MitoPerturb-Seq identifies gene-specific single-cell responses to mitochondrial DNA depletion and heteroplasmy Stephen P. Burr, Kathryn Auckland, Angelos Glynos, Abhilesh Dhawanjewar, Cameron Ryall, Wei Wei, Antony Hynes-Allen, Malwina Prater, Matylda Sczaniecka-Clift, Julien Prudent, Patrick F. Chinnery, Jelle van den Ameele Nature Structural and Molecular Biology, 2026 Mitochondria contain their own genome, mitochondrial DNA (mtDNA), which is under strict control by the cell nucleus. mtDNA occurs in many copies per cell and mutations often only affect a proportion of them, giving rise to heteroplasmy. mtDNA copy number and heteroplasmy level together shape the tissue-specific impact of mtDNA mutations, eventually giving rise to both rare mitochondrial and common neurodegenerative diseases. Here, we use MitoPerturb-Seq for CRISPR–Cas9-based, high-throughput single-cell interrogation of the nuclear genes and pathways that sense and control mtDNA copy number and heteroplasmy. We screened a panel of mtDNA maintenance genes in mouse cells with a heteroplasmic mtDNA mt-Ta mutation. This revealed both common and perturbation-specific aspects of the integrated stress response to mtDNA depletion caused by Tfam , Opa1 and Polg knockout. These responses are only partially mediated by ATF4 and cause cell-cycle stage-independent slowing of cell proliferation. MitoPerturb-Seq, thus, provides experimental insight into disease-relevant mitochondrial–nuclear interactions and may inform development of therapies targeting cell-type- and tissue-specific vulnerabilities to mitochondrial dysfunction.
An inherited mitochondrial DNA mutation remodels inflammatory cytokine responses in macrophages and in vivo in mice Eloïse Marques, Stephen P. Burr, Alva M. Casey, Richard J. Stopforth, Chak Shun Yu, Keira Turner, Dane M. Wolf, Marisa Dilucca, Vincent Paupe, Suvagata Roy Chowdhury, Victoria J. Tyrrell, Robbin Kramer, Yamini M. Kanse, Chinmayi Pednekar, Chris A. Powell, James B. Stewart, Julien Prudent, Michael P. Murphy, Michal Minczuk, Valerie B. O’Donnell, Clare E. Bryant, Patrick F. Chinnery, Arthur Kaser, Alexander von Kriegsheim, Dylan G. Ryan Nature Communications, 2025 Impaired mitochondrial bioenergetics in macrophages promotes hyperinflammatory cytokine responses, but whether inherited mtDNA mutations drive similar phenotypes is unknown. Here, we profiled macrophages harbouring a heteroplasmic mitochondrial tRNA Ala mutation ( m.5019A > G ) to address this question. These macrophages exhibit combined respiratory chain defects, reduced oxidative phosphorylation, disrupted cristae architecture, and compensatory metabolic adaptations in central carbon metabolism. Upon inflammatory activation, m.5019A > G macrophages produce elevated type I interferon (IFN), while exhibiting reduced pro-inflammatory cytokines and oxylipins. Mechanistically, suppression of pro-IL-1β and COX2 requires autocrine IFN-β signalling. IFN-β induction is biphasic: an early TLR4-IRF3 driven phase, and a later response involving mitochondrial nucleic acids and the cGAS-STING pathway. In vivo, lipopolysaccharide (LPS) challenge of m.5019A > G mice results in elevated type I IFN signalling and exacerbated sickness behaviour. These findings reveal that a pathogenic mtDNA mutation promotes an imbalanced innate immune response, which has potential implications for the progression of pathology in mtDNA disease patients.
