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Apoptosis, autophagy and unfolded protein response pathways in Arbovirus replication and pathogenesis.

Iranpour M, Moghadam AR, Yazdi M, Ande SR, Alizadeh J, Wiechec E, Lindsay R, Drebot M, Coombs KM, Ghavami S - Expert Rev Mol Med (2016)

Bottom Line: Recently, a few successful approaches toward production of effective vaccines against some of these pathogens have been developed, but treatment and prevention of the resulting diseases remain a major health and research concern.The arbovirus infection and replication processes are complex, and many factors are involved in their regulation.In this review, we focus on the importance of these pathways in the arbovirus replication and infection processes.

View Article: PubMed Central - PubMed

Affiliation: Zoonotic Diseases and Special Pathogens,National Microbiology Laboratory,Public Health Agency of Canada,1015 Arlington St.,Winnipeg,Manitoba,Canada.

ABSTRACT
Arboviruses are pathogens that widely affect the health of people in different communities around the world. Recently, a few successful approaches toward production of effective vaccines against some of these pathogens have been developed, but treatment and prevention of the resulting diseases remain a major health and research concern. The arbovirus infection and replication processes are complex, and many factors are involved in their regulation. Apoptosis, autophagy and the unfolded protein response (UPR) are three mechanisms that are involved in pathogenesis of many viruses. In this review, we focus on the importance of these pathways in the arbovirus replication and infection processes. We provide a brief introduction on how apoptosis, autophagy and the UPR are initiated and regulated, and then discuss the involvement of these pathways in regulation of arbovirus pathogenesis.

No MeSH data available.


Related in: MedlinePlus

Graphic representation of apoptosis signalling pathways. Apoptosis is initiated via two different routes including extrinsic and intrinsic apoptotic pathways. The extrinsic signals are initiated by cell death ligands (e.g. FasL, APO-2L, TRAIL, TNF) and activate FADD and subsequently cleave pro-caspase-8. Cleavage of pro-caspases-8 and -10 initiate activation of caspases-8 and -10, which later can directly trigger effector caspases including caspases-3, -6 and -7. The intrinsic pathway is stimulated via DNA damage. Once DNA damage occurs, p53 is activated and induces apoptosis in a mitochondria-dependent manner. In this pathway, pro-apoptotic and antiapoptotic proteins are up- and down-regulated, leading to release of cytochrome c. Released cytochrome c later can activate caspase 9 which in turn activates caspase-3. FasL, Fas (Apo-1/CD95) ligand; TNF, tumour necrosis factor receptor TRAIL, TNF, tumour necrosis factor receptor.
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fig04: Graphic representation of apoptosis signalling pathways. Apoptosis is initiated via two different routes including extrinsic and intrinsic apoptotic pathways. The extrinsic signals are initiated by cell death ligands (e.g. FasL, APO-2L, TRAIL, TNF) and activate FADD and subsequently cleave pro-caspase-8. Cleavage of pro-caspases-8 and -10 initiate activation of caspases-8 and -10, which later can directly trigger effector caspases including caspases-3, -6 and -7. The intrinsic pathway is stimulated via DNA damage. Once DNA damage occurs, p53 is activated and induces apoptosis in a mitochondria-dependent manner. In this pathway, pro-apoptotic and antiapoptotic proteins are up- and down-regulated, leading to release of cytochrome c. Released cytochrome c later can activate caspase 9 which in turn activates caspase-3. FasL, Fas (Apo-1/CD95) ligand; TNF, tumour necrosis factor receptor TRAIL, TNF, tumour necrosis factor receptor.

Mentions: There are two main functionally distinct pathways for apoptosis induction (Fig. 4): the extrinsic and the intrinsic mitochondrial pathways (Refs 137, 138, 139). Caspases are involved in most of the apoptotic processes and are activated by ligation of death receptors [tumour necrosis factor receptor (TNFR), Fas, TNF-related apoptosis-inducing ligand (TRAIL)] or release of specific proteins from the mitochondria (Refs 140, 141). However, accumulating evidence suggests that the two pathways are intimately intertwined (Refs 138, 142), which will be described in the next sections. The extrinsic apoptosis cascade is stimulated after the binding of cell surface receptors to their ligands, resulting in Fas-associated protein with death domain (FADD)-dependent activation of initiator caspases, namely caspase-8, and subsequently caspase-3 and -7 (Refs 143, 144). As a consequence, effector caspases (i.e. caspase-3 and caspase-7) are dimerized and activated and, once active they can cause apoptosis (Refs 141, 145).Figure 4.


