Persistent Coxsackievirus B3 Infection in Pancreatic Ductal Cells
            <i>In Vitro</i>
            Downregulates Cellular Polyamine Metabolism

Mastrodomenico, Vincent; LoMascolo, Natalie J; Firpo, Mason R; Guzman, Maria Del Mar Villanueva; Zaporowski, Adam; Mounce, Bryan C.

doi:10.1128/msphere.00036-23

Cited by 5 publications

(2 citation statements)

References 32 publications

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“…In contrast, SARS-CoV-2 [51], porcine reproductive and respiratory syndrome virus (PRRSV) [52], and porcine endemic diarrhoea virus (PEDV) [53] upregulate expression of SSAT and thus decrease polyamine levels in infected cells. Exhaustion of spermine and spermidine levels due to lowered expression of ODC is also a feature of lytic KSAV [50] and Coxsackie virus B3 (CVB3) [54] infections. So, our data expand the list of viral pathogens that deregulate expression of polyamine-metabolising enzymes and decrease polyamine content.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis C Virus Dysregulates Polyamine and Proline Metabolism and Perturbs Urea Cycle

Zakirova,

Khomich,

Smirnova

et al. 2024

Preprint

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Hepatitis C virus (HCV) is an oncogenic virus that causes chronic liver disease in more than 80% of patients. During the last decade, efficient direct acting antivirals were introduced into clinical practice. However, clearance of the virus does not reduce risk of end-stage liver diseases to the level observed in patients that have never been infected. So, investigation of HCV pathogenesis is still warranted. Virus-induced changes in cell metabolism contribute to the development of HCV-associated liver pathologies. Here we studied the impact of the virus on the metabolism of polyamines and proline as well as on the urea cycle, which plays a crucial role in liver function. It was found that HCV strongly suppresses the expression of arginase, a key enzyme of the urea cycle, leading to accumulation of arginine and upregulates proline oxidase with a concomitant decrease in proline concentrations. Addition of exogenous proline moderately suppressed viral replication. HCV upregulated transcription but suppressed protein levels of polyamine-metabolizing enzymes. This resulted in a decrease in polyamine content in infected cells. Finally, compounds targeting polyamine metabolism demonstrated pronounced antiviral activity pointing to spermine and spermidine as compounds affecting HCV replication. These data expand our understanding of HCV’s imprint on cell metabolism.

show abstract

Section: Discussionmentioning

confidence: 99%

Hepatitis C Virus Dysregulates Polyamine and Proline Metabolism and Perturbs Urea Cycle

Zakirova,

Khomich,

Smirnova

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…In contrast, SARS-CoV-2 [ 55 ], porcine reproductive and respiratory syndrome virus (PRRSV) [ 56 ], and porcine endemic diarrhoea virus (PEDV) [ 57 ] up-regulate expression of SSAT and thus decrease polyamine levels in infected cells. Exhaustion of spermine and spermidine levels due to lowered expression of ODC is also a feature of lytic KSAV [ 54 ] and Coxsackie virus B3 (CVB3) [ 58 ] infections. So, our data expand the list of viral pathogens that deregulate the expression of polyamine-metabolizing enzymes and decrease polyamine content.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis C Virus Dysregulates Polyamine and Proline Metabolism and Perturbs the Urea Cycle

Zakirova,

Khomich,

Smirnova

et al. 2024

Cells

View full text Add to dashboard Cite

Hepatitis C virus (HCV) is an oncogenic virus that causes chronic liver disease in more than 80% of patients. During the last decade, efficient direct-acting antivirals were introduced into clinical practice. However, clearance of the virus does not reduce the risk of end-stage liver diseases to the level observed in patients who have never been infected. So, investigation of HCV pathogenesis is still warranted. Virus-induced changes in cell metabolism contribute to the development of HCV-associated liver pathologies. Here, we studied the impact of the virus on the metabolism of polyamines and proline as well as on the urea cycle, which plays a crucial role in liver function. It was found that HCV strongly suppresses the expression of arginase, a key enzyme of the urea cycle, leading to the accumulation of arginine, and up-regulates proline oxidase with a concomitant decrease in proline concentrations. The addition of exogenous proline moderately suppressed viral replication. HCV up-regulated transcription but suppressed protein levels of polyamine-metabolizing enzymes. This resulted in a decrease in polyamine content in infected cells. Finally, compounds targeting polyamine metabolism demonstrated pronounced antiviral activity, pointing to spermine and spermidine as compounds affecting HCV replication. These data expand our understanding of HCV’s imprint on cell metabolism.

show abstract

Global landscape of coxsackieviruses in human health

Machado,

Tavares,

Sousa

2024

Virus Research

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Persistent Coxsackievirus B3 Infection in Pancreatic Ductal Cells In Vitro Downregulates Cellular Polyamine Metabolism

Cited by 5 publications

References 32 publications

Hepatitis C Virus Dysregulates Polyamine and Proline Metabolism and Perturbs Urea Cycle

Hepatitis C Virus Dysregulates Polyamine and Proline Metabolism and Perturbs Urea Cycle

Hepatitis C Virus Dysregulates Polyamine and Proline Metabolism and Perturbs the Urea Cycle

Global landscape of coxsackieviruses in human health

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