Institut für Virologie und Immunbiologie
Refine
Has Fulltext
- yes (267)
Is part of the Bibliography
- yes (267) (remove)
Year of publication
Document Type
- Journal article (221)
- Doctoral Thesis (41)
- Conference Proceeding (3)
- Preprint (2)
Language
- English (267) (remove)
Keywords
- Virologie (33)
- HIV (18)
- Immunologie (16)
- T cells (15)
- measles virus (12)
- SARS-CoV-2 (11)
- Dendritische Zelle (7)
- dendritic cells (7)
- regulatory T cells (7)
- T-Lymphozyt (5)
- immune evasion (5)
- CD28 (4)
- COVID-19 (4)
- Lymphozyt (4)
- Ratte (4)
- T cell (4)
- autoimmunity (4)
- cell staining (4)
- ceramides (4)
- monocytes (4)
- sphingolipids (4)
- sphingomyelinase (4)
- Dendritic cells (3)
- Immunreaktion (3)
- Masernvirus (3)
- Maus (3)
- Medizin (3)
- Parkinson’s disease (3)
- South Africa (3)
- T cell receptor (3)
- Toleranz (3)
- antiretroviral therapy (3)
- ceramide (3)
- evolution (3)
- flow cytometry (3)
- gene expression (3)
- herpesvirus (3)
- immunology (3)
- macrophages (3)
- phosphoantigen (3)
- 3D tissue model (2)
- AIDS (2)
- Antigen CD8 (2)
- Antikörper (2)
- Apoptosis (2)
- BTN3 (2)
- Blimp-1 (2)
- CD1d (2)
- CD4(+) (2)
- CTLA-4 (2)
- Candida albicans (2)
- Dendritic cell (2)
- GFAP (2)
- GM-CSF (2)
- HHV-6 (2)
- HIV-Infektion (2)
- Herpes (2)
- Herpesvirus (2)
- Human papillomavirus (2)
- Immunology (2)
- KDELR2 (2)
- ME/CFS (2)
- Natürliche Killerzelle (2)
- Parkinson (2)
- Prion (2)
- Proteinkinase B (2)
- RNA polymerase II (2)
- Spumaviren (2)
- T cell receptors (2)
- TCR (2)
- TGF-BETA (2)
- TNF-alpha (2)
- Tansania (2)
- Tanzania (2)
- Treg (2)
- VLA-1 (2)
- Viren (2)
- Virology (2)
- Virus (2)
- acid ceramidase inhibitor ceranib-2 (2)
- acid sphingomyelinase (2)
- activation (2)
- alpaca (2)
- antibodies (2)
- antigen presentation (2)
- binding protein (2)
- bone marrow (2)
- butyrophilin (2)
- butyrophilin 3 (2)
- cytokine secretion (2)
- cytokines (2)
- cytotoxic T cells (2)
- dendritic cell (2)
- depression (2)
- domain (2)
- expression (2)
- foamy virus (2)
- foamy viruses (2)
- fusion and fission (2)
- gene regulation (2)
- herpes simplex virus (2)
- human (2)
- identification (2)
- in-vivo (2)
- infection (2)
- inflammation (2)
- latency (2)
- lymph nodes (2)
- measels virus (2)
- measles (2)
- miR-30 (2)
- miRNA processing (2)
- mitochondria (2)
- mouse (2)
- neuroprotection (2)
- neutral sphingomyelinase-2 (2)
- peripheral nervous system (2)
- phylogenetic analysis (2)
- plasma membrane (2)
- rat (2)
- replication (2)
- reverse transcriptase (2)
- sialic acid (2)
- small interfering RNAs (2)
- sphingolipid (2)
- sphingosine kinase inhibitor SKI-II (2)
- sphingosine-1-phosphate (2)
- tolerance (2)
- transcription (2)
- translation (2)
- type I interferon (2)
- viral infection (2)
- viral load (2)
- virology (2)
- virus (2)
- virus reactivation (2)
- γδ T cell (2)
- 1,2-benzisothiazolinone (1)
- 2',7'-dichlorofluorescin (1)
- 3D Ko-kulture (1)
- 3D cell culture (1)
- 3D-Modell (1)
- 5`-UTR (1)
- 60-nucleotide duplication (1)
- ABCG2 (1)
- ACH-2 (1)
- AKT-signaling (1)
- APOBEC3G (1)
- ASM (1)
- ATP-adenosine triphosphate (1)
- ATRA (1)
- Actinomycetes (1)
- Activation (1)
- Adaptive cell transfer (1)
- Aktivierung (1)
- Aktivierung <Physiologie> (1)
- Allotransplantation (1)
- Alpha therapy (1)
- Alzheimer’s disease (1)
- Aminobisphosphonat (1)
- Aminobisphosphonate (1)
- Antibody (1)
- Antibody responses (1)
- Antigen CD4 (1)
- Antigen presentation (1)
- Antigenpräsentation (1)
- Antikörperantworten (1)
- Antisense (1)
- Apoptose (1)
- Aspergillus fumigatus (1)
- Auto-antibodies (1)
- Autoimmune diseases (1)
- Autoimmunity (1)
- Autoimmunität (1)
- Autophagie (1)
- Autophagy (1)
- B cells (1)
- B-Lymphozyt (1)
- B-cell (1)
- B-cells (1)
- B-zells (1)
- BBC3 (1)
- BCG (1)
- BK virus (1)
- BTN (1)
- BTN2 (1)
- BTN2A1 (1)
- BTN3A1 (1)
- Bakterien (1)
- Bauchspeicheldrüsenkrebs (1)
- Biologie (1)
- Biomarkers (1)
- Blutbildendes Gewebe (1)
- Bone marrow transplantantation (1)
- Bowen’s disease, periungual (1)
- Braak (1)
- Brugia Malayi (1)
- Bruton Tyrosine Kinase (1)
- Bryophyta (1)
- C-terminal domain (1)
- CCS (1)
- CD 8 (1)
- CD25+CD4+ regulatory T cells (1)
- CD28 costimulation (1)
- CD28 superagonist (1)
- CD28 superagonists (1)
- CD28-SA (1)