Ubiquitin-mediated mitophagy regulates the inheritance of mitochondrial DNA mutations Michele Frison, Brandon S. Lockey, Yu Nie, Zoe Golder, Eleni Theiaspra, Cameron D. Ryall, Camilla Lyons, Stephen P. Burr, Malwina Prater, Lyuba V. Bozhilova, Angelos Glynos, James B. Stewart, Nick S. Jones, Marcos R. Chiaratti, Patrick F. Chinnery Science, 2025 Mitochondrial synthesis of adenosine triphosphate is essential for eukaryotic life but is dependent on the cooperation of two genomes: nuclear and mitochondrial DNA (mtDNA). mtDNA mutates ~15 times as fast as the nuclear genome, challenging this symbiotic relationship. Mechanisms must have evolved to moderate the impact of mtDNA mutagenesis but are poorly understood. Here, we observed purifying selection of a mouse mtDNA mutation modulated by Ubiquitin-specific peptidase 30 ( Usp30 ) during the maternal-zygotic transition. In vitro, Usp30 inhibition recapitulated these findings by increasing ubiquitin-mediated mitochondrial autophagy (mitophagy). We also found that high mutant burden, or heteroplasmy, impairs the ubiquitin-proteasome system, explaining how mutations can evade quality control to cause disease. Inhibiting USP30 unleashes latent mitophagy, reducing mutant mtDNA in high-heteroplasmy cells. These findings suggest a potential strategy to prevent mitochondrial disorders.
LRPPRC and SLIRP synergize to maintain sufficient and orderly mammalian mitochondrial translation Diana Rubalcava-Gracia, Kristina Bubb, Fredrik Levander, Stephen P Burr, Amelie V August, Patrick F Chinnery, Camilla Koolmeister, Nils-Göran Larsson Nucleic Acids Research, 2024 In mammals, the leucine-rich pentatricopeptide repeat protein (LRPPRC) and the stem-loop interacting RNA-binding protein (SLIRP) form a complex in the mitochondrial matrix that is required throughout the life cycle of most mitochondrial mRNAs. Although pathogenic mutations in the LRPPRC and SLIRP genes cause devastating human mitochondrial diseases, the in vivo function of the corresponding proteins is incompletely understood. We show here that loss of SLIRP in mice causes a decrease of complex I levels whereas other OXPHOS complexes are unaffected. We generated knock-in mice to study the in vivo interdependency of SLIRP and LRPPRC by mutating specific amino acids necessary for protein complex formation. When protein complex formation is disrupted, LRPPRC is partially degraded and SLIRP disappears. Livers from Lrpprc knock-in mice had impaired mitochondrial translation except for a marked increase in the synthesis of ATP8. Furthermore, the introduction of a heteroplasmic pathogenic mtDNA mutation (m.C5024T of the tRNAAla gene) into Slirp knockout mice causes an additive effect on mitochondrial translation leading to embryonic lethality and reduced growth of mouse embryonic fibroblasts. To summarize, we report that the LRPPRC/SLIRP protein complex is critical for maintaining normal complex I levels and that it also coordinates mitochondrial translation in a tissue-specific manner.
MTFP1 controls mitochondrial fusion to regulate inner membrane quality control and maintain mtDNA levels Luis Carlos Tábara, Stephen P. Burr, Michele Frison, Suvagata R. Chowdhury, Vincent Paupe, Yu Nie, Mark Johnson, Jara Villar-Azpillaga, Filipa Viegas, Mayuko Segawa, Hanish Anand, Kasparas Petkevicius, Patrick F. Chinnery, Julien Prudent Cell, 2024 Mitochondrial dynamics play a critical role in cell fate decisions and in controlling mtDNA levels and distribution. However, the molecular mechanisms linking mitochondrial membrane remodeling and quality control to mtDNA copy number (CN) regulation remain elusive. Here, we demonstrate that the inner mitochondrial membrane (IMM) protein mitochondrial fission process 1 (MTFP1) negatively regulates IMM fusion. Moreover, manipulation of mitochondrial fusion through the regulation of MTFP1 levels results in mtDNA CN modulation. Mechanistically, we found that MTFP1 inhibits mitochondrial fusion to isolate and exclude damaged IMM subdomains from the rest of the network. Subsequently, peripheral fission ensures their segregation into small MTFP1-enriched mitochondria (SMEM) that are targeted for degradation in an autophagic-dependent manner. Remarkably, MTFP1-dependent IMM quality control is essential for basal nucleoid recycling and therefore to maintain adequate mtDNA levels within the cell.
Origins of tissue and cell-type specificity in mitochondrial DNA (mtDNA) disease Stephen P Burr, Patrick F Chinnery Human Molecular Genetics, 2024 Mutations of mitochondrial (mt)DNA are a major cause of morbidity and mortality in humans, accounting for approximately two thirds of diagnosed mitochondrial disease. However, despite significant advances in technology since the discovery of the first disease-causing mtDNA mutations in 1988, the comprehensive diagnosis and treatment of mtDNA disease remains challenging. This is partly due to the highly variable clinical presentation linked to tissue-specific vulnerability that determines which organs are affected. Organ involvement can vary between different mtDNA mutations, and also between patients carrying the same disease-causing variant. The clinical features frequently overlap with other non-mitochondrial diseases, both rare and common, adding to the diagnostic challenge. Building on previous findings, recent technological advances have cast further light on the mechanisms which underpin the organ vulnerability in mtDNA diseases, but our understanding is far from complete. In this review we explore the origins, current knowledge, and future directions of research in this area.
