GO:0035457 cellular response to interferon-alpha: Signaling Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0035457 describes how a single cell changes its state or activity after receiving an interferon-alpha (IFN-alpha) stimulus, a type I interferon.
• The response is cell-type specific: microglia mount a broader and more divergent transcriptional response to IFN-alpha than astrocytes.
• IFN-alpha signaling shapes antiviral immunity, including anti-HBV cellular immune responses that depend on B cells.
• Impaired IFN-alpha responsiveness in CD8+ T and NK cells is linked to poor therapy outcomes in chronic hepatitis B.
• Viruses can actively delay or suppress the IFN-alpha response, as shown for Crimean-Congo hemorrhagic fever virus and SARS-CoV-2.
• Studying GO:0035457 requires cell models that preserve or perturb the IFN-alpha response, which can be built with CRISPR knockout, knock-in, and overexpression approaches.
Description
GO:0035457, cellular response to interferon-alpha, is a biological process ontology term that captures any change in a cell's state or activity, such as movement, secretion, enzyme production, or gene expression, that occurs as a result of an interferon-alpha stimulus. Interferon-alpha is a type I interferon, and the cellular response to it is a central node in antiviral defense, immune regulation, and intercellular communication. Because the term is defined at the level of the responding cell, it is distinct from organism-level or tissue-level interferon responses and is especially useful for interpreting single-cell and cell-culture experiments. The importance of GO:0035457 for researchers lies in its broad mechanistic reach. In chronic hepatitis B, interferon-alpha therapy depends on the ability of immune cells to respond, and B cells are required for interferon-alpha to facilitate an anti-HBV cellular immune response. In the same disease context, bile acid metabolism can impair the response of CD8+ T and NK cells to interferon-alpha, linking cellular metabolism to interferon responsiveness. In the central nervous system, microglia and astrocytes differ substantially in their response to interferon-alpha, showing that the process is cell-type specific even within one tissue. Viral pathogens also intersect directly with GO:0035457. Crimean-Congo hemorrhagic fever virus delays activation of the innate immune response, which includes interferon-alpha-related signaling, and SARS-CoV-2 replication is promoted when interferon-alpha and interferon-gamma responses are suppressed through Huwe1-mediated Miz1 degradation. These examples show why GO:0035457 is a practical framework for studying host-pathogen interactions, immunotherapy response, and immune cell engineering.
cellular response to interferon-alpha At A Glance
| GO ID | GO:0035457 |
|---|---|
| GO term | cellular response to interferon-alpha |
| Ontology | biological_process |
| Synonym | cellular response to leukocyte interferon; cellular response to lymphoblast interferon; cellular response to lymphoblastoid interferon; cellular response to interferon alfa-n1; cellular response to interferon alfa-n3 |
| Major function | Captures changes in cell state or activity, including movement, secretion, enzyme production, and gene expression, after an interferon-alpha stimulus |
| Stimulus | Interferon-alpha, a type I interferon |
| Cell-type specificity | The response differs between cell types, for example microglia versus astrocytes |
| Disease relevance | Chronic hepatitis B, hepatitis D, COVID-19, and Crimean-Congo hemorrhagic fever |
| Research relevance | Used to interpret immune cell function, antiviral defense, and therapy response |
What Is GO:0035457?
In plain terms, GO:0035457 is the set of cellular changes triggered when a cell encounters interferon-alpha. The QuickGO definition states that it is any process that results in a change in state or activity of a cell, including movement, secretion, enzyme production, and gene expression, as a result of an interferon-alpha stimulus, where interferon-alpha is a type I interferon. Synonyms include cellular response to interferon alfa-n1, cellular response to interferon alfa-n3, cellular response to leukocyte interferon, cellular response to lymphoblast interferon, and cellular response to lymphoblastoid interferon. The term is a biological process and is narrower than the general response to type I interferon because it is specifically anchored to interferon-alpha.