- CD39 (1)
- CD4(+) T-cells (1)
- CD4(+)CD25(+) (1)
- CD4+ T cells (1)
- CD46 (1)
- CD4\(^{+}\) T cells (1)
- CD4\(^{+}\) T helper cells (1)
- CD73 (1)
- CD8+ T cells (1)
- CLEC16A (1)
- CMV (1)
- CNS infection (1)
- COVID‐19 (1)
- COVID‐19 vaccination (1)
- CRAC (1)
- CSF (1)
- Ca2+ (1)
- Calu-3 (1)
- Cancer (1)
- Candida (1)
- Cell migration (1)
- Cell signalling (1)
- Ceramid (1)
- Ceramide (1)
- ChIP-seq (1)
- Children (1)
- Cytomegalie-Virus (1)
- Cytotoxicity (1)
- Cytotoxizität (1)
- D665 (1)
- DAPI staining (1)
- DAT (1)
- DETC (1)
- DNA sequence (1)
- DNA transcription (1)
- DNA traps (1)
- Desaktivierung (1)
- Diabetes mellitus (1)
- Diabetes mellitus Typ 1 (1)
- Diagnostik (1)
- Disease genetics (1)
- Disease severity (1)
- Dolutegravir (1)
- Donor lymphocytes (1)
- EBV (1)
- EVER1 (1)
- EVER2 (1)
- Einfluss (1)
- Enterovirus (1)
- Enzyme-linked immunosorbent assay (1)
- Epidemiology (1)
- Epithelzelle (1)
- Escherichia coli infections (1)
- Evaluation (1)
- Expression (1)
- Extracellular domain (1)
- Factor receptor (1)
- Fanconi Anemia (1)
- Farnesyl Pyrophosphate Synthase (1)
- Farnesylpyrophosphatsynthase (FPPS) (1)
- Fibroblasten (1)
- Flt3L (1)
- Flymphozyt (1)
- Foamy virus (1)
- Frühe Gene (1)
- G glycoprotein (1)
- GBS (1)
- GRP78 (1)
- GagPol fusion protein (1)
- Gen (1)
- German people (1)
- Germany (1)
- Glucocorticoid receptor (1)
- Glucocorticosteroide (1)
- Glukocorticioid (1)
- Glukokortikoid Rezeptor (1)
- Golgi (1)
- Graft versus Tumor (1)
- Graft-versus-leukemia (1)
- Granzyme B (1)
- Grippe (1)
- Guillain-Barré-Syndrom (1)
- HAND (1)
- HCMV (1)
- HHV-6A (1)
- HIV Drug resistance (1)
- HIV South Africa (1)
- HIV diagnosis and management (1)
- HIV infections (1)
- HIV neurocognitive impairment (1)
- HIV-1 (1)
- HIV-1 subtype AG (1)
- HIV-1-infected patients (1)
- HIV-1; subtype C; proviral plasmid; viral replication; resistance assays; Vpu; CD317; CD4 (1)
- HTLV-I (1)
- Hamburg (1)
- Herpesviren (1)
- Herpesviruses (1)
- Homing (1)
- Hsp90 (1)
- Human foamy virus bel-l transactivator; Expression in insect cells (1)
- Hypnales (1)
- ICP27 (1)
- ICP4 (1)
- IE3 (1)
- IFN-gamma (1)
- IL-2 (1)
- IL-3 (1)
- IL1RA (1)
- IL‐10 (1)
- Ibrutinib (1)
- IgG (1)
- Immunesupression (1)
- Immunisierung (1)
- Immunität <Medizin> (1)
- Immunological synapse (1)
- Immunosuppression (1)
- Immunstimulation (1)
- Immunsuppression (1)
- Immunsupression (1)
- Immuntoleranz (1)
- Impfstoff (1)
- Impfung (1)
- IncRNA (1)
- Infectious disease (1)
- Influenza (1)
- Integrase (1)
- Integrase inhibitor (1)
- Integrin (1)
- Interaction (1)
- Interferon (1)
- Interferon <gamma-> (1)
- Interferon gamma (1)
- Interferonantagonism (1)
- Interferonantagonismus (1)
- Isopentenyl pyrophosphate (IPP) (1)
- Isopentenyl-pyrophosphat (IPP) (1)
- Isoprenoid Synthesis (1)
- Isoprenoide (1)
- Isoprenoidsynthese (1)
- JCV (1)
- Jurkat cells (1)
- KRAS (1)
- Karibisches Meer (1)
- Kerinokeratosis papulosa (1)
- Kohlenstoff (1)
- Kongress (1)
- Krebs <Medizin> (1)
- LAD (1)
- LFA-1 (1)
- LIF (1)
- Langerhans cells (1)
- Lentivirus (1)
- Ligand (1)
- MCMV (1)
- MEK/ERK-signaling (1)
- MHC I (1)
- MHC II (1)
- MIR-155 (1)
- MPO (1)
- MRI (1)
- MS (1)
- MV receptor (1)
- MV transcription (1)
- Macrophage (1)
- Major depression (1)
- Major splice donor (1)
- Makrophagen (1)
- Malignancies (1)
- Masern (1)
- Masern-Virus (1)
- Measles virus (1)
- Mechanismus (1)
- Medicine (1)
- Mesocestoides corti (1)
- Mineralocorticoid receptor (1)
- Mineralokortikoid Rezeptor (1)
- Mitochondria (1)
- Molekularpathologie (1)
- Monocytes and macrophages (1)
- Monozytendifferenzierung (1)
- Moose (1)
- Motoneuron (1)
- Multiple Sklerose (1)
- Multiple myeloma (1)
- Multiple sclerosis (1)
- Mycobacterium tuberculosis (1)
- Myelin Basic Protein Promoter (1)
- Myeloid-derived suppressor cells (1)
- Myeloma (1)
- N-CAM (1)
- N-oleoyl serinol (1)
- NFAT (1)
- NFATc1 (1)
- NFKB (1)
- NK cells (1)
- NKT (1)
- NKT Zellen (1)
- NKT cells (1)
- NRF2 (1)
- Nail unit (1)
- Nanoröhre (1)
- Neisseria meningitidis (1)
- Neuritis (1)
- NfL (1)
- Notch1 (1)
- Nucleus (1)
- Ovalbumin (1)
- PAR-CLIP (1)
- PARM (1)
- PCI-32765 (1)
- PCLS (1)
- PKB (1)
- PKB/Akt (1)
- PKCζ, (1)
- PML (1)
- PO (1)
- PVM (1)
- Parkinsonism (1)
