109660 – ident: e_1_3_3_10_2 doi: 10.1016/j.meegid.2022.105277 – ident: e_1_3_3_39_2 doi: 10.1038/nrm.2017.125 – ident: e_1_3_3_37_2 doi: 10.4161/auto.23465 – ident: e_1_3_3_45_2 doi: 10.1016/j.immuni.2022.06.007 – ident: e_1_3_3_29_2 doi: 10.1016/j.chom.2017.06.005 – ident: e_1_3_3_18_2 doi: 10.1016/j.molcel.2010.09.023 – ident: e_1_3_3_38_2 doi: 10.1128/JVI.01850-18 – ident: e_1_3_3_35_2 doi: 10.1128/JVI.01255-20 – ident: e_1_3_3_11_2 doi: 10.3382/ps/pez042 – ident: e_1_3_3_21_2 doi: 10.3389/fmicb.2018.01091 – ident: e_1_3_3_25_2 doi: 10.1080/15548627.2015.1017184 – ident: e_1_3_3_4_2 doi: 10.1007/s00705-022-05390-1 – ident: e_1_3_3_27_2 doi: 10.3390/biom10010100 – ident: e_1_3_3_33_2 doi: 10.1128/jvi.01957-21 – ident: e_1_3_3_46_2 doi: 10.1038/cdd.2009.33 – ident: e_1_3_3_16_2 doi: 10.1186/s13567-021-00907-z – ident: e_1_3_3_30_2 doi: 10.1038/nrm2245 – ident: e_1_3_3_41_2 doi: 10.1038/nature12029 – ident: e_1_3_3_20_2 doi: 10.1038/s41579-018-0003-6 – ident: e_1_3_3_15_2 doi: 10.1016/j.ijbiomac.2020.01.015 – ident: e_1_3_3_12_2 doi: 10.1016/j.psj.2024.103831 – ident: e_1_3_3_36_2 doi: 10.1128/jvi.00181-24 – ident: e_1_3_3_13_2 doi: 10.1016/j.vetmic.2018.07.014 – ident: e_1_3_3_31_2 doi: 10.3390/cells9092101 – ident: e_1_3_3_5_2 doi: 10.1038/emi.2016.115 – ident: e_1_3_3_40_2 doi: 10.1016/j.cell.2015.01.032 – ident: e_1_3_3_23_2 doi: 10.1016/j.vetmic.2022.109617 – ident: e_1_3_3_3_2 doi: 10.1016/j.psj.2019.12.059 – ident: e_1_3_3_42_2 doi: 10.1016/j.mib.2016.05.004 – ident: e_1_3_3_22_2 doi: 10.1016/j.vetmic.2022.109388 – ident: e_1_3_3_7_2 doi: 10.1177/10406387211019962 – ident: e_1_3_3_9_2 doi: 10.1371/journal.pone.0077601 – ident: e_1_3_3_32_2 doi: 10.1371/journal.ppat.1011201 – ident: e_1_3_3_2_2 doi: 10.1136/vr.128.25.591 – volume: 8 start-page: 931 year: 2007 end-page: 937 ident: B29 article-title: Autophagy: from phenomenology to molecular understanding in less than a decade publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm2245 – volume: 99 start-page: 2459 year: 2020 end-page: 2468 ident: B2 article-title: Research Note: molecular and pathologic characterization of avian adenovirus isolated from the oviducts of laying hens in eastern Japan publication-title: Poult Sci doi: 10.1016/j.psj.2019.12.059 – volume: 93 year: 2019 ident: B37 article-title: Biogenesis of extracellular vesicles during herpes simplex virus 1 infection: role of the CD63 tetraspanin publication-title: J Virol doi: 10.1128/JVI.01850-18 – volume: 223 start-page: 34 year: 2018 end-page: 41 ident: B12 article-title: Fowl adenovirus serotype 4-induced apoptosis, autophagy, and a severe inflammatory response in liver publication-title: Vet Microbiol doi: 10.1016/j.vetmic.2018.07.014 – volume: 82 start-page: 297 year: 2020 end-page: 322 ident: B27 article-title: Autophagy in kidney disease publication-title: Annu Rev Physiol doi: 10.1146/annurev-physiol-021119-034658 – volume: 95 year: 2021 ident: B16 article-title: Fowl adenovirus serotype 4 induces hepatic steatosis via activation of liver X receptor-α publication-title: J Virol doi: 10.1128/JVI.01938-20 – volume: 167 start-page: 1191 year: 2022 end-page: 1195 ident: B3 article-title: Genomic characterization of a fowl adenovirus serotype 4 strain isolated from a chicken with hydropericardium syndrome in Japan publication-title: Arch Virol doi: 10.1007/s00705-022-05390-1 – volume: 8 year: 2013 ident: B8 article-title: Pathogenicity and cytokine gene