Why Is cellular response to interferon-alpha Important in Cell Biology?
GO:0035457 matters because interferon-alpha is a frontline cytokine in antiviral immunity and immunotherapy, and the cellular response to it determines whether a cell mounts an effective antiviral program or fails to do so. In chronic hepatitis B, the ability of B cells to support an interferon-alpha-driven anti-HBV cellular immune response is a measurable determinant of immune control, and impaired CD8+ T and NK cell responses to interferon-alpha are associated with poor therapy response. In viral infections such as Crimean-Congo hemorrhagic fever and SARS-CoV-2, the virus can delay or suppress the interferon-alpha response to promote replication. Because the response is cell-type specific, as shown by microglia versus astrocytes, GO:0035457 provides a precise framework for designing cell models and interpreting single-cell data.
• Defines the cell-intrinsic changes caused by interferon-alpha, enabling precise annotation of antiviral and immune experiments.
• Links interferon-alpha responsiveness to chronic hepatitis B therapy outcomes through CD8+ T and NK cell function.
• Highlights the role of B cells in interferon-alpha-facilitated anti-HBV cellular immunity.
• Explains how viruses such as Crimean-Congo hemorrhagic fever virus delay innate immune activation.
• Connects suppression of interferon-alpha and interferon-gamma responses to SARS-CoV-2 replication.
• Shows that the response is cell-type specific, as demonstrated for microglia versus astrocytes.
• Supports research on hepatitis D virus genotype-specific responsiveness to interferon-alpha.
• Provides a framework for studying plasmacytoid dendritic cell recovery during interferon-alpha treatment in chronic hepatitis B.
• Helps interpret stress-related immune modulation, such as the interferon-alpha response of pigs to weaning stress.
• Guides CRISPR cell model design for testing causal roles of interferon-alpha response genes.
What Happens During cellular response to interferon-alpha?
Interferon-alpha recognition and early signaling
In simple terms: The cell first detects interferon-alpha and switches on its antiviral program.
The cellular response to interferon-alpha begins when a cell receives an interferon-alpha stimulus, which is a type I interferon. This stimulus initiates changes in cell state or activity, including gene expression, enzyme production, and secretion. In the central nervous system, microglia and astrocytes both respond to interferon-alpha, but microglia show a more extensive and divergent response, indicating that early signaling outcomes are cell-type dependent. In chronic hepatitis B, interferon-alpha can facilitate an anti-HBV cellular immune response in a B cell-dependent manner, showing that the response is not restricted to infected cells but also shapes immune cell behavior.
Transcriptional and functional reprogramming
In simple terms: The cell changes which genes it uses and what jobs it performs.
After the interferon-alpha stimulus, the cell undergoes changes in gene expression and activity that define GO:0035457. These changes can include movement, secretion, and enzyme production, as stated in the ontology definition. In microglia, the response to interferon-alpha is more extensive and divergent than in astrocytes, which means the same stimulus produces different functional reprogramming across cell types. In hepatitis B, interferon-alpha treatment correlates with recovery of blood plasmacytoid dendritic cells in children with chronic hepatitis B, linking the cellular response to measurable immune cell recovery.
Immune cell activation and antiviral effector function
In simple terms: Immune cells become better at attacking viruses, or sometimes fail to do so.
The cellular response to interferon-alpha includes functional changes in immune cells that affect antiviral control. Interferon-alpha facilitates an anti-HBV cellular immune response in a B cell-dependent manner, indicating that B cells are required for this effect. In patients with HBeAg-positive chronic hepatitis B, taurocholic acid inhibits the response to interferon-alpha therapy by impairing CD8+ T and NK cell function, directly connecting the cellular response to effector immune cell performance. These findings show that GO:0035457 can be studied as a determinant of therapy response in human disease.
Viral interference with the interferon-alpha response
In simple terms: Some viruses try to block or delay the cell's interferon-alpha response.
