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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 proviral functions of autophagy. There are five possible mechanisms for modulating viral replication by autophagy. Amphisome formation is thought to be beneficial for viral cellular entry and replication. Induction of autophagosome formation is also important for some virus’ replication. Furthermore, viruses initiate autophagy to benefit from lipid droplets as an energy source during viral replication. Free fatty acids are liberated from lipid droplets during autophagy to produce ATP. Viruses also stimulate autophagy to subvert immune responses by selectively degrading key regulatory molecules. Another mechanism is that viruses promote their replication by prolonging cell survival and suppressing cell death. The mechanistic details related to proviral functions of autophagy are discussed in the text.
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fig06: Graphic proviral functions of autophagy. There are five possible mechanisms for modulating viral replication by autophagy. Amphisome formation is thought to be beneficial for viral cellular entry and replication. Induction of autophagosome formation is also important for some virus’ replication. Furthermore, viruses initiate autophagy to benefit from lipid droplets as an energy source during viral replication. Free fatty acids are liberated from lipid droplets during autophagy to produce ATP. Viruses also stimulate autophagy to subvert immune responses by selectively degrading key regulatory molecules. Another mechanism is that viruses promote their replication by prolonging cell survival and suppressing cell death. The mechanistic details related to proviral functions of autophagy are discussed in the text.

Mentions: Although autophagy was initially proposed as a physiological cellular response to environmental stress followed by virus amplification, increasing evidence now indicates that several viruses may use autophagy as a survival strategy to support their life cycle, which is known as ‘pro-viral autophagy’ (Refs 131, 138, 184, 185) (Fig. 6). Virus-induced induction of autophagy seems to be associated with replication/translation of many arboviruses like DENV, JEV, CHIKV, rotavirus, and epizootic haemorrhagic disease virus (EHDV, an orbivirus) (Refs 186, 187, 188, 189, 190, 191). The results that were obtained by monitoring LC3 lipidation in JEV-infected NT-2 cells, a pluripotent human testicular embryonal carcinoma cell line treated with Rapamycin and 3-methyladenine, revealed that there was a direct relationship between autophagy and viral replication The results were confirmed using an Atg5/Beclin-1 knock down model (Ref. 187). Most commonly, in many eukaryotic cells, it is apparent that the initiation of autophagy can be enhanced in infected DENV cells; in addition, the replication of DENV is positively linked to autophagy induction (Ref. 192). However, DENV viral replication has been shown to be limited in monocytes, which suggests a possible cell-specific relationship between activated autophagy and DENV production (Ref. 193). WNV induces autophagy even though its replication is autophagy independent (Ref. 194). The importance of virus-induced autophagy and up-regulation of viral replication has also been shown in CHIKV-infected cells (Ref. 188). The Orbivirus EHDV induces autophagy, apoptosis and c-Jun N-terminal kinase (JNK) activation, and phosphorylates c-Jun, all of which seem to benefit viral replication (Ref. 190). JEV also induces autophagy in the early stage of infection and the inoculated viral particles traffic to autophagosomes for subsequent steps of viral infection (Ref. 187). In vivo studies showed that autophagy played a supporting role in DENV-2 replication and pathogenesis (Ref. 195).Figure 6.


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 proviral functions of autophagy. There are five possible mechanisms for modulating viral replication by autophagy. Amphisome formation is thought to be beneficial for viral cellular entry and replication. Induction of autophagosome formation is also important for some virus’ replication. Furthermore, viruses initiate autophagy to benefit from lipid droplets as an energy source during viral replication. Free fatty acids are liberated from lipid droplets during autophagy to produce ATP. Viruses also stimulate autophagy to subvert immune responses by selectively degrading key regulatory molecules. Another mechanism is that viruses promote their replication by prolonging cell survival and suppressing cell death. The mechanistic details related to proviral functions of autophagy are discussed in the text.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig06: Graphic proviral functions of autophagy. There are five possible mechanisms for modulating viral replication by autophagy. Amphisome formation is thought to be beneficial for viral cellular entry and replication. Induction of autophagosome formation is also important for some virus’ replication. Furthermore, viruses initiate autophagy to benefit from lipid droplets as an energy source during viral replication. Free fatty acids are liberated from lipid droplets during autophagy to produce ATP. Viruses also stimulate autophagy to subvert immune responses by selectively degrading key regulatory molecules. Another mechanism is that viruses promote their replication by prolonging cell survival and suppressing cell death. The mechanistic details related to proviral functions of autophagy are discussed in the text.
Mentions: Although autophagy was initially proposed as a physiological cellular response to environmental stress followed by virus amplification, increasing evidence now indicates that several viruses may use autophagy as a survival strategy to support their life cycle, which is known as ‘pro-viral autophagy’ (Refs 131, 138, 184, 185) (Fig. 6). Virus-induced induction of autophagy seems to be associated with replication/translation of many arboviruses like DENV, JEV, CHIKV, rotavirus, and epizootic haemorrhagic disease virus (EHDV, an orbivirus) (Refs 186, 187, 188, 189, 190, 191). The results that were obtained by monitoring LC3 lipidation in JEV-infected NT-2 cells, a pluripotent human testicular embryonal carcinoma cell line treated with Rapamycin and 3-methyladenine, revealed that there was a direct relationship between autophagy and viral replication The results were confirmed using an Atg5/Beclin-1 knock down model (Ref. 187). Most commonly, in many eukaryotic cells, it is apparent that the initiation of autophagy can be enhanced in infected DENV cells; in addition, the replication of DENV is positively linked to autophagy induction (Ref. 192). However, DENV viral replication has been shown to be limited in monocytes, which suggests a possible cell-specific relationship between activated autophagy and DENV production (Ref. 193). WNV induces autophagy even though its replication is autophagy independent (Ref. 194). The importance of virus-induced autophagy and up-regulation of viral replication has also been shown in CHIKV-infected cells (Ref. 188). The Orbivirus EHDV induces autophagy, apoptosis and c-Jun N-terminal kinase (JNK) activation, and phosphorylates c-Jun, all of which seem to benefit viral replication (Ref. 190). JEV also induces autophagy in the early stage of infection and the inoculated viral particles traffic to autophagosomes for subsequent steps of viral infection (Ref. 187). In vivo studies showed that autophagy played a supporting role in DENV-2 replication and pathogenesis (Ref. 195).Figure 6.

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