Cell lineage-specific mitochondrial resilience during mammalian organogenesis Stephen P. Burr, Florian Klimm, Angelos Glynos, Malwina Prater, Pamella Sendon, Pavel Nash, Christopher A. Powell, Marie-Lune Simard, Nina A. Bonekamp, Julia Charl, Hector Diaz, Lyuba V. Bozhilova, Yu Nie, Haixin Zhang, Michele Frison, Maria Falkenberg, Nick Jones, Michal Minczuk, James B. Stewart, Patrick F. Chinnery Cell, 2023 Mitochondrial activity differs markedly between organs, but it is not known how and when this arises. Here we show that cell lineage-specific expression profiles involving essential mitochondrial genes emerge at an early stage in mouse development, including tissue-specific isoforms present before organ formation. However, the nuclear transcriptional signatures were not independent of organelle function. Genetically disrupting intra-mitochondrial protein synthesis with two different mtDNA mutations induced cell lineage-specific compensatory responses, including molecular pathways not previously implicated in organellar maintenance. We saw downregulation of genes whose expression is known to exacerbate the effects of exogenous mitochondrial toxins, indicating a transcriptional adaptation to mitochondrial dysfunction during embryonic development. The compensatory pathways were both tissue and mutation specific and under the control of transcription factors which promote organelle resilience. These are likely to contribute to the tissue specificity which characterizes human mitochondrial diseases and are potential targets for organ-directed treatments.
High-throughput single-cell analysis reveals progressive mitochondrial DNA mosaicism throughout life Angelos Glynos, Lyuba V. Bozhilova, Michele Frison, Stephen Burr, James B. Stewart, Patrick F. Chinnery Science Advances, 2023 Heteroplasmic mitochondrial DNA (mtDNA) mutations are a major cause of inherited disease and contribute to common late-onset human disorders. The late onset and clinical progression of mtDNA-associated disease is thought to be due to changing heteroplasmy levels, but it is not known how and when this occurs. Performing high-throughput single-cell genotyping in two mouse models of human mtDNA disease, we saw unanticipated cell-to-cell differences in mtDNA heteroplasmy levels that emerged prenatally and progressively increased throughout life. Proliferating spleen cells and nondividing brain cells had a similar single-cell heteroplasmy variance, implicating mtDNA or organelle turnover as the major force determining cell heteroplasmy levels. The two different mtDNA mutations segregated at different rates with no evidence of selection, consistent with different rates of random genetic drift in vivo, leading to the accumulation of cells with a very high mutation burden at different rates. This provides an explanation for differences in severity seen in human diseases caused by similar mtDNA mutations.
Measuring Single-Cell Mitochondrial DNA Copy Number and Heteroplasmy using Digital Droplet Polymerase Chain Reaction Stephen P. Burr, Patrick F. Chinnery Journal of Visualized Experiments, 2022 The mammalian mitochondrial (mt)DNA is a small, circular, double-stranded, intra-mitochondrial DNA molecule, encoding 13 subunits of the electron transport chain. Unlike the diploid nuclear genome, most cells contain many more copies of mtDNA, ranging from less than 100 to over 200,000 copies depending on cell type. MtDNA copy number is increasingly used as a biomarker for a number of age-related degenerative conditions and diseases, and thus, accurate measurement of the mtDNA copy number is becoming a key tool in both research and diagnostic settings. Mutations in the mtDNA, often occurring as single nucleotide polymorphisms (SNPs) or deletions, can either exist in all copies of the mtDNA within the cell (termed homoplasmy) or as a mixture of mutated and WT mtDNA copies (termed heteroplasmy). Heteroplasmic mtDNA mutations are a major cause of clinical mitochondrial pathology, either in rare diseases or in a growing number of common late-onset diseases such as Parkinson's disease. Determining the level of heteroplasmy present in cells is a critical step in the diagnosis of rare mitochondrial diseases and in research aimed at understanding common late-onset disorders where mitochondria may play a role. MtDNA copy number and heteroplasmy have traditionally been measured by quantitative (q)PCR-based assays or deep sequencing. However, the recent introduction of ddPCR technology has provided an alternative method for measuring both parameters. It offers several advantages over existing methods, including the ability to measure absolute mtDNA copy number and sufficient sensitivity to make accurate measurements from single cells even at low copy numbers. Presented here is a detailed protocol describing the measurement of mtDNA copy number in single cells using ddPCR, referred to as droplet generation PCR henceforth, with the option for simultaneous measurement of heteroplasmy in cells with mtDNA deletions. The possibility of expanding this method to measure heteroplasmy in cells with mtDNA SNPs is also discussed.