- Pathogenese (1)
- Pathway (1)
- Persistenz (1)
- Phage Display (1)
- Placebo (1)
- Pneumoviruses (1)
- Po (1)
- Polyadenylation (1)
- Polyadenylierung (1)
- Polymerase chain reaction (1)
- Polyoma-Virus (1)
- Polyomaviren (1)
- Polyomavirus JC (1)
- Prednisolon (1)
- Primaten (1)
- Priming (1)
- Prion protein (1)
- Prionkrankheit (1)
- Prionprotein (1)
- Prodigy (1)
- Prognose (1)
- Proliferation (1)
- Proteine (1)
- R0 (1)
- RAG1 (1)
- REDD1 (1)
- RNA (1)
- RNA Interferenz (1)
- RNA export (1)
- RNA interference (1)
- RNA structure (1)
- RNS (1)
- RNS-Viren (1)
- RQQ domain (1)
- RSV (1)
- RSV-A ON1 (1)
- RT-qPCR (1)
- Regluation (1)
- Regulation (1)
- Regulation of protease activity (1)
- Regulatorische T Zellen (1)
- Regulatorischer T-Lymphozyt (1)
- Regulatory T cells (1)
- Regulatory-cells (1)
- RelB (1)
- Replikation (1)
- Respiratory tract infection (1)
- Retroviren (1)
- Retroviren-Infektion (1)
- Rheumatoid arthritis (1)
- SARS-CoV-2 brain disorders (1)
- SARS‐CoV‐2 (1)
- SARS‐CoV‐2 infection (1)
- SLAM CDW150 (1)
- STEMI (1)
- STIM1 (1)
- STIM2 (1)
- Salmo trutta fario (1)
- Schwämme (1)
- Seahorse XF (1)
- Sekundärmetabolit (1)
- Sequenzanalyse (1)
- Sialylsäure (1)
- Skint1 (1)
- Sphingosine-1-phosphate (1)
- Sphingosine-1-phosphats (1)
- Subtyp C (1)
- Superagonistic antibody (1)
- Suppression (1)
- Synthese (1)
- Südafrika (1)
- T Cells (1)
- T Lymphozyt (1)
- T Zell Selektion (1)
- T Zellen (1)
- T cell activation (1)
- T cell acute lymphoblastic leukemia (1)
- T cell development (1)
- T cell migration (1)
- T cell selection (1)
- T cell silencing (1)
- T cell suppression (1)
- T helper 1 cells (1)
- T helper cell responses (1)
- T- Zelle (1)
- T-ALL (1)
- T-Zelle (1)
- T-cell (1)
- T-zellen (1)
- TAB08 (1)
- TAMs (1)
- TCF1 (1)
- TCF12 (1)
- TCR signaling cascade (1)
- TCRb (1)
- TGN1412 (1)
- TLR2 (1)
- TLR4 (1)
- TNF (1)
- TRDV2 (1)
- TRGV9 (1)
- Tamoxifen (1)
- Targeted Therapies (1)
- Th1 cells (1)
- Thymozyten (1)
- Thymus (1)
- Tiermodell (1)
- Tierversuch (1)
- Tissue engineering (1)
- Tr1 (1)
- Transcription (1)
- Transgen (1)
- Transgene (1)
- Transgene Tiere (1)
- Transkriptionsfaktor (1)
- Tumor Microenvironment (1)
- Tumor-necrosis-factor (1)
- Tumorwachstum (1)
- Uganda (1)
- Vaccination (1)
- Vaccine (1)
- Vero E6 (1)
- Vg9Vd2 T Zellaktivierung (1)
- Vg9Vd2 T cell (1)
- Vgamma9Vdelta2 (1)
- Vietnam (1)
- Viral infections (1)
- Virus-like particles (1)
- Virus-ähnliche Partikel (1)
- Vγ9Vδ2 (1)
- Vγ9Vδ2 T cell (1)
- WASp (1)
- Waxy papulosis of childhood (1)
- Wiskott-Aldrich syndrome (1)
- Zell Migration (1)
- Zelldifferenzierung (1)
- Zellkonjugation (1)
- Zellrezeptor (1)
- Zentralnervensystem (1)
- Zytokine (1)
- acetylsalicylic acid (1)
- acid ceramidase (1)
- acquisition of host regulators (1)
- actins (1)
- acute Graft versus Host Disease (1)
- acute graft-versus-host disease (1)
- acute heart failure (1)
- acute kidney injury (1)
- adaptive immune response (1)
- adenosine (1)
- adhesion (1)
- admission screening (1)
- adoptive transfer (1)
- adult (1)
- age groups (1)
- aging (1)
- allogeneic stem cell transplantation (1)
- alpha-globin (1)
- alternative splicing (1)
- alveoar echinococcosis (1)
- amplicon sequencing (1)
- anemia (1)
- anergy (1)
- angiogenesis (1)
- animal models (1)
- anthocyanin (1)
- anti-depressant drug (1)
- anti-hiv agents (1)
- anti-myocardial (1)
- anti-protease (1)
- anti-retroviral agents (1)
- antidepressants (1)
- antigen-B (1)
- antigenic recall (1)
- antimicrobial resistance (1)
- antiretrovirals (1)
- antiviral activity (1)
- antiviral treatment (1)
- antivirals (1)
- anti‐SARS‐CoV‐2‐spike IgG (1)
- anxiety (1)
- aorta (1)
- aorta ring (1)
- apoptosis (1)
- arthritis (1)
- aspirin (1)
- astaxanthin (1)
- attachment glycoprotein (1)
- autoantibodies (1)
- autoantibody (1)
- azapeptide nitriles (1)
- azido-ceramides (1)
- azidothymidine (1)
- bacteria (1)
- bacterial pathogens (1)
- bilberry (1)
- binding analysis (1)
- biochemical assays (1)
- bioinformatic (1)
- black currant (1)
- black trout syndrome (1)
- blocking opsonization (1)
- blocking phagocytosis (1)
- brain (1)
- brain bank (1)
- brain pathology (1)
- brain stem (1)
- branch point (1)
- brown trout (1)
- butyrophilin 2A1 (1)
- butyrophilins (1)