Viruses can actively interfere with the cellular response to interferon-alpha. Crimean-Congo hemorrhagic fever virus delays activation of the innate immune response, which includes interferon-alpha-related signaling. SARS-CoV-2 replication is promoted when interferon-alpha and interferon-gamma responses are suppressed through Huwe1-mediated Miz1 degradation. These examples show that GO:0035457 is not only a host defense process but also a target of viral countermeasures.
Genotype- and context-dependent responsiveness
In simple terms: Different viral strains and host conditions can change how well the cell responds.
The responsiveness of the cellular response to interferon-alpha can vary by viral genotype and host context. Multimodal characterization of eight hepatitis D virus genotype isolates showed differences in responsiveness to interferon-alpha treatment. In pigs, the interferon-alpha response is characterized in the context of weaning stress, showing that physiological stress can be a variable in this process. Together, these studies support the idea that GO:0035457 should be assessed in a context-specific manner.
Key Genes Involved in GO:0035457 cellular response to interferon-alpha
The following genes and proteins are experimentally linked to the cellular response to interferon-alpha in the cited literature and are useful entry points for CRISPR cell model design.
| Gene | Major Role | Research Relevance |
|---|---|---|
| IFNA | Encodes interferon-alpha, the type I interferon stimulus for GO:0035457 | Used to define the stimulus in cellular response experiments |
| IFNAR1 | Type I interferon receptor component that initiates interferon-alpha signaling | Candidate for knockout to block the cellular response to interferon-alpha |
| IFNAR2 | Type I interferon receptor component required for interferon-alpha signal transduction | Candidate for knockout to test receptor-dependent effects |
| JAK1 | Janus kinase that propagates type I interferon receptor signaling | Candidate for point mutation to dissect signaling steps |
| TYK2 | Janus kinase that propagates type I interferon receptor signaling | Candidate for knockout to test interferon-alpha response dependence |
| STAT1 | Transcription factor activated downstream of interferon-alpha signaling | Candidate for knockout to test transcriptional reprogramming |
| STAT2 | Transcription factor activated downstream of interferon-alpha signaling | Candidate for knockout to test transcriptional reprogramming |
| IRF9 | Forms the ISGF3 complex with STAT1 and STAT2 | Candidate for knockout to test interferon-stimulated gene induction |
| Miz1 | Degraded by Huwe1 to suppress interferon-alpha and interferon-gamma responses | Candidate for knockout or knock-in to study SARS-CoV-2 replication |
| Huwe1 | Mediates Miz1 degradation and suppresses interferon-alpha response | Candidate for knockout to test interferon-alpha response restoration |
| CD8A | Marker of CD8+ T cells whose function is impaired in poor interferon-alpha therapy response | Relevant to immune cell response studies in chronic hepatitis B |
| NK cell receptors | Mediate NK cell function that is impaired in poor interferon-alpha therapy response | Relevant to immune cell response studies in chronic hepatitis B |
| B cell markers | B cells are required for interferon-alpha-facilitated anti-HBV cellular immune response | Relevant to B cell-dependent interferon-alpha response studies |
| Plasmacytoid dendritic cells | Recovery correlates with response to interferon-alpha treatment in children with chronic hepatitis B | Relevant to immune recovery studies during interferon-alpha therapy |
| Taurocholic acid pathway genes | Taurocholic acid inhibits interferon-alpha therapy response by impairing CD8+ T and NK cell function | Relevant to metabolic regulation of interferon-alpha response |
| Hepatitis D virus genotype factors | Genotype isolates differ in responsiveness to interferon-alpha treatment | Relevant to genotype-specific interferon-alpha response studies |
| Crimean-Congo hemorrhagic fever virus innate immune antagonists | Delay activation of the innate immune response including interferon-alpha signaling | Relevant to viral interference studies |
| Weaning stress response genes | Characterized in the interferon-alpha response of pigs to weaning stress | Relevant to stress-context interferon-alpha response studies |
How Is cellular response to interferon-alpha Regulated?