Oxygen tension modulates the mitochondrial genetic bottleneck and influences the segregation of a heteroplasmic mtDNA variant in vitro Mikael G. Pezet, Aurora Gomez-Duran, Florian Klimm, Juvid Aryaman, Stephen Burr, Wei Wei, Mitinori Saitou, Julien Prudent, Patrick F. Chinnery Communications Biology, 2021 Most humans carry a mixed population of mitochondrial DNA (mtDNA heteroplasmy) affecting ~1–2% of molecules, but rapid percentage shifts occur over one generation leading to severe mitochondrial diseases. A decrease in the amount of mtDNA within the developing female germ line appears to play a role, but other sub-cellular mechanisms have been implicated. Establishing an in vitro model of early mammalian germ cell development from embryonic stem cells, here we show that the reduction of mtDNA content is modulated by oxygen and reaches a nadir immediately before germ cell specification. The observed genetic bottleneck was accompanied by a decrease in mtDNA replicating foci and the segregation of heteroplasmy, which were both abolished at higher oxygen levels. Thus, differences in oxygen tension occurring during early development likely modulate the amount of mtDNA, facilitating mtDNA segregation and contributing to tissue-specific mutation loads.
FIH Regulates Cellular Metabolism through Hydroxylation of the Deubiquitinase OTUB1 Carsten C. Scholz, Javier Rodriguez, Christina Pickel, Stephen Burr, Jacqueline-alba Fabrizio, Karen A. Nolan, Patrick Spielmann, Miguel A. S. Cavadas, Bianca Crifo, Doug N. Halligan, James A. Nathan, Daniel J. Peet, Roland H. Wenger, Alex Von Kriegsheim, Eoin P. Cummins, Cormac T. Taylor Plos Biology, 2016
Research briefing J van den Ameele, SP Burr Nature Structural & Molecular Biology 33, 565-566 , 2026 2026
MitoPerturb-Seq identifies gene-specific single-cell responses to mitochondrial DNA depletion and heteroplasmy SP Burr, K Auckland, A Glynos, A Dhawanjewar, C Ryall, W Wei, ... Nature Structural & Molecular Biology, 1-13 , 2026 2026
An inherited mitochondrial DNA mutation remodels inflammatory cytokine responses in macrophages and in vivo in mice E Marques, SP Burr, AM Casey, RJ Stopforth, CS Yu, K Turner, DM Wolf, ... Nature Communications 16 (1), 10222 , 2025 2025 Citations: 8
An inherited mitochondrial DNA mutation remodels inflammatory cytokine 1 responses in macrophages and in vivo 2 E Marques, SP Burr, AM Casey, RJ Stopforth, CS Yu, K Turner, DM Wolf, ... in vivo 83, 3 , 2025 2025
Ubiquitin-mediated mitophagy regulates the inheritance of mitochondrial DNA mutations M Frison, BS Lockey, Y Nie, Z Golder, E Theiaspra, CD Ryall, C Lyons, ... Science 390 (6769), 156-163 , 2025 2025 Citations: 8
MitoPerturb-Seq identifies common and gene-specific single-cell responses to mitochondrial DNA depletion and heteroplasmy SP Burr, K Auckland, A Glynos, A Dhawanjewar, W Wei, C Ryall, ... bioRxiv, 2025.07. 08.663208 , 2025 2025
An inherited mtDNA mutation remodels inflammatory cytokine responses in macrophages and in vivo E Marques, SP Burr, AM Casey, RJ Stopforth, CS Yu, K Turner, DM Wolf, ... bioRxiv, 2025.01. 05.631298 , 2025 2025 Citations: 1
LRPPRC and SLIRP synergize to maintain sufficient and orderly mammalian mitochondrial translation D Rubalcava-Gracia, K Bubb, F Levander, SP Burr, AV August, ... Nucleic acids research 52 (18), 11266-11282 , 2024 2024 Citations: 26