- cDC2 subset (1)
- calcium (1)
- calnexin (1)
- cancer microenvironment (1)
- canine distemper virus (1)
- cardiac magnetic resonance imaging (1)
- cardiorespiratory centre (1)
- caveolin-1 (Cav-1) (1)
- cell cycle and cell division (1)
- cell differentiation (1)
- cell line specificity pyridyl indole carboxylates (1)
- cell line-specificity (1)
- cell membrane (1)
- cell membrane model (1)
- cell migration (1)
- cell-cycle dependence (1)
- cells (1)
- cellular receptor (1)
- cellular stress responses (1)
- central-nervous-system (1)
- ceramidase (1)
- cerebrospinal fluid (1)
- channel (1)
- characterization and analytical techniques (1)
- chikungunya virus (1)
- child (1)
- children (1)
- cholera (1)
- cholesteryl ester (1)
- chondrogenesis (1)
- chromatin (1)
- chronic rhinosinusitis (1)
- circulation patterns (1)
- cis-acting sequences (1)
- co-evolution (1)
- co-stimulation, (1)
- coevolution (1)
- cognitive dysfunction (1)
- complement (1)
- complement factor H (1)
- complex (1)
- conversion (1)
- coronavirus (1)
- criteria (1)
- critically ill (1)
- cross-linking (1)
- cryptic peptides (1)
- cytokine release (1)
- cytokine release syndrome (1)
- cytokine responses (1)
- cytoskeleton (1)
- decay (1)
- defective ribosomal products (1)
- degradation (1)
- demyelination (1)
- dengue virus (1)
- diacylglycerol (1)
- diagnostic (1)
- diet (1)
- differential diagnosis (1)
- differentiation (1)
- direct-acting antivirals (1)
- disease severity (1)
- diversity (1)
- dmrt1 (1)
- dna-binding protein (1)
- dogs (1)
- dopamine (1)
- drug adherence (1)
- drug discovery (1)
- drug interactions (1)
- embryo (1)
- encephalitis (1)
- endothelial cell infection (1)
- endothelial cells (1)
- enhance viral transcription (1)
- env leader protein (1)
- enzyme-linked immunoassays (1)
- enzymes (1)
- epicutaneous (1)
- epitope mapping (1)
- epitope specificity (1)
- epstein-barr virus (1)
- exclusion criteria (1)
- excretory-secretory (1)
- factor H (1)
- fibroblasts (1)
- fluorescence-activated cell sorting (1)
- fluoxetine (1)
- foamy retrovirus (1)
- foamyviruses (1)
- fungal infection (1)
- gamma-interferon (1)
- gammadelta T cells (1)
- gene delivery (1)
- gene-expression (1)
- genetic conservation (1)
- genetic interference (1)
- genetic variability (1)
- genetics (1)
- glial damage (1)
- glial fibrillary acidic protein (1)
- glucocorticoid (1)
- glycolipids (1)
- glycoproteins (1)
- glycosphingolipids (1)
- granulosus (1)
- granzyme B (1)
- group B genotype (1)
- group-A (1)
- guidelines (1)
- hACE2 (1)
- healthcare workers (1)
- heart (1)
- heart failure (1)
- helminth infection (1)
- helminths (1)
- hemagglutinin (1)
- hematological disorders (1)
- hepadnaviruses (1)
- heroine (1)
- herpes virus (1)
- highly-active antiretroviral therapy (1)
- histones (1)
- homeostasis (1)
- homing (1)
- host shutoff (1)
- host-pathogen interactions (1)
- human behaviour (1)
- human bocavirus (1)
- human cytomegalovirus (HCMV) (1)
- human immunodeficiency virus (1)
- human peripheral blood (1)
- humans (1)
- hydatid disease (1)
- immediate early genes (1)
- immune activation (1)
- immune cells (1)
- immune control (1)
- immune escape (1)
- immune neuromelanin (1)
- immune response (1)
- immune suppression (1)
- immune therapy (1)
- immuno suppression (1)
- immunoglobulin superfamily (1)
- immunomodulatory (1)
- immunoprecipitation (1)
- immunosuppression (1)
- immunosurveillance (1)
- immunotherapy (1)
- improves survival (1)
- in vitro culture (1)
- in vivo (1)
- indinavir (1)
- inducible deletion (1)
- inducible nitric oxide synthase (1)
- infarction size (1)
- infected mice (1)
- infected-cell protein (1)
- infection control (1)
- infection spread (1)
- infectivity assays (1)
- influenza (1)
- influenza A virus (1)
- influenza virus (1)
- injecting drug users (1)
- innate immune response (1)
- innate lymphoid cells (1)
- interferon (1)
- interferon signaling (1)
- interferon γ (1)
- interleukin 1 receptor antagonist (1)
- interleukins (1)
- kidneys (1)
- large gene lists (1)
- larvae (1)
- lethality rate (1)
- leukemia (1)
- lipids (1)
- liposome (1)
- lithium (1)
- long terminal repeat (1)
- luciferase assay (1)
- lymphocyte activation (1)
- lymphomas (1)
- lyso-phospholipids (1)
- lytic infection (1)
