4.3 Mitochondrial ROS and viruses
Examples of mitochondrial ROS in the context of host-virus interactions
indicate varying effects. For example, systemic infection by TMV was
exacerbated in SHAM-treated tomato plants (Liao et al., 2012). SHAM is
an inhibitor of the mitochondrial alternative oxidase (AOX), resulting
in elevated mitochondrial ROS levels in plants (see above). In contrast,
treatment with potassium cyanide (KCN), a cytochrome pathway inhibitor,
decreased ROS levels and enhanced resistance to TMV (Liao et al., 2012).
These results contrast with the effects reported by Stonebloom et al.,
where increased mtROS led to increased intercellular trafficking
(Stonebloom et al., 2012).
While relatively little is known about the involvement of mtROS in plant
responses to plant viruses, more is known in animal systems. The NS1
protein from Mink Enteritis Virus (MEV), an autonomous parvovirus
causing acute hemorrhagic enteritis in minks, induces apoptosis in
HEK293T cells through the mitochondrial pathway. NS1-transfected cells
show increased ROS production and activation of p38-MAPK, leading to p53
phosphorylation that mediates the mitochondrial apoptotic process. These
findings suggest that MEV pathogenicity depends on disrupting various
aspects of mitochondrial function, including disruption of redox status
(Lin et al., 2019) (Lin et al., 2019 J. Virology doi:
10.1128/JVI.01249-19.). Mitochondrial TRXs can also be involved
in viral disruption of host defense systems. For instance, TRX2, which
is localized in mitochondria, negatively regulates innate immunity in
Hela cells by disrupting the assembly of the virus-induced signaling
adaptor (VISA) complex (Li et al., 2020). This complex is crucial for
inducing type I interferons and eliciting innate antiviral responses.
TRX2 achieves this inhibition by suppressing ROS production. Knockdown
of TRX2 enhances Sendai virus replication by triggering IFN-B
induction. It will be interesting to see how commonly plant viruses
manipulate mitochondrial ROS during infection.