expression pattern of a serotype 4 fowl adenovirus isolate publication-title: PLoS One doi: 10.1371/journal.pone.0077601 – volume: 101 start-page: 105277 year: 2022 ident: B9 article-title: Epidemiological survey of avian adenovirus in China from 2015 to 2021 and the genetic variability of highly pathogenic Fadv-4 isolates publication-title: Infect Genet Evol doi: 10.1016/j.meegid.2022.105277 – volume: 9 year: 2021 ident: B25 article-title: Autophagy and mitochondrial homeostasis during infection: a double-edged sword publication-title: Front Cell Dev Biol doi: 10.3389/fcell.2021.738932 – volume: 19 start-page: 213 year: 2018 end-page: 228 ident: B38 article-title: Shedding light on the cell biology of extracellular vesicles publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm.2017.125 – volume: 89 start-page: 8026 year: 2015 end-page: 8041 ident: B18 article-title: Dengue virus inhibition of autophagic flux and dependency of viral replication on proteasomal degradation of the autophagy receptor p62 publication-title: J Virol doi: 10.1128/JVI.00787-15 – volume: 16 start-page: 341 year: 2018 end-page: 354 ident: B19 article-title: Autophagy during viral infection — a double-edged sword publication-title: Nat Rev Microbiol doi: 10.1038/s41579-018-0003-6 – volume: 32 start-page: 77 year: 2016 end-page: 81 ident: B41 article-title: Extracellular vesicles are the Trojan horses of viral infection publication-title: Curr Opin Microbiol doi: 10.1016/j.mib.2016.05.004 – volume: 52 year: 2021 ident: B15 article-title: A novel fiber-2-edited live attenuated vaccine candidate against the highly pathogenic serotype 4 fowl adenovirus publication-title: Vet Res doi: 10.1186/s13567-021-00907-z – volume: 22 start-page: 74 year: 2017 end-page: 85 ident: B28 article-title: Viral replication complexes are targeted by LC3-guided interferon-inducible GTpases publication-title: Cell Host Microbe doi: 10.1016/j.chom.2017.06.005 – volume: 85 start-page: 596 year: 2011 end-page: 605 ident: B42 article-title: Neutralizing antibody-resistant hepatitis C virus cell-to-cell transmission publication-title: J Virol doi: 10.1128/JVI.01592-10 – volume: 276 start-page: 109617 year: 2023 ident: B22 article-title: β-catenin facilitates fowl adenovirus serotype 4 replication through enhancing virus-induced autophagy publication-title: Vet Microbiol doi: 10.1016/j.vetmic.2022.109617 – volume: 10 start-page: 93 year: 2014 end-page: 110 ident: B33 article-title: Autophagy enhances the replication of classical swine fever virus in vitro publication-title: Autophagy doi: 10.4161/auto.26843 – volume: 98 year: 2024 ident: B35 article-title: OASL suppresses infectious bursal disease virus replication by targeting VP2 for degrading through the autophagy pathway publication-title: J Virol doi: 10.1128/jvi.00181-24 – volume: 128 start-page: 591 year: 1991 end-page: 593 ident: B1 article-title: Studies on the aetiology of hydropericardium syndrome (Angara disease) in broilers publication-title: Vet Rec doi: 10.1136/vr.128.25.591 – volume: 103 year: 2024 ident: B11 article-title: Hypervirulent fowl adenovirus serotype 4 elicits early innate immune response and promotes virus-induced cellular autophagy in the spleen publication-title: Poult Sci doi: 10.1016/j.psj.2024.103831 – volume: 5 year: 2016 ident: B4 article-title: Genetic characterization of novel fowl aviadenovirus 4 isolates from outbreaks of hepatitis-hydropericardium