RETRACTED ARTICLE: Mitochondrial bioenergy alterations in avian HD11 macrophages infected with infectious bronchitis virus

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.

Protective effects of hypericin against infectious bronchitis virus induced apoptosis and reactive oxygen species in chicken embryo kidney cells

“…Therefore, we investigated whether HY ameliorated IBV-induced ROS generation. Our results revealed that HY could inhibit ROS production in the absence of phototherapy ( Figure 6), which was consistent with other report (Da Silva et al, 2018).…”

Comparative features of infections of two Massachusetts (Mass) infectious bronchitis virus (IBV) variants isolated from Western Canadian layer flocks

“…The current study shows that minor genetic differences in Mass IBV variants do not lead to differences in macrophage responses in the respiratory tract although each of the tested IBV isolates were able to elicit significant macrophage responses in these tissues. IBV M41 and ConnA5968 strains have been shown to replicate in macrophages in vivo and in vitro [65][66][67]. The IBV Beaudette strain is able to infect the HD11 macrophage cell line [68].…”