RETRACTED ARTICLE: Mitochondrial bioenergyalterations in avian HD11 macrophages infected with infectious bronchitisvirus
Authors: Roberto Gameiro
Dielson S Vieira
Sergio E L da Silva
Carolina U F Fabri
Felipe E S Silva
Tereza C Cardoso
Andrea F Garcia
Helena L Ferreira
Journal: Archives of Virology (2018)
Discipline: MICROBIOLOGY
Keywords: mitochondrial dysfunction; apoptosis; infectious bronchitis virus; HD11 avian macrophage cells; Massachusetts 41 (M41) strain
Affiliations: Faculdade de Medicina Veterinária (FAMEV), Universidade Federal Uberlândia (UFU), Uberlândia, MG, Brazil., Department of Veterinary Medicine, FZEA-USP-University of Sao Paulo, Pirassununga, SP, Brazil., Centro Universitário Católico Salesiano Auxilium, UniSLESIANO, Araçatuba, SP, Brazil., College of Veterinary Medicine, UNESP-University of São Paulo State, Araçatuba, SP, Brazil., College of Veterinary Medicine, UNESP-University of São Paulo State, Araçatuba, SP, Brazil. .

Abstract:  To establish an association between mitochondrial dysfunction and apoptosis following infectious bronchitis virus (IBV) infection, HD11 avian macrophage cells were infected with the Massachusetts 41 (M41) strain. Our results show that the M41 strain of IBV induced cytopathic effects followed by the release of new viral particles. Elevated numbers of apoptotic cells were observed at 24, 48 and 72 h post-infection (p.i.). Viral infection was associated with mitochondrial membrane depolarization and reactive oxygen species (ROS) production at all of the examined timepoints p.i. In summary, IBV M41 replication in infected HD11 macrophages seems to induce mitochondrial bioenergy failure, acting as a respiratory chain uncoupler, without compromising viral replication. 

Retracted: Yes

PubPeer comments:
 2019 retraction. https: link.springer.com article 10.1007%2Fs00705-019-04481-w The Editor-in-Chief has retracted this article [1]. Figures 1A, 1D and 2B (bottom right) are identical with Figures 1A, 1H and 1B respectively in another article [2] which reports a study in a different species. In addition, Table 1 contains data presented in a third article [3], which also reports a study in a different species. The Editor-in-Chief therefore no longer has confidence in the validity of the data and the conclusions drawn. Tereza C. Cardoso disagrees with this retraction. Helena L. Ferreira agrees with this retraction. Sergio E. L. da Silva, Andrea F. Garcia, Felipe E. S. Silva, Roberto Gameiro, Carolina U. F. Fabri and Dielson S. Vieira have not responded to any correspondence about this retraction. [1] da Silva, Sergio EL, et al. u201cMitochondrial bioenergy alterations in avian HD11 macrophages infected with infectious bronchitis virus.u201d Archives of Virology 163.4 (2018): 1043-1049. [2] Cardoso, Tereza C., et al. u201cBovine Herpesvirus 5 promotes mitochondrial dysfunction in cultured bovine monocyte-derived macrophages and not affect virus replication.u201d Veterinary Microbiology 229 (2019): 153u2013158. [3] Garcia, Juliana Albarracin, et al. u201cTumour necrosis factoru2010alphau2010induced protein 8 (TNFAIP8) expression associated with cell survival and death in cancer cell lines infected with canine distemper virus.u201d Veterinary and Comparative Oncology 15.2 (2017): 336u2013344. , 
 Also, retraction of: https: www.sciencedirect.com science article pii S0378113518309350 Cardoso, Tereza C., et al. u201cBovine Herpesvirus 5 promotes mitochondrial dysfunction in cultured bovine monocyte-derived macrophages and not affect virus replication.u201d Veterinary Microbiology 229 (2019): 153u2013158. This article has been retracted at the request of the Editors-in-Chief and Authors. Fig 1A is a duplicate of a figure that has already been published in da Silva SEL et al. Archives of Virology 2018;163:1043-1049; 10.1007 s00705-018-3704-2. These two papers report studies performed with cells from two different animal species (bovine cells for the Veterinary Microbiology paper and chicken cells for the Archives of Virology paper). The reuse of the same figure in the Veterinary Microbiology paper to describe cells that were supposed to be from a different species is thus inappropriate and also puts into question the reliability of the other results presented in this paper. In addition, the Editors-in-Chief have remaining concerns about the strong similarities of other data presented in the two papers. Even if these concerns were addressed, the re-use of any data has to be clearly indicated and appropriately cited. As such this article represents a misuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of the journal that this was not detected during the submission process. ,