• E-mailValentyn.Oksenych@uib.no
  • Visitor Address
    Haukeland universitetssykehus, Laboratoriebygget
    5009 Bergen
  • Postal Address
    Postboks 7804
    5020 Bergen

Academic interests

DNA in our cells is constantly damaged by various internal and external factors. To maintain genomic stability, the cells develop multiple DNA repair pathways. Mutations in DNA repair genes lead to disorders in humans. Non-Homologous End-Joining (NHEJ) fixes the DNA double-strand breaks (DSB) throughout the cell cycle. NHEJ is required for the development of immune and nervous systems and to suppress medulloblastoma.

NHEJ consists of Ku70, Ku80, XLF, XRCC4, DNA Ligase 4, DNA-PKcs, Artemis, XLS/PAXX, APLF, Mri/Cyren. There is a complex genetic interaction between the NHEJ factors (eg, Oksenych et al., PNAS, 2013; Xing et al., DNA repair, 2017; Castaneda-Zegarra et al., DNA repair, 2019; Xing and Oksenych, FEBS open bio, 2019; Castaneda-Zegarra et al., Aging, 2020; Castaneda-Zegarra et al., Scandinavian Journal of Immunology, 2020).

In response to DNA damage, there is a complex process that includes the activation of multiple enzymes and modifications of proteins, such as histones surrounding the DSBs. This process is called the DNA damage response (DDR) pathway. It is facilitated by protein kinases ATM and DNA-PKcs, scaffold proteins MDC1 and 53BP1, ubiquitin-ligases RNF8 and RNF168, and many other proteins. During the DDR, histones are phosphorylated, ubiquitylated, methylated, acetylated, SUMOylated, NEDDylated, etc (Zha et al., Nature, 2011; Oksencyh et al., PNAS, 2012; Kumar et al., DNA repair, 2014; Beck et al. al., Biomolecules, 2020). I am attempting to understand the complexity of DDR, as well as its role in the development of the immune system and in cancer suppression.

Both NHEJ and DDR pathways are involved in immune system development, including the V(D)J recombination in developing B and T lymphocytes, and the Class Switch Recombination (CSR) in mature B cells.

Translocations associated with V(D)J recombination and class switch recombination (CSR) can be detected using High Throughput Genome-Wide Translocation sequencing (HTGTS). I collaborate with researchers at Karolinska Institutet and Harvard Medical School to develop HTGTS-based assays using primary human B cells.

Several drug candidates were identified to be used in cancer and immune disease treatments. I collaborate with researchers at UiO and local hospitals to validate and select the best options for further translation to the clinic. 


2015-2022. Researcher, principal investigator. NTNU – Trondheim, Norway

2021-2022. Lecturer. University of Stavanger, Stavanger, Norway

2020-2022.Researcher. University of Oslo, Oslo, Norway

2020-2020. Researcher. The Arctic University of Norway – Tromsø (UiT)

2018-2020. Visiting Researcher. Karolinska Institutet, Sweden

2014-2015. Postdoc. University of Copenhagen, Denmark

2010-2014. Postdoc. Harvard Medical School, USA

2005-2009. PhD candidate. IGBMC, University of Strasbourg, France

Past projects and awards 

2020-2021. Karolinska Institutet (KI Foundations and Funds). #2020-02155

2020-2021. Health Authority of Central Norway#38811

2019-2022. Award in innovation, enabling technologies, NTNU, Norway

2018-2019. NTNU PES and POS grants, Norway

2018-2019. Research Council of Norway, FRIPRO#291217

2017-2021. Outstanding Academic Fellow Award, NTNU, Norway

2017-2020. Norwegian Cancer Society, Open call#182355

2016-2019. Research Council of Norway, FRIMEDBIO#249774

2016-2018. Research Council of Norway, FRIPRO#270491

2016-2018. Health Authority of Central Norway#13477

2015-2017. Lundbeck Fellowship, University of Copenhagen, Denmark

2008-2009. Anti-Cancer Research Association (ARC), France

2007-2008. Anti-Cancer Research Association (ARC), France

2005 Mobility grant, IBB – Academy of Science, Warsaw, Poland

HUIMM320 Basal immunologi (Basic immunology)