MTFP1 controls mitochondrial fusion to regulate inner membrane quality control and maintain mtDNA levels LC Tábara, SP Burr, M Frison, SR Chowdhury, V Paupe, Y Nie, ... Cell 187 (14), 3619-3637. e27 , 2024 2024 Citations: 111
Origins of tissue and cell-type specificity in mitochondrial DNA (mtDNA) disease SP Burr, PF Chinnery Human Molecular Genetics 33 (R1), R3-R11 , 2024 2024 Citations: 29
High-throughput single-cell analysis reveals progressive mitochondrial DNA mosaicism throughout life A Glynos, LV Bozhilova, M Frison, S Burr, JB Stewart, PF Chinnery Science advances 9 (43), eadi4038 , 2023 2023 Citations: 26
Cell lineage-specific mitochondrial resilience during mammalian organogenesis SP Burr, F Klimm, A Glynos, M Prater, P Sendon, P Nash, CA Powell, ... Cell 186 (6), 1212-1229. e21 , 2023 2023 Citations: 37
Measuring single-cell mitochondrial DNA copy number and heteroplasmy using digital droplet polymerase chain reaction SP Burr, PF Chinnery JoVE (Journal of Visualized Experiments), e63870 , 2022 2022 Citations: 20
Mitochondrial DNA heteroplasmy is modulated during oocyte development propagating mutation transmission H Zhang, M Esposito, MG Pezet, J Aryaman, W Wei, F Klimm, ... Science Advances 7 (50), eabi5657 , 2021 2021 Citations: 46
Oxygen tension modulates the mitochondrial genetic bottleneck and influences the segregation of a heteroplasmic mtDNA variant in vitro MG Pezet, A Gomez-Duran, F Klimm, J Aryaman, S Burr, W Wei, M Saitou, ... Communications Biology 4 (1), 584 , 2021 2021 Citations: 14
Haploid genetic screening identifies a novel regulator of BMPR2 B Dunmore, S Burr, P Upton, J Nathan, N Morrell European Respiratory Journal 56 (suppl 64) , 2020 2020
ABHD11 maintains 2-oxoglutarate metabolism by preserving functional lipoylation of the 2-oxoglutarate dehydrogenase complex PSJ Bailey, BM Ortmann, AW Martinelli, JW Houghton, ASH Costa, ... Nature communications 11 (1), 4046 , 2020 2020 Citations: 57
Heredity and segregation of mtDNA SP Burr, PF Chinnery The Human Mitochondrial Genome, 87-107 , 2020 2020 Citations: 6
The mitochondrial DNA genetic bottleneck: inheritance and beyond H Zhang, SP Burr, PF Chinnery Essays in biochemistry 62 (3), 225-234 , 2018 2018 Citations: 181
MARCH6 and TRC8 facilitate the quality control of cytosolic and tail‐anchored proteins S Stefanovic‐Barrett, AS Dickson, SP Burr, JC Williamson, IT Lobb, ... The EMBO Reports 19 (5), EMBR201745603 , 2018 2018 Citations: 97
MOST CITED SCHOLAR PUBLICATIONS
Mitochondrial protein lipoylation and the 2-oxoglutarate dehydrogenase complex controls HIF1α stability in aerobic conditions SP Burr, ASH Costa, GL Grice, RT Timms, IT Lobb, P Freisinger, RB Dodd, ... Cell metabolism 24 (5), 740-752 , 2016 2016 Citations: 184
The mitochondrial DNA genetic bottleneck: inheritance and beyond H Zhang, SP Burr, PF Chinnery Essays in biochemistry 62 (3), 225-234 , 2018 2018 Citations: 181
Mesenchymal stromal cells and regulatory T cells: the Yin and Yang of peripheral tolerance? SP Burr, F Dazzi, OA Garden Immunology and cell biology 91 (1), 12-18 , 2013 2013 Citations: 167
The vacuolar-ATPase complex and assembly factors, TMEM199 and CCDC115, control HIF1α prolyl hydroxylation by regulating cellular iron levels AL Miles, SP Burr, GL Grice, JA Nathan elife 6, e22693 , 2017 2017 Citations: 119
MTFP1 controls mitochondrial fusion to regulate inner membrane quality control and maintain mtDNA levels LC Tábara, SP Burr, M Frison, SR Chowdhury, V Paupe, Y Nie, ... Cell 187 (14), 3619-3637. e27 , 2024 2024 Citations: 111