syndrome in broiler chickens in China publication-title: Emerg Microbes Infect doi: 10.1038/emi.2016.115 – volume: 19 year: 2023 ident: B31 article-title: Autophagy is induced by swine acute diarrhea syndrome coronavirus through the cellular IRE1-JNK-Beclin 1 signaling pathway after an interaction of viral membrane-associated papain-like protease and GRP78 publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1011201 – volume: 55 start-page: 1370 year: 2022 end-page: 1385 ident: B44 article-title: Oxidized DNA fragments exit mitochondria via mPTP- and VDAC-dependent channels to activate NLRP3 inflammasome and interferon signaling publication-title: Immunity doi: 10.1016/j.immuni.2022.06.007 – volume: 96 year: 2022 ident: B32 article-title: The A137R protein of african swine fever virus inhibits type I interferon production via the autophagy-mediated lysosomal degradation of TBK1 publication-title: J Virol doi: 10.1128/jvi.01957-21 – volume: 94 year: 2020 ident: B34 article-title: Cytoplasmic cargo receptor p62 inhibits avibirnavirus replication by mediating autophagic degradation of viral protein VP2 publication-title: J Virol doi: 10.1128/JVI.01255-20 – volume: 50 start-page: 182 year: 2021 end-page: 189 ident: B7 article-title: Epidemiology of fowl adenovirus (FAdV) infections in South Korean chickens during 2013-2019 following introduction of FAdV-4 vaccines publication-title: Avian Pathol doi: 10.1080/03079457.2021.1872766 – volume: 98 start-page: 2765 year: 2019 end-page: 2771 ident: B10 article-title: Pathogenicity of a fowl adenovirus serotype 4 isolated from chickens associated with hydropericardium-hepatitis syndrome in China publication-title: Poult Sci doi: 10.3382/ps/pez042 – volume: 5 year: 2016 ident: B5 article-title: Outbreaks of serotype 4 fowl adenovirus with novel genotype, China publication-title: Emerg Microbes Infect doi: 10.1038/emi.2016.50 – volume: 40 start-page: 280 year: 2010 end-page: 293 ident: B17 article-title: Autophagy and the integrated stress response publication-title: Mol Cell doi: 10.1016/j.molcel.2010.09.023 – volume: 9 year: 2018 ident: B20 article-title: Autophagy benefits the replication of egg drop syndrome virus in duck embryo fibroblasts publication-title: Front Microbiol doi: 10.3389/fmicb.2018.01091 – volume: 10 year: 2020 ident: B26 article-title: Autophagy function and regulation in kidney disease publication-title: Biomolecules doi: 10.3390/biom10010100 – volume: 496 start-page: 367 year: 2013 end-page: 371 ident: B40 article-title: A pathogenic picornavirus acquires an envelope by hijacking cellular membranes publication-title: Nature doi: 10.1038/nature12029 – volume: 33 start-page: 806 year: 2021 end-page: 809 ident: B6 article-title: Emergence of fowl aviadenovirus C-4 in a backyard chicken flock in California publication-title: J Vet Diagn Invest doi: 10.1177/10406387211019962 – volume: 11 start-page: 503 year: 2015 end-page: 515 ident: B24 article-title: Binding of the pathogen receptor HSP90AA1 to avibirnavirus VP2 induces autophagy by inactivating the AKT-MTOR pathway publication-title: Autophagy doi: 10.1080/15548627.2015.1017184 – volume: 16 start-page: 966 year: 2009 end-page: 975 ident: B45 article-title: Life and death partners: apoptosis, autophagy and the cross-talk between them publication-title: Cell Death Differ doi: 10.1038/cdd.2009.33 – volume: 10 year: 2022 ident: B13 article-title: The role of hexon amino