Host Mitochondrial Requirements of Cytomegalovirus Replication

Monk, Chandler H.; Zwezdaryk, Kevin J.

doi:10.1007/s40588-020-00153-5

Cited by 7 publications

(5 citation statements)

References 56 publications

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“…97,98 It is interesting that HCMV UL37 activates calmodulindependent kinase (CaMKK) via increasing calcium signaling and promoting viral induction of glycolysis. 99,100 Tuberous sclerosis complex 2 (TSC2) negatively regulates mTOR complex I, thus acting as a metabolic sensor with a critical role in glucose transport. UL38 induces the mTOR pathway by inhibiting tuberous TSC2 to increase viral replication.…”

Section: Human Cytomegalovirus (Hcmv)mentioning

confidence: 99%

Interplay between cellular metabolism and DNA viruses

Zandi¹,

Shokri

Mahmoudvand

et al. 2022

Journal of Medical Virology

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Viruses as intracellular pathogens take over the host metabolism and reprogram to facilitate optimal virus production. DNA viruses can cause alterations in several metabolic pathways, including aerobic glycolysis also known as the Warburg effect, pentose phosphate pathway activation, and amino acid catabolism such as glutaminolysis, nucleotide biosynthesis, lipid metabolism, and amino acid biosynthesis. The available energy for productive infection can be increased in infected cells via modification of different carbon source utilization. This review discusses the metabolic alterations of the DNA viruses that will be the basis for future novel therapeutic approaches.

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Section: Human Cytomegalovirus (Hcmv)mentioning

confidence: 99%

Interplay between cellular metabolism and DNA viruses

Zandi¹,

Shokri

Mahmoudvand

et al. 2022

Journal of Medical Virology

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“…On the other hand, two pathways related to mitochondrial functions (i.e., "consumption of oxygen" and "ATP synthesis") were found to be lower in sEVs from hCMV-infected HIPECs than in NI HIPECs (Figure 2b). This may also be the consequence of hCMV-induced mitochondrial dysfunctions [45][46][47][48], likely via interference with the antiviral Viperin protein, which leads to decreased cellular ATP levels [49]. S2 for bibliography references).…”

Section: Sevs Secreted By Infected Hipecs Harbor a Potential Proviral...mentioning

confidence: 99%

Human Cytomegalovirus Modifies Placental Small Extracellular Vesicle Composition to Enhance Infection of Fetal Neural Cells In Vitro

Bergamelli

Martin

Aubert

et al. 2022

Viruses

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Although placental small extracellular vesicles (sEVs) are extensively studied in the context of pregnancy, little is known about their role during viral congenital infection, especially at the beginning of pregnancy. In this study, we examined the consequences of human cytomegalovirus (hCMV) infection on sEVs production, composition, and function using an immortalized human cytotrophoblast cell line derived from first trimester placenta. By combining complementary approaches of biochemistry, electron microscopy, and quantitative proteomic analysis, we showed that hCMV infection increases the yield of sEVs produced by cytotrophoblasts and modifies their protein content towards a potential proviral phenotype. We further demonstrate that sEVs secreted by hCMV-infected cytotrophoblasts potentiate infection in naive recipient cells of fetal origin, including human neural stem cells. Importantly, these functional consequences are also observed with sEVs prepared from an ex vivo model of infected histocultures from early placenta. Based on these findings, we propose that placental sEVs could be important actors favoring viral dissemination to the fetal brain during hCMV congenital infection.

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“…On the other hand, two pathways related to mitochondrial functions (i.e., "consumption of oxygen" and "ATP synthesis ") were found to be lower in sEVs from hCMV-infected HIPECs than in NI HIPECs (Figure 2B). This may also be the consequence of hCMV-induced mitochondrial dysfunctions (33)(34)(35)(36), likely via interference with the antiviral Viperin protein, which leads to decreased cellular ATP levels (37).…”

Section: Sevs Secreted By Infected Hipecs Harbor a Proviral Protein C...mentioning

confidence: 99%

Human Cytomegalovirus modifies placental small extracellular vesicle secretion and composition towards a proviral phenotype to enhance infection of fetal recipient cells

Bergamelli¹,

Martin²,

Aubert³

et al. 2021

Preprint

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Although placental small extracellular vesicles (sEVs) are extensively studied in the context of pregnancy, little is known about their role during human cytomegalovirus (hCMV) congenital infection, especially at the beginning of pregnancy. In this study, we examined the consequences of hCMV infection on sEVs production and composition using an immortalized human cytotrophoblast cell line derived from first trimester placenta. By combining complementary approaches of biochemistry, imaging techniques and quantitative proteomic analysis, we showed that hCMV infection increased the yield of sEVs produced by cytotrophoblasts and modified their protein composition towards a proviral phenotype. We further demonstrated that sEVs secreted by hCMV-infected cytotrophoblasts potentiated infection in naive recipient cells of fetal origin, including neural stem cells. Importantly, the enhancement of hCMV infection was also observed with sEVs prepared from either an ex vivo model of infected histocultures from early placenta or from the amniotic fluid of patients naturally infected by hCMV at the beginning of pregnancy. Based on these findings, we propose that placental sEVs could be key actors favoring viral dissemination to the fetal brain during hCMV congenital infection.

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Host Mitochondrial Requirements of Cytomegalovirus Replication

Cited by 7 publications

References 56 publications

Interplay between cellular metabolism and DNA viruses

Interplay between cellular metabolism and DNA viruses

Human Cytomegalovirus Modifies Placental Small Extracellular Vesicle Composition to Enhance Infection of Fetal Neural Cells In Vitro

Human Cytomegalovirus modifies placental small extracellular vesicle secretion and composition towards a proviral phenotype to enhance infection of fetal recipient cells

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