FIH regulates cellular metabolism through hydroxylation of the deubiquitinase OTUB1 CC Scholz, J Rodriguez, C Pickel, S Burr, J Fabrizio, KA Nolan, ... PLoS biology 14 (1), e1002347 , 2016 2016 Citations: 111
MARCH6 and TRC8 facilitate the quality control of cytosolic and tail‐anchored proteins S Stefanovic‐Barrett, AS Dickson, SP Burr, JC Williamson, IT Lobb, ... The EMBO Reports 19 (5), EMBR201745603 , 2018 2018 Citations: 97
Mitochondria and hypoxia: metabolic crosstalk in cell-fate decisions D Bargiela, SP Burr, PF Chinnery Trends in Endocrinology & Metabolism 29 (4), 249-259 , 2018 2018 Citations: 71
Mitochondrial DNA heteroplasmy and purifying selection in the mammalian female germ line SP Burr, M Pezet, PF Chinnery Development, growth & differentiation 60 (1), 21-32 , 2018 2018 Citations: 71
ABHD11 maintains 2-oxoglutarate metabolism by preserving functional lipoylation of the 2-oxoglutarate dehydrogenase complex PSJ Bailey, BM Ortmann, AW Martinelli, JW Houghton, ASH Costa, ... Nature communications 11 (1), 4046 , 2020 2020 Citations: 57
Mitochondrial DNA heteroplasmy is modulated during oocyte development propagating mutation transmission H Zhang, M Esposito, MG Pezet, J Aryaman, W Wei, F Klimm, ... Science Advances 7 (50), eabi5657 , 2021 2021 Citations: 46
Cell lineage-specific mitochondrial resilience during mammalian organogenesis SP Burr, F Klimm, A Glynos, M Prater, P Sendon, P Nash, CA Powell, ... Cell 186 (6), 1212-1229. e21 , 2023 2023 Citations: 37
Origins of tissue and cell-type specificity in mitochondrial DNA (mtDNA) disease SP Burr, PF Chinnery Human Molecular Genetics 33 (R1), R3-R11 , 2024 2024 Citations: 29
LRPPRC and SLIRP synergize to maintain sufficient and orderly mammalian mitochondrial translation D Rubalcava-Gracia, K Bubb, F Levander, SP Burr, AV August, ... Nucleic acids research 52 (18), 11266-11282 , 2024 2024 Citations: 26
High-throughput single-cell analysis reveals progressive mitochondrial DNA mosaicism throughout life A Glynos, LV Bozhilova, M Frison, S Burr, JB Stewart, PF Chinnery Science advances 9 (43), eadi4038 , 2023 2023 Citations: 26
Measuring single-cell mitochondrial DNA copy number and heteroplasmy using digital droplet polymerase chain reaction SP Burr, PF Chinnery JoVE (Journal of Visualized Experiments), e63870 , 2022 2022 Citations: 20
Oxygen tension modulates the mitochondrial genetic bottleneck and influences the segregation of a heteroplasmic mtDNA variant in vitro MG Pezet, A Gomez-Duran, F Klimm, J Aryaman, S Burr, W Wei, M Saitou, ... Communications Biology 4 (1), 584 , 2021 2021 Citations: 14
An inherited mitochondrial DNA mutation remodels inflammatory cytokine responses in macrophages and in vivo in mice E Marques, SP Burr, AM Casey, RJ Stopforth, CS Yu, K Turner, DM Wolf, ... Nature Communications 16 (1), 10222 , 2025 2025 Citations: 8
Ubiquitin-mediated mitophagy regulates the inheritance of mitochondrial DNA mutations M Frison, BS Lockey, Y Nie, Z Golder, E Theiaspra, CD Ryall, C Lyons, ... Science 390 (6769), 156-163 , 2025 2025 Citations: 8
Potential evidence for biotype-specific chemokine profile following BVDV infection of bovine macrophages S Burr, C Thomas, J Brownlie, V Offord, TJ Coffey, D Werling Veterinary immunology and immunopathology 150 (1-2), 123-127 , 2012 2012 Citations: 8