- mTORC1 (1)
- magnetic properties and materials (1)
- major depression (1)
- major histocompatibility complex (1)
- management (1)
- marine sponge (1)
- mechanism (1)
- mediated suppression (1)
- medical (1)
- medical research (1)
- memory B cells (1)
- meningococcal disease (1)
- mesenchymal stem cell (1)
- messenger RNA (1)
- metacestode vesicles (1)
- mevalonate pathway (1)
- miRNA (1)
- miRNA target (1)
- miRNS (1)
- mice (1)
- microRNA (1)
- microbial mutation (1)
- microbiology (1)
- migration (1)
- molecular biology (1)
- molecular characterization (1)
- monocyte (1)
- monocyte differentiation (1)
- moonlighting (1)
- morbilliviruses (1)
- morphine (1)
- mortality (1)
- mothers (1)
- motif discovery (1)
- motifs (1)
- motility (1)
- mouse models (1)
- movement disorders (1)
- mukosale Immunantwort (1)
- multi-drug resistance (1)
- multihit targeting (1)
- multiple myeloma (1)
- multiple sclerosis (1)
- murine cytomegalovirus (MCMV) (1)
- murine model (1)
- mutant mice (1)
- mutation databases (1)
- mycobacteria (1)
- myelin (1)
- myeloid-derived suppressor cell (MDSC) (1)
- myeloid-derived suppressor cells (MDSC) (1)
- myeloid-derived suppressor cells (MDSCs) (1)
- myocardial infarction (1)
- naloxone (1)
- nanobiocomposites (1)
- nanoparticles (1)
- nasal polyps (1)
- necrosis-factor-alpha (1)
- nervous-system (1)
- neurodegeneration (1)
- neurofilament light chain (1)
- neuroinflammation (1)
- neuroinvasion (1)
- neurological symptoms/disorders (1)
- neurovirulence (1)
- neutral sphingomyelinase (1)
- neutral sphingomyelinase 2 (1)
- next generation sequencing (1)
- nine-banded armadillo (1)
- non-canonical translation (1)
- non-nucleoside reverse transcriptase inhibitors (1)
- nucleosides (1)
- oligomers (1)
- opioids (1)
- ortholog (1)
- orthoreovirus (1)
- outpatients (1)
- ovarian cancer (1)
- oxidative phosphorylation (1)
- oxidative stress (1)
- pH-regulated antigen 1 (Pra1) (1)
- pancreatic cancer (1)
- parainfluenza virus (1)
- parasitic diseases (1)
- parasitology (1)
- pathogenesis (1)
- pediatric infections (1)
- pediatrics (1)
- pellet culture (1)
- peptidomimetics (1)
- peripheral tolerance (1)
- persistierende Infektion (1)
- perspectives (1)
- phagocytosis (1)
- phosphoantigens (1)
- phospholipidosis (1)
- piscine orthoreovirus (1)
- placental mammals (1)
- plasminogen (1)
- pneumona virus (1)
- pol messenger-rna (1)
- polarization (1)
- poly(A) site usage (1)
- polyadenylation (1)
- polymicrobial sepsis (1)
- polymorphism (1)
- polyomavirus (1)
- polyomaviruses (1)
- population coverage (1)
- postmortem studies (1)
- pre-messenger RNA (1)
- precision-cut lung slices (1)
- prediction (1)
- prevention (1)
- primary cells (1)
- proliferative darkening syndrome (1)
- promoter-proximal pausing (1)
- protease inhibitors (1)
- protein regulation and expression (1)
- protein sequencing (1)
- proteomic analysis (1)
- protocol (1)
- public health medicine (1)
- purine-rich element (1)
- quality of life (1)
- randomized controlled clinical trial (1)
- randomized controlled-trial (1)
- reactivation (1)
- recognition (1)
- recombinant proteins (1)
- recombination (1)
- regulation (1)
- regulatory T cells (Treg) (1)
- regulatory protein ICP27 (1)
- remdesivir (1)
- resistance (1)
- respiratory syncytial virus (1)
- respiratory tract (1)
- restriction factors (1)
- retroviral infection (1)
- retroviral proteins (1)
- retroviral vectors (1)
- retroviruses (1)
- reverse transcriptase inhibitors (1)
- reverse transcriptase-polymerase chain reaction (1)
- reverse-transcriptase (1)
- reverse-transcriptase inhibitors (1)
- ribonuclease H (1)
- routine clinical-practice (1)
- salicylic acid (1)
- self-reactivity (1)
- sepsis (1)
- sequence (1)
- sequence databases (1)
- seroprevalence (1)
- serum (1)
- sex-determining gene (1)
- shock (1)
- signal transduction (1)
- simian foamy viruses (1)
- sphingomonads (1)
- sphingosine 1-phosphate (1)
- sphingosine kinase (1)
- spleen (1)
- splice regulation (1)
- splicing (1)
- splicing inhibition (1)
- spread (1)
- steady state (1)
- steady-state dendritic cells (1)
- sterol pathway (1)
- strains (1)
- stress (1)
- stroke (1)
- subacute sclerosing-panencephalitis (1)
- subgroup-B (1)
- subviral particle release (1)