Academic article
  • Show author(s) (2023). Tyrosine Kinase Inhibitors Target B Lymphocytes. Biomolecules.
  • Show author(s) (2023). Therapeutic Effectiveness of Interferon-α2b against COVID-19 with Community-Acquired Pneumonia: The Ukrainian Experience. International Journal of Molecular Sciences.
  • Show author(s) (2023). The F/B ratio as a biomarker for inflammation in COVID-19 and T2D: Impact of metformin. Biomedicine & Pharmacotherapy.
  • Show author(s) (2023). Metformin Therapy Changes Gut Microbiota Alpha-Diversity in COVID-19 Patients with Type 2 Diabetes: The Role of SARS-CoV-2 Variants and Antibiotic Treatment. Pharmaceuticals.
  • Show author(s) (2022). Seven classes of antiviral agents. Cellular and Molecular Life Sciences (CMLS).
  • Show author(s) (2022). Oral Administration of Myelin Oligodendrocyte Glycoprotein Attenuates Experimental Autoimmune Encephalomyelitis through Induction of Th2/Treg Cells and Suppression of Th1/Th17 Immune Responses. Current Issues in Molecular Biology. 5728-5740.
  • Show author(s) (2022). Novel Synergistic Anti-Enteroviral Drug Combinations. Viruses. 7 pages.
  • Show author(s) (2022). DrugVirus.info 2.0: an integrative data portal for broad-spectrum antivirals (BSA) and BSA-containing drug combinations (BCCs). Nucleic Acids Research (NAR). W272-W275.
  • Show author(s) (2021). Synergistic interferon-alpha-based combinations for treatment of sars-cov-2 and other viral infections. Viruses. 1-18.
  • Show author(s) (2021). Nafamostat–interferon-α combination suppresses sars-cov-2 infection in vitro and in vivo by cooperatively targeting host tmprss2. Viruses. 1-8.
  • Show author(s) (2021). Active components of commonly prescribed medicines affect influenza a virus–host cell interaction: A pilot study. Viruses. 1-14.
  • Show author(s) (2021). Acetyltransferases GCN5 and PCAF Are Required for B Lymphocyte Maturation in Mice. Biomolecules. 1-10.
  • Show author(s) (2020). Potential Antiviral Options against SARS-CoV-2 Infection. Viruses. Viruses. E642.
  • Show author(s) (2020). Non-Homologous End Joining Factors XLF, PAXX and DNA-PKcs Maintain the Neural Stem and Progenitor Cell Population. Biomolecules. 1-13.
  • Show author(s) (2020). Mediator of DNA Damage Checkpoint Protein 1 Facilitates V(D)J Recombination in Cells Lacking DNA Repair Factor XLF. Biomolecules.
  • Show author(s) (2020). Leaky severe combined immunodeficiency in mice lacking non-homologous end joining factors XLF and MRI. Aging. 23578-23597.
  • Show author(s) (2020). Identification and Tracking of Antiviral Drug Combinations. Viruses.
  • Show author(s) (2020). Chemical, Physical and Biological Triggers of Evolutionary Sonserved Bcl-xL-Mediated Apoptosis. Cancers. 1-19.
  • Show author(s) (2019). Synthetic lethality between DNA repair factors Xlf and Paxx is rescued by inactivation of Trp53. DNA Repair. 164-169.
  • Show author(s) (2019). Low temperature and low UV indexes correlated with peaks of influenza virus activity in Northern Europe during 2010-2018. Viruses. 1-10.
  • Show author(s) (2019). Genetic interaction between DNA repair factors PAXX, XLF, XRCC4 and DNA-PKcs in human cells. FEBS Open Bio. 1315-1326.
  • Show author(s) (2019). Generation of a mouse model lacking the non-homologous end-joining factor Mri/Cyren. Biomolecules. 1-13.
  • Show author(s) (2019). Common nodes of virus-host interaction revealed through an integrated network analysis. Frontiers in Immunology. 12 pages.
  • Show author(s) (2018). Robust DNA repair in PAXX-deficient mammalian cells. FEBS Open Bio. 442-448.
  • Show author(s) (2018). Novel activities of safe-in-human broad-spectrum antiviral agents. Antiviral Research. 174-182.
  • Show author(s) (2018). Normal development of mice lacking PAXX, the paralogue of XRCC4 and XLF. FEBS Open Bio. 426-434.
  • Show author(s) (2017). Synthetic lethality between murine DNA repair factors XLF and DNA-PKcs is rescued by inactivation of Ku70. DNA Repair. 133-138.
  • Show author(s) (2017). Antiviral properties of chemical inhibitors of cellular anti-apoptotic Bcl-2 proteins. Viruses.
Academic lecture
  • Show author(s) (2019). Critical Nodes of Virus–Host Interaction Revealed Through an Integrated Network Analysis.
  • Show author(s) (2019). Critical Nodes of Viral Modulation Revealed Through an Integrated Network Analysis of Host-Virus Interaction Landscape.
  • Show author(s) (2023). Editorial: Plasticity of immune cells in tumor microenvironment. Frontiers in Oncology.
  • Show author(s) (2023). DNA Repair and Immune Response: Editorial. Biomolecules.
  • Show author(s) (2022). Broad-Spectrum Antivirals and Antiviral Drug Combinations. Viruses.
  • Show author(s) (2022). Broad-Spectrum Antivirals and Antiviral Combinations: An Editorial Update. Viruses.
  • Show author(s) (2021). DNA Damage Response. Biomolecules. 1-3.
  • Show author(s) (2021). DNA Damage Response. Biomolecules.
Academic literature review
  • Show author(s) (2023). The Intersection of COVID-19 and Metabolic-Associated Fatty Liver Disease: An Overview of the Current Evidence. Viruses.
  • Show author(s) (2023). Efficacy of interferon alpha for the treatment of hospitalized patients with COVID-19: A meta-analysis. Frontiers in Immunology. 8 pages.
  • Show author(s) (2022). Weil’s Disease — Immunopathogenesis, Multiple Organ Failure, and Potential Role of Gut Microbiota. Biomolecules. 1-17.
  • Show author(s) (2022). Seven classes of antiviral agents. Cellular and Molecular Life Sciences (CMLS).
  • Show author(s) (2022). Mono- and combinational drug therapies for global viral pandemic preparedness. iScience.
  • Show author(s) (2022). Immunoregulatory Intestinal Microbiota and COVID-19 in Patients with Type Two Diabetes: A Double-Edged Sword. Viruses. 1-21.
  • Show author(s) (2020). Interaction between Fibroblasts and Immune Cells Following DNA Damage Induced by Ionizing Radiation . International Journal of Molecular Sciences. 1-15.
  • Show author(s) (2020). Genetic interaction between the non‐homologous end joining factors during B and T lymphocyte development: in vivo mouse models. Scandinavian Journal of Immunology. 1-9.
  • Show author(s) (2020). Discovery and development of safe-in-man broad-spectrum antiviral agents. International Journal of Infectious Diseases. 268-276.

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