Apoptosis, autophagy and unfolded protein response pathways in Arbovirus replication and pathogenesis.

Iranpour M, Moghadam AR, Yazdi M, Ande SR, Alizadeh J, Wiechec E, Lindsay R, Drebot M, Coombs KM, Ghavami S - Expert Rev Mol Med (2016)

Graphic representation of apoptosis signalling pathways. Apoptosis is initiated via two different routes including extrinsic and intrinsic apoptotic pathways. The extrinsic signals are initiated by cell death ligands (e.g. FasL, APO-2L, TRAIL, TNF) and activate FADD and subsequently cleave pro-caspase-8. Cleavage of pro-caspases-8 and -10 initiate activation of caspases-8 and -10, which later can directly trigger effector caspases including caspases-3, -6 and -7. The intrinsic pathway is stimulated via DNA damage. Once DNA damage occurs, p53 is activated and induces apoptosis in a mitochondria-dependent manner. In this pathway, pro-apoptotic and antiapoptotic proteins are up- and down-regulated, leading to release of cytochrome c. Released cytochrome c later can activate caspase 9 which in turn activates caspase-3. FasL, Fas (Apo-1/CD95) ligand; TNF, tumour necrosis factor receptor TRAIL, TNF, tumour necrosis factor receptor.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4836210&req=5

fig04: Graphic representation of apoptosis signalling pathways. Apoptosis is initiated via two different routes including extrinsic and intrinsic apoptotic pathways. The extrinsic signals are initiated by cell death ligands (e.g. FasL, APO-2L, TRAIL, TNF) and activate FADD and subsequently cleave pro-caspase-8. Cleavage of pro-caspases-8 and -10 initiate activation of caspases-8 and -10, which later can directly trigger effector caspases including caspases-3, -6 and -7. The intrinsic pathway is stimulated via DNA damage. Once DNA damage occurs, p53 is activated and induces apoptosis in a mitochondria-dependent manner. In this pathway, pro-apoptotic and antiapoptotic proteins are up- and down-regulated, leading to release of cytochrome c. Released cytochrome c later can activate caspase 9 which in turn activates caspase-3. FasL, Fas (Apo-1/CD95) ligand; TNF, tumour necrosis factor receptor TRAIL, TNF, tumour necrosis factor receptor.
Mentions: There are two main functionally distinct pathways for apoptosis induction (Fig. 4): the extrinsic and the intrinsic mitochondrial pathways (Refs 137, 138, 139). Caspases are involved in most of the apoptotic processes and are activated by ligation of death receptors [tumour necrosis factor receptor (TNFR), Fas, TNF-related apoptosis-inducing ligand (TRAIL)] or release of specific proteins from the mitochondria (Refs 140, 141). However, accumulating evidence suggests that the two pathways are intimately intertwined (Refs 138, 142), which will be described in the next sections. The extrinsic apoptosis cascade is stimulated after the binding of cell surface receptors to their ligands, resulting in Fas-associated protein with death domain (FADD)-dependent activation of initiator caspases, namely caspase-8, and subsequently caspase-3 and -7 (Refs 143, 144). As a consequence, effector caspases (i.e. caspase-3 and caspase-7) are dimerized and activated and, once active they can cause apoptosis (Refs 141, 145).Figure 4.

Bottom Line: Recently, a few successful approaches toward production of effective vaccines against some of these pathogens have been developed, but treatment and prevention of the resulting diseases remain a major health and research concern.The arbovirus infection and replication processes are complex, and many factors are involved in their regulation.In this review, we focus on the importance of these pathways in the arbovirus replication and infection processes.

View Article: PubMed Central - PubMed

Affiliation: Zoonotic Diseases and Special Pathogens,National Microbiology Laboratory,Public Health Agency of Canada,1015 Arlington St.,Winnipeg,Manitoba,Canada.

ABSTRACT
Arboviruses are pathogens that widely affect the health of people in different communities around the world. Recently, a few successful approaches toward production of effective vaccines against some of these pathogens have been developed, but treatment and prevention of the resulting diseases remain a major health and research concern. The arbovirus infection and replication processes are complex, and many factors are involved in their regulation. Apoptosis, autophagy and the unfolded protein response (UPR) are three mechanisms that are involved in pathogenesis of many viruses. In this review, we focus on the importance of these pathways in the arbovirus replication and infection processes. We provide a brief introduction on how apoptosis, autophagy and the UPR are initiated and regulated, and then discuss the involvement of these pathways in regulation of arbovirus pathogenesis.

No MeSH data available.


Related in: MedlinePlus