- surface transport (1)
- surfactants (1)
- surveillance (1)
- tanzania (1)
- terminal gag domain (1)
- testing strategy (1)
- the microtubule-organizing center (1)
- therapy (1)
- thermal stresses (1)
- thymocyte (1)
- tissue (1)
- tolerogenic dendritic cells (1)
- toll-like receptors (1)
- toxins (1)
- transcription factors (1)
- transcriptional profiling (1)
- transcriptional termination (1)
- transcriptomics (1)
- transcutaneous (1)
- transduction (1)
- transient regulatory T-cell targeting (1)
- transmembrane protein (1)
- tumor (1)
- tumor associated macrophages (1)
- tumour immunology (1)
- type 1 (1)
- type 1 ICP27 (1)
- tyrosine (1)
- ultraviolet radiation (1)
- unwindase (1)
- vaccination and immunization (1)
- vaccinia virus (1)
- vero cells (1)
- vesicles (1)
- viral epidemiology (1)
- viral miRNAs (1)
- viral microRNAs (1)
- viral pathology (1)
- viral replication (1)
- viral shedding (1)
- virale Proteine (1)
- virulence (1)
- virus budding (1)
- virus entry (1)
- virus host interaction (1)
- virus replication (1)
- virus vectors (1)
- virus-induced encephalitis (1)
- viruses (1)
- vitamin-D-receptor (1)
- vivo (1)
- wild-type (1)
- world health organization (1)
- α-synuclein-specific T cells (1)
- γδ T cells (1)
- γδ TCR (1)
Institute
- Institut für Virologie und Immunbiologie (267)
- Theodor-Boveri-Institut für Biowissenschaften (26)
- Graduate School of Life Sciences (18)
- Medizinische Klinik und Poliklinik II (13)
- Institut für Hygiene und Mikrobiologie (8)
- Institut für Organische Chemie (8)
- Pathologisches Institut (8)
- Neurologische Klinik und Poliklinik (7)
- Kinderklinik und Poliklinik (5)
- Klinik und Poliklinik für Dermatologie, Venerologie und Allergologie (5)
Sonstige beteiligte Institutionen
- Datenintegrationszentrum Würzburg (DIZ) (1)
- Interdisziplinäre Biomaterial- und Datenbank Würzburg (ibdw) (1)
- Interdisziplinäres Zentrum für Klinische Forschung (ZIKF), Würzburg (1)
- Joslin Diabetes Center, Harvard Medical School (1)
- Roche Diagnostics GmbH Penzberg (1)
- University of Stellenbosch, Division of Medical Virology (1)
EU-Project number / Contract (GA) number
- 721016 (4)
- 101041177 (1)
- 249177 (1)
- 677673 (1)
- 825575 (1)
- 955974 (1)
- CoG 721016–HERPES (1)
- ERC-2016-CoG 721016-HERPES (1)
MDSCs are suppressive immune cells with a high relevance in various pathologies including cancer, autoimmunity, and chronic infections. Surface marker expression of MDSCs resembles monocytes and neutrophils which have immunostimulatory functions instead of suppressing T cells. Therefore, finding specific surface markers for MDSCs is important for MDSC research and therapeutic MDSC manipulation. In this study, we analyzed if the integrin VLA-1 has the potential as a novel MDSC marker. VLA-1 was expressed by M-MDSCs but not by G-MDSCs as well as by Teff cells. VLA-1 deficiency did not impact iNOS expression, the distribution of M-MDSC and G-MDSC subsets, and the suppressive capacity of MDSCs towards naïve and Teff cells in vitro. In mice, VLA-1 had no effect on the homing capability of MDSCs to the spleen, which is a major reservoir for MDSCs. Since the splenic red pulp contains collagen IV and VLA-1 binds collagen IV with a high affinity, we found MDSCs and Teff cells in this area as expected. We showed that T cell suppression in the spleen, indicated by reduced T cell recovery and proliferation as well as increased apoptosis and cell death, partially depended on VLA-1 expression by the MDSCs. In a mouse model of multiple sclerosis, MDSC injection prior to disease onset led to a decrease of the disease score, and this effect was significantly reduced when MDSCs were VLA-1 deficient. The expression of Sema7A by Teff cells, a ligand for VLA-1 which is implicated in negative T cell regulation, resulted in a slightly stronger Teff cell suppression by MDSCs compared to Sema7A deficient T cells. Live cell imaging and intravital 2-photon microscopy showed that the interaction time of MDSCs and Teff cells was shorter when MDSCs lacked VLA 1 expression, however VLA-1 expression had no impact on MDSC mobility. Therefore, the VLA-1-dependent interaction of MDSC and Teff cells on collagen IV in the splenic red pulp is implicated MDSC-mediated Teff cell suppression.
