ArticleThe Journal of biological chemistry2016
The Non-structural Protein of Crimean-Congo Hemorrhagic Fever Virus Disrupts the Mitochondrial Membrane Potential and Induces Apoptosis.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 91 citations in OpenAlex.
- Pathogenicity and virulence of Crimean-Congo hemorrhagic fever virus: From enzootic maintenance to severe human disease.Virulence · 2026Review
- Evaluation of hematological and biochemical parameters in the differential diagnosis of Crimean-Congo hemorrhagic fever and brucellosis: insights from a large patient cohort.BMC infectious diseases · 2026Article
- Review
- Venturing into host-pathogen interaction in Crimean-Congo hemorrhagic fever to highlight terra incognita.Frontiers in immunology · 2026Review
- Crimean-Congo hemorrhagic fever virus NSm protein inhibits the type I interferon signaling by binding to STAT2.PLoS neglected tropical diseases · 2025Article
- NSs: the multifaceted bunyavirus virulence factor.Npj viruses · 2025Review
- Crimean-Congo Hemorrhagic Fever Disease: Relationship Between Clinical Course and Apoptosis.Infectious diseases & clinical microbiology · 2025Article
- Lymphopenia: An early indicator of Crimean-Congo haemorrhagic fever.Tropical medicine & international health : TM & IH · 2025Article
- Review
- Article
- The Role of Nucleocapsid Protein (NP) in the Immunology of Crimean-Congo Hemorrhagic Fever Virus (CCHFV).Viruses · 2024Review
- Cellular immunity to nucleoproteins (NP) of Crimean-Congo hemorrhagic fever virus (CCHFV) and Hazara Virus (HAZV).Medical microbiology and immunology · 2024Article
- Article
- Recent Advances in Crimean-Congo Hemorrhagic Fever Virus Detection, Treatment, and Vaccination: Overview of Current Status and Challenges.Biological procedures online · 2024Review
- Article
- Vaccine approaches and treatment aspects against Crimean Congo hemorrhagic fever.Virusdisease · 2024Review
- Alternative translation contributes to the generation of a cytoplasmic subpopulation of the Junín virus nucleoprotein that inhibits caspase activation and innate immunity.Journal of virology · 2024Article
- Screening for Mitochondrial tRNA Variants in 200 Patients with Systemic Lupus Erythematosus.Human heredity · 2024Article
- Indirubin, an Active Component of Indigo Naturalis, Exhibits Inhibitory Effects on Leukemia CellsAnti-cancer agents in medicinal chemistry · 2024Article
- Nonstructural protein NS17 of grass carp reovirus Honghu strain promotes virus infection by mediating cell-cell fusion and apoptosis.Virus research · 2023Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viruses have developed distinct strategies to overcome the host defense system. Regulation of apoptosis in response to viral infection is important for virus survival and dissemination. Like other viruses, Crimean-Congo hemorrhagic fever virus (CCHFV) is known to regulate apoptosis. This study, for the first time, suggests that the non-structural protein NSs of CCHFV, a member of the genus Nairovirus, induces apoptosis. In this report, we demonstrated the expression of CCHFV NSs, which contains 150 amino acid residues, in CCHFV-infected cells. CCHFV NSs undergoes active degradation during infection. We further demonstrated that ectopic expression of CCHFV NSs induces apoptosis, as reflected by caspase-3/7 activity and cleaved poly(ADP-ribose) polymerase, in different cell lines that support CCHFV replication. Using specific inhibitors, we showed that CCHFV NSs induces apoptosis via both intrinsic and extrinsic pathways. The minimal active region of the CCHFV NSs protein was determined to be 93-140 amino acid residues. Using alanine scanning, we demonstrated that Leu-127 and Leu-135 are the key residues for NSs-induced apoptosis. Interestingly, CCHFV NSs co-localizes in mitochondria and also disrupts the mitochondrial membrane potential. We also demonstrated that Leu-127 and Leu-135 are important residues for disruption of the mitochondrial membrane potential by NSs. Therefore, these results indicate that the C terminus of CCHFV NSs triggers mitochondrial membrane permeabilization, leading to activation of caspases, which, ultimately, leads to apoptosis. Given that multiple factors contribute to apoptosis during CCHFV infection, further studies are needed to define the involvement of CCHFV NSs in regulating apoptosis in infected cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.