acid 188 varies in fowl adenovirus serotype 4 strains with different virulence publication-title: Microbiol Spectr doi: 10.1128/spectrum.01493-22 – volume: 9 year: 2020 ident: B30 article-title: Interplay between cellular autophagy and hepatitis B virus replication: a systematic review publication-title: Cells doi: 10.3390/cells9092101 – volume: 97 year: 2023 ident: B23 article-title: Critical role of viral protein hexon in hypervirulent fowl adenovirus serotype-4-induced autophagy by interaction with BAG3 and promotion of viral replication in LMH cells publication-title: J Virol doi: 10.1128/jvi.00284-23 – volume: 269 start-page: 109388 year: 2022 ident: B21 article-title: FAdV-4 induce autophagy via the endoplasmic reticulum stress-related unfolded protein response publication-title: Vet Microbiol doi: 10.1016/j.vetmic.2022.109388 – volume: 9 start-page: 496 year: 2013 end-page: 509 ident: B36 article-title: Visualizing the autophagy pathway in avian cells and its application to studying infectious bronchitis virus publication-title: Autophagy doi: 10.4161/auto.23465 – volume: 160 start-page: 619 year: 2015 end-page: 630 ident: B39 article-title: Phosphatidylserine vesicles enable efficient en bloc transmission of enteroviruses publication-title: Cell doi: 10.1016/j.cell.2015.01.032 – volume: 278 start-page: 109660 year: 2023 ident: B43 article-title: Fowl adenovirus serotype 4 52/55k protein triggers PKR degradation by ubiquitin-proteasome system to evade effective innate immunity publication-title: Vet Microbiol doi: 10.1016/j.vetmic.2023.109660 – volume: 146 start-page: 497 year: 2020 end-page: 507 ident: B14 article-title: Cyclic GMP-AMP synthase is essential for cytosolic double-stranded DNA and fowl adenovirus serotype 4 triggered innate immune responses in chickens publication-title: Int J Biol Macromol doi: 10.1016/j.ijbiomac.2020.01.015 |
| SSID | ssj0001105252 |
| Score | 2.3250427 |
| Snippet | Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has become globally prevalent since 2015 as a predominant pathogen on poultry farms, leading to substantial... Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has emerged as a significant poultry pathogen since 2015, exhibiting clinical multi-organ and multi-tissue... ABSTRACT Hypervirulent fowl adenovirus serotype 4 (FAdV-4) has emerged as a significant poultry pathogen since 2015, exhibiting clinical multi-organ and... |
| SourceID | doaj pubmedcentral proquest asm2 pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database |
| StartPage | e0005825 |
| SubjectTerms | autophagosome-like vesicles' delivery hypervirulent fowl adenovirus serotype 4 inflammation kidney injury Research Article Veterinary Microbiology |
| SummonAdditionalLinks | – databaseName: DOAJ Open Access Full Text dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Za9wwEBZlIdCX0qSXe6FCoVAw0e31YxsSQiF9aiBvQrLGZLuNXeJdyv77zMjesFtK-9IX34eY-TyHJH_D2HvTJJVSlUrn2rpE62fKuTUJFyJg-tyEKtGI7sVXd35pvlzZq51SXzQnbKQHHgV3rFJDpEwBQ-dgaE6OAHQzIG0jQIOJZH3R5-0kU7l3RVJ9NjUNY6INPs4_Lt6ub4iw0CI40JnMwnCj9vxRpu3_U6z5-5TJHR909pg9moJH_mls9CF7AN0ROxjLSW6esOUF0H-8mXqZL7qB8u4BN1Y9xzCPLxepgw3uf0c54opTGZQlprG4nVDDiccNv8a8FK3H7Zq8EW_7Xz94QNPU06GBI1576rTl5im7PDv9dnJeTsUUymBsvSq1gzpWLganYzCVanW0WgRobI0e2-rGGkBUhRYUiNBgVBddJpeTTRsBrdAzNuv6Dl4wLmoRgk1Suzg3OomoIcgkY6In4o0F-0CS9dPXMPicaKi53-rAZx14ZQv2cSt8_3Nk1_jbxZ9JPfcXEjF2PoBw8RNc_L_gUrB3W-V6_JBodCR00K8Hr4nJDE2uqQv2fFT2_asoCcXcTxZsvgeDvbbsn-kW15msWyoMimXlXv6P1r9iDxXVHxYaAfyazVA-8AaDolV8m_F_B6ElDCo priority: 102 providerName: Directory of Open Access Journals |