Gene expression in eukaryotic cells is regulated by the combinatorial action of numerous gene-regulatory factors, among which microRNAs (miRNAs) play a fundamental role at the post-transcriptional level. miRNAs are single-stranded, small non-coding RNA molecules that emerge in a cascade-like fashion via the generation of primary and precursor miRNAs. Mature miRNAs become functional when incorporated into the RNA induced silencing complex (RISC). miRNAs guide RISCs to target mRNAs in a sequence-specific fashion. To this end, base-pairs are usually formed between the miRNA seed region, spanning nucleotide positions 2 to 8 (from the 5' end) and the 3'UTR of the target mRNA. Once miRNA-mRNA interaction is established, RISC represses translation and occasionally induces direct or indirect target mRNA degradation. Interestingly, miRNAs are expressed not only in every multicellular organism but are also encoded by several viruses, predominately by herpesviruses. By controlling both, cellular as well as viral mRNA transcripts, virus-encoded miRNAs confer many beneficial effects on viral growth and persistence. Murine cytomegalovirus (MCMV) is a ß-herpesvirus and so far, 29 mature MCMV-encoded miRNAs have been identified during lytic infection. Computational analysis of previously conducted photoactivated ribonucleotide-enhanced individual nucleotide resolution crosslinking immunoprecipitation (PAR-iCLIP) experiments identified a read cluster within the 3' untranslated region (3'UTR) of the immediate early 3 (IE3) transcript in MCMV. Based on miRNA target predictions, two highly abundant MCMV miRNAs, namely miR-m01-2-3p and miR-M23-2-3p were found to potentially bind to two closely positioned target sites within the IE3 PAR-iCLIP peak. To confirm this hypothesis, we performed luciferase assays and showed that activity values of a luciferase fused with the 3'UTR of IE3 were downregulated in the presence of miR-m01- 2 and miR-M23-2. In a second step, we investigated the effect of pre-expression of miR-m01-2 and miR-M23-2 on the induction of virus replication. After optimizing the transfection procedure by comparing different reagents and conditions, plaque formation was monitored. We could demonstrate that the replication cycle of the wild-type but not of our MCMV mutant that harbored point mutations in both miRNA binding sites within the IE3-3'UTR, was significantly delayed in the presence of miR-m01-2 and miR-M23-2. This confirmed that miR-m01-2 and miR-M23-2 functionally target the major transcription factor IE3 which acts as an indispensable regulator of viral gene expression during MCMV lytic infection. Repression of the major immediate early genes by viral miRNAs is a conserved feature of cytomegaloviruses. The functional role of this type of regulation can now be studied in the MCMV mouse model.
Recently, Tummino et al. reported that 34 compounds, including Chloroquine and Fluoxetine, inhibit SARS-CoV-2 replication by inducing phospholipidosis, although Chloroquine failed to suppress viral replication in Calu-3 cells and patients. In contrast, Fluoxetine represses viral replication in human precision-cut lung slices (PCLS) and Calu-3 cells. Thus, it is unlikely that these compounds have similar mechanisms of action. Here, we analysed a subset of these compounds in the viral replication and phospholipidosis assays using the Calu-3 cells and PCLS as the patient-near system. Trimipramine and Chloroquine induced phospholipidosis but failed to inhibit SARS-CoV-2 replication in Calu-3 cells, which contradicts the reported findings and the proposed mechanism. Fluoxetine, only slightly induced phospholipidosis in Calu-3 cells but reduced viral replication by 2.7 orders of magnitude. Tilorone suppressed viral replication by 1.9 orders of magnitude in Calu-3 cells without causing phospholipidosis. Thus, induction of phospholipidosis is not correlated with the inhibition of SARS-CoV-2, and the compounds act via other mechanisms. However, we show that compounds, such as Amiodarone, Tamoxifen and Tilorone, with antiviral activity on Calu-3 cells, also inhibited viral replication in human PCLS. Our results indicate that antiviral assays against SARS-CoV-2 are cell-line specific. Data from Vero E6 can lead to non-transferable results, underlining the importance of an appropriate cell system for analysing antiviral compounds against SARS-CoV-2. We observed a correlation between the active compounds in Calu-3 cells and PCLS.
Psychosocial factors affect mental health and health-related quality of life (HRQL) in a complex manner, yet gender differences in these interactions remain poorly understood. We investigated whether psychosocial factors such as social support and personal and work-related concerns impact mental health and HRQL differentially in women and men during the first year of the COVID-19 pandemic. Between June and October 2020, the first part of a COVID-19-specific program was conducted within the “Characteristics and Course of Heart Failure Stages A-B and Determinants of Progression (STAAB)” cohort study, a representative age- and gender-stratified sample of the general population of Würzburg, Germany. Using psychometric networks, we first established the complex relations between personal social support, personal and work-related concerns, and their interactions with anxiety, depression, and HRQL. Second, we tested for gender differences by comparing expected influence, edge weight differences, and stability of the networks. The network comparison revealed a significant difference in the overall network structure. The male (N = 1370) but not the female network (N = 1520) showed a positive link between work-related concern and anxiety. In both networks, anxiety was the most central variable. These findings provide further evidence that the complex interplay of psychosocial factors with mental health and HRQL decisively depends on gender. Our results are relevant for the development of gender-specific interventions to increase resilience in times of pandemic crisis.
Immune checkpoint blockade therapy is beneficial and even curative for some cancer patients. However, the majority don’t respond to immune therapy. Across different tumor types, pre-existing T cell infiltrates predict response to checkpoint-based immunotherapy. Based on in vitro pharmacological studies, mouse models and analyses of human melanoma patients, we show that the cytokine GDF-15 impairs LFA-1/β2-integrin-mediated adhesion of T cells to activated endothelial cells, which is a pre-requisite of T cell extravasation. In melanoma patients, GDF-15 serum levels strongly correlate with failure of PD-1-based immune checkpoint blockade therapy. Neutralization of GDF-15 improves both T cell trafficking and therapy efficiency in murine tumor models. Thus GDF-15, beside its known role in cancer-related anorexia and cachexia, emerges as a regulator of T cell extravasation into the tumor microenvironment, which provides an even stronger rationale for therapeutic anti-GDF-15 antibody development.
