Неструктурный Белок 1 Вируса Клещевого Энцефалита Активирует Экспрессию Субъединиц Иммунопротеасомы

Кузьменко, Ю. В.; Kuzmenko, Yulia; Starodubova, Elizaveta; Karganova, Galina G.; Тимофеев, А В; Карпов, В.Л.

doi:10.7868/s0026898416020129

Cited by 2 publications

(1 citation statement)

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“…The authors believe that in this case an active antioxidant process in combination with the prevalence of a constitutive proteasome is beneficial for the survival of the infected cell. In our previous studies we have shown that in TBEV NS1-expressing cells the concentration of immunoproteasome subunits is increased [42]. This upregulation can be caused by increased ROS as was shown in the current study.…”

Section: Discussionmentioning

confidence: 72%

Nonstructural Protein 1 of Tick-Borne Encephalitis Virus Induces Oxidative Stress and Activates Antioxidant Defense by the Nrf2/ARE Pathway

Kuzmenko

Smirnova²,

Ivanov³

et al. 2016

Intervirology

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Background: Infection with tick-borne encephalitis virus (TBEV) causes pathological changes in the central nervous system. However, the possible redox alterations in the infected cells that can contribute to the virus pathogenicity remain unknown. Objective: In the current study we explored the ability of TBEV nonstructural protein 1 (NS1) to induce oxidative stress and activate antioxidant defense via the nuclear factor (erythroid-derived-2)-like 2/antioxidant response element (Nrf2/ARE) pathway. Methods: HEK 293T cells were transfected with plasmid encoding NS1 protein, and the production of reactive oxygen species (ROS) was measured using oxidation-sensitive dyes, the activation of the ARE promoter was estimated using a reporter plasmid, and the expression of phase II detoxifying enzymes was quantified by measuring their mRNA levels using RT-qPCR. Results: A high level of ROS production was detected in cells transfected with NS1-expressing plasmid. In addition, this protein activated the promoter with an ARE and upregulated the transcription of ARE-dependent genes that encode phase II enzymes. Conclusion: TBEV NS1 protein both triggers ROS production and activates a defense Nrf2/ARE pathway. These data suggest that a role of redox-mediated processes in TBEV-induced damage of the central nervous system should also be explored. These data can contribute to a better understanding of TBEV pathogenicity, further improvement of TBE treatment, and the development of vaccine candidates against this infection.

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Section: Discussionmentioning

confidence: 72%

Nonstructural Protein 1 of Tick-Borne Encephalitis Virus Induces Oxidative Stress and Activates Antioxidant Defense by the Nrf2/ARE Pathway

Kuzmenko

Smirnova²,

Ivanov³

et al. 2016

Intervirology

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Activation of Early Proinflammatory Responses by TBEV NS1 Varies between the Strains of Various Subtypes

Starodubova

Tuchynskaya

Kuzmenko

et al. 2023

IJMS

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Tick-borne encephalitis (TBE) is an emerging zoonosis that may cause long-term neurological sequelae or even death. Thus, there is a growing interest in understanding the factors of TBE pathogenesis. Viral genetic determinants may greatly affect the severity and consequences of TBE. In this study, nonstructural protein 1 (NS1) of the tick-borne encephalitis virus (TBEV) was tested as such a determinant. NS1s of three strains with similar neuroinvasiveness belonging to the European, Siberian and Far-Eastern subtypes of TBEV were studied. Transfection of mouse cells with plasmids encoding NS1 of the three TBEV subtypes led to different levels of NS1 protein accumulation in and secretion from the cells. NS1s of TBEV were able to trigger cytokine production either in isolated mouse splenocytes or in mice after delivery of NS1 encoding plasmids. The profile and dynamics of TNF-α, IL-6, IL-10 and IFN-γ differed between the strains. These results demonstrated the involvement of TBEV NS1 in triggering an immune response and indicated the diversity of NS1 as one of the genetic factors of TBEV pathogenicity.

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Неструктурный Белок 1 Вируса Клещевого Энцефалита Активирует Экспрессию Субъединиц Иммунопротеасомы

Cited by 2 publications

References 0 publications

Nonstructural Protein 1 of Tick-Borne Encephalitis Virus Induces Oxidative Stress and Activates Antioxidant Defense by the Nrf2/ARE Pathway

Nonstructural Protein 1 of Tick-Borne Encephalitis Virus Induces Oxidative Stress and Activates Antioxidant Defense by the Nrf2/ARE Pathway

Activation of Early Proinflammatory Responses by TBEV NS1 Varies between the Strains of Various Subtypes

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