| Title | Mechanistic insights into the kidney injury in chickens induced by hypervirulent fowl adenovirus serotype 4 |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/40130861 https://journals.asm.org/doi/10.1128/spectrum.00058-25 https://www.proquest.com/docview/3180988749 https://pubmed.ncbi.nlm.nih.gov/PMC12054176 https://doaj.org/article/2dc8140a217a408890e023e15c0e3e4b |
| Volume | 13 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3di9QwEB_OOwRfxG_rxxFBEIRqmq-2j6t4HMrpiwv3FpIm5db1WrnuIvvfO5NtV1cO8aXfacr8JpOZpPkNwEvVBBFCGXJj2jpH66fySquAG-4wfG5cGWhG9-yzOZ2rj-f6_ADMtBZmlODwxg2XaSJ_17JF9TYtPrxaXxLpoEaA9Q040qJW2CCPZrP5l0-_R1cKys8mxmnMa8uiDcY6xF5_lGj7r_M1__5l8o8-6OQO3B6dRzbbon0XDmJ3D25u00lu7sPyLNI63kS9zBbdQHH3gAernqGbx5aL0MUNnn9DOeKOURqUJYaxeBwQ4cD8hl1gXIrW42pNvRFr-5_fmUPT1NOlgaG-9jRoy9QDmJ98-Pr-NB-TKeRO6XqVSxNrXxrvjPROlaKVXkvuYqNr7LG1bLSKqFWujSJy16BX500ilyua1ke0Qg_hsOu7-BgYr7lzOhTS-ErJwL2MrgiFD_RGLJjBK5KsnbC0KdAQlZ0wsAkDK3QGryfh2x9bdo1_PfyO4Nk9SMTY6QKqiR3bmRWhIQ4vh5GWU_QLF4_olcRCNzzKqHwGLyZwLTYkmh1xXezXg5XEZIYmV9UZPNqCvauKglCM_YoMqj012PuW_Tvd4iKRdRcCneKiNE_-WyhP4ZagJMNcopY-g0O8GZ-j57Pyx6OaH6eRg1_ijgV4 |
| linkProvider | American Society for Microbiology |
| linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1Zb9QwELagFYIXxE04jYSEhBTwneRxQVQL7ZaXrtQ3y44ddbttUjW7qvbfM-PNFhZViJecziHPeDyfx_6GkPeqDiKEIuTGNFUO1k_lpVYBNswBfK5dETCiOzk046n6cayPh1mVuBbmFPPynvWfXH-e4vjYsHEgeshHWH5OCxAvl-dIPKhByPo22cXYIQCv3dFo-nP_9wgLxxxtYghl3vgs2GH4kNjqkxJ1_03-5t_TJv_oh_YekPuDA0lHa4k_JLdi-4jcWaeUXD0m80nEtbyJfpnO2h6xdw8Hi46Cq0fns9DGFZyfQl3CjmIqlDlAWTgOIOVA_YqeADYFC3K5xB6JNt3VGXVgnjq81FPQ2Q4Hbql6QqZ7346-jvMhoULulK4WuTSx8oXxzkjvVCEa6bVkLta6gl5by1qrCJrlmigiczV4dt4kgjleNz6CJXpKdtqujc8JZRVzTgcujS-VDMzL6HjgPuAb4cGMfMCatUOL6G0CG6K0GxnYJAMrdEY-birfXqwZNv5V-AuK57ogkmOnC6ArdmhrVoQaebwcoC2ncBoXi-CZRK5rFmVUPiPvNsK10JgwQuLa2C17K5HNDMyuqjLybC3s608hEAX8xzNSbqnB1r9s32lnJ4mwmwtwjHlhXvx3pbwld8dHkwN78P1w_yW5JzDpMJOgsa_IDhSMr8ETWvg3g8r_Ag38COY |
| linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV3db9MwED9BJxAviG8yvoyEhIQUlvgryWP5qAZjgwcq7c2yY0cr3ZJpaYX633PnpoOiCfHSJqmdVPc7n-9y9u8AXsnac-8Ln2rdVClaP5mWSnr8yCyGz7UtPGV0D4_0_lR-PlbHw6pK2gszSLB_a_uzmMinkX3um6EeYbkXNyBeLM-IeFAhyOo67MRk1Qh2xuPp14Pfb1hyqtHGh1TmlX3RDuNz-NacFKn7r_I3_142-cc8NLkDtwcHko3XiN-Fa6G9BzfWJSVX92F-GGgvb6RfZrO2p9i7x4NFx9DVY_OZb8MKz3-gLPGLUSmUOYayeOwRZc_cip1gbIoW5GJJMxJrup-nzKJ56uhSz1BnO3pxy-QDmE4-fn-_nw4FFVIrVbVIhQ6VK7SzWjgrC94Ip0RmQ60qnLWVqJUMqFm2CTxktkbPzulIMJfXjQtoiR7CqO3a8BhYVmXWKp8L7UopfOZEsLnPnac7YscEXpNkzQZPE4MNXpoNBiZiYLhK4M1G-OZ8zbDxr8bvCJ7LhkSOHS-gqphhrBnua-LxshhtWUnLuLKAnknIVZ0FEaRL4OUGXIODiTIktg3dsjeC2MzQ7MoqgUdrsC8fRYEoxn95AuWWGmz9l-1f2tlJJOzOOTrGeaF3_1soL-Dmtw8T8-XT0cETuMWp5nAmUGGfwgjbhWfoCC3c80HjfwHowwiC |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Mechanistic+insights+into+the+kidney+injury+in+chickens+induced+by+hypervirulent+fowl+adenovirus+serotype+4&rft.jtitle=Microbiology+spectrum&rft.au=Zhu%2C+Chunhua&rft.au=Zhou%2C+Jiayu&rft.au=Chen%2C+Zhen&rft.au=Chen%2C+Cuiteng&rft.date=2025-03-25&rft.issn=2165-0497&rft.eissn=2165-0497&rft.spage=e0005825&rft_id=info:doi/10.1128%2Fspectrum.00058-25&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2165-0497&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2165-0497&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2165-0497&client=summon |