Herpes simplex virus 1 (HSV-1) infection and stress responses disrupt transcription termination by RNA Polymerase II (Pol II). In HSV-1 infection, but not upon salt or heat stress, this is accompanied by a dramatic increase in chromatin accessibility downstream of genes. Here, we show that the HSV-1 immediate-early protein ICP22 is both necessary and sufficient to induce downstream open chromatin regions (dOCRs) when transcription termination is disrupted by the viral ICP27 protein. This is accompanied by a marked ICP22-dependent loss of histones downstream of affected genes consistent with impaired histone repositioning in the wake of Pol II. Efficient knock-down of the ICP22-interacting histone chaperone FACT is not sufficient to induce dOCRs in ΔICP22 infection but increases dOCR induction in wild-type HSV-1 infection. Interestingly, this is accompanied by a marked increase in chromatin accessibility within gene bodies. We propose a model in which allosteric changes in Pol II composition downstream of genes and ICP22-mediated interference with FACT activity explain the differential impairment of histone repositioning downstream of genes in the wake of Pol II in HSV-1 infection.
Recently, we have shown that C6-ceramides efficiently suppress viral replication by trapping the virus in lysosomes. Here, we use antiviral assays to evaluate a synthetic ceramide derivative α-NH2-ω-N3-C6-ceramide (AKS461) and to confirm the biological activity of C6-ceramides inhibiting SARS-CoV-2. Click-labeling with a fluorophore demonstrated that AKS461 accumulates in lysosomes. Previously, it has been shown that suppression of SARS-CoV-2 replication can be cell-type specific. Thus, AKS461 inhibited SARS-CoV-2 replication in Huh-7, Vero, and Calu-3 cells up to 2.5 orders of magnitude. The results were confirmed by CoronaFISH, indicating that AKS461 acts comparable to the unmodified C6-ceramide. Thus, AKS461 serves as a tool to study ceramide-associated cellular and viral pathways, such as SARS-CoV-2 infections, and it helped to identify lysosomes as the central organelle of C6-ceramides to inhibit viral replication.
Recently, we have described novel pyridyl indole esters and peptidomimetics as potent inhibitors of the severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) main protease. Here, we analysed the impact of these compounds on viral replication. It has been shown that some antivirals against SARS-CoV-2 act in a cell line-specific way. Thus, the compounds were tested in Vero, Huh-7, and Calu-3 cells. We showed that the protease inhibitors at 30 µM suppress viral replication by up to 5 orders of magnitude in Huh-7 cells, while in Calu-3 cells, suppression by 2 orders of magnitude was achieved. Three pyridin-3-yl indole-carboxylates inhibited viral replication in all cell lines, indicating that they might repress viral replication in human tissue as well. Thus, we investigated three compounds in human precision-cut lung slices and observed donor-dependent antiviral activity in this patient-near system. Our results provide evidence that even direct-acting antivirals may act in a cell line-specific manner.
Butyrophilin (BTN)–3A and BTN2A1 molecules control the activation of human Vγ9Vδ2 T cells during T cell receptor (TCR)-mediated sensing of phosphoantigens (PAg) derived from microbes and tumors. However, the molecular rules governing PAg sensing remain largely unknown. Here, we establish three mechanistic principles of PAg-mediated γδ T cell activation. First, in humans, following PAg binding to the intracellular BTN3A1-B30.2 domain, Vγ9Vδ2 TCR triggering involves the extracellular V-domain of BTN3A2/BTN3A3. Moreover, the localization of both protein domains on different chains of the BTN3A homo-or heteromers is essential for efficient PAg-mediated activation. Second, the formation of BTN3A homo-or heteromers, which differ in intracellular trafficking and conformation, is controlled by molecular interactions between the juxtamembrane regions of the BTN3A chains. Finally, the ability of PAg not simply to bind BTN3A-B30.2, but to promote its subsequent interaction with the BTN2A1-B30.2 domain, is essential for T-cell activation. Defining these determinants of cooperation and the division of labor in BTN proteins improves our understanding of PAg sensing and elucidates a mode of action that may apply to other BTN family members.
The genomes of both human cytomegalovirus (HCMV) and murine cytomegalovirus (MCMV) were first sequenced over 20 years ago. Similar to HCMV, the MCMV genome had initially been proposed to harbor ≈170 open reading frames (ORFs). More recently, omics approaches revealed HCMV gene expression to be substantially more complex comprising several hundred viral ORFs. Here, we provide a state-of-the art reannotation of lytic MCMV gene expression based on integrative analysis of a large set of omics data. Our data reveal 365 viral transcription start sites (TiSS) that give rise to 380 and 454 viral transcripts and ORFs, respectively. The latter include 200 small ORFs, some of which represented the most highly expressed viral gene products. By combining TiSS profiling with metabolic RNA labelling and chemical nucleotide conversion sequencing (dSLAM-seq), we provide a detailed picture of the expression kinetics of viral transcription. This not only resulted in the identification of a novel MCMV immediate early transcript encoding the m166.5 ORF, which we termed ie4, but also revealed a group of well-expressed viral transcripts that are induced later than canonical true late genes and contain an initiator element (Inr) but no TATA- or TATT-box in their core promoters. We show that viral upstream ORFs (uORFs) tune gene expression of longer viral ORFs expressed in cis at translational level. Finally, we identify a truncated isoform of the viral NK-cell immune evasin m145 arising from a viral TiSS downstream of the canonical m145 mRNA. Despite being ≈5-fold more abundantly expressed than the canonical m145 protein it was not required for downregulating the NK cell ligand, MULT-I. In summary, our work will pave the way for future mechanistic studies on previously unknown cytomegalovirus gene products in an important virus animal model.