The cellular response to interferon-alpha is regulated at multiple levels. Viral proteins can suppress it, as shown by Huwe1-mediated Miz1 degradation, which suppresses interferon-alpha and interferon-gamma responses and promotes SARS-CoV-2 replication. Crimean-Congo hemorrhagic fever virus delays activation of the innate immune response, providing another example of negative regulation by a pathogen. Host metabolic factors can also regulate the response: taurocholic acid inhibits the response to interferon-alpha therapy in patients with HBeAg-positive chronic hepatitis B by impairing CD8+ T and NK cell function. In addition, the response is modulated by cell type, as microglia have a more extensive and divergent response to interferon-alpha compared with astrocytes, and by physiological context, as shown by the interferon-alpha response of pigs to weaning stress. These layers of regulation mean that GO:0035457 should be interpreted with attention to pathogen, metabolic, cell-type, and stress variables.
cellular response to interferon-alpha and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| IFNA / IFNAR1 / IFNAR2 | Chronic hepatitis B and interferon-alpha therapy response | Knockout cell model to block the cellular response to interferon-alpha |
| Huwe1 / Miz1 | COVID-19 and SARS-CoV-2 replication | Knockout or knock-in cell model to test interferon-alpha response suppression |
| Hepatitis D virus genotype factors | Hepatitis D virus responsiveness to interferon-alpha | Genotype-specific infection model with interferon-alpha treatment |
| Crimean-Congo hemorrhagic fever virus innate immune antagonists | Crimean-Congo hemorrhagic fever and innate immune delay | Infection model with innate immune activation readouts |
| Taurocholic acid pathway genes | HBeAg-positive chronic hepatitis B and therapy failure | Immune cell model with taurocholic acid treatment and interferon-alpha stimulation |
Chronic hepatitis B and interferon-alpha therapy response
Chronic hepatitis B is a major context for GO:0035457. Interferon-alpha facilitates an anti-HBV cellular immune response in a B cell-dependent manner, showing that the cellular response to interferon-alpha is part of the therapeutic mechanism. However, taurocholic acid inhibits the response to interferon-alpha therapy in patients with HBeAg-positive chronic hepatitis B by impairing CD8+ T and NK cell function, linking metabolic status to treatment failure. Recovery of blood plasmacytoid dendritic cells correlates with response to interferon-alpha treatment in children with chronic hepatitis B, providing a cellular biomarker of the response.
Hepatitis D virus genotype-specific responsiveness
Hepatitis D virus provides a clear example of genotype-dependent responsiveness to interferon-alpha. Multimodal characterization of eight hepatitis D virus genotype isolates demonstrated differences in responsiveness to interferon-alpha treatment, indicating that the cellular response to interferon-alpha can vary with viral genotype. This has direct implications for interpreting GO:0035457 in the context of hepatitis D research and for designing experiments that account for genotype diversity.
COVID-19 and SARS-CoV-2 immune evasion
SARS-CoV-2 can suppress the cellular response to interferon-alpha. Suppression of interferon-alpha and interferon-gamma responses by Huwe1-mediated Miz1 degradation promotes SARS-CoV-2 replication, directly connecting GO:0035457 to COVID-19 biology. This finding suggests that the cellular response to interferon-alpha is a determinant of viral replication efficiency and a potential target for host-directed research.
Crimean-Congo hemorrhagic fever and innate immune delay
Crimean-Congo hemorrhagic fever virus delays activation of the innate immune response, which includes interferon-alpha-related signaling. This delay is an example of a pathogen interfering with GO:0035457, and it supports the use of this ontology term when studying hemorrhagic fever virus-host interactions.
From cellular response to interferon-alpha-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for the cellular response to interferon-alpha? | CRISPR knockout cell model with interferon-alpha stimulation |
| Does a specific point mutation alter interferon-alpha signaling? | CRISPR point-mutation knock-in cell model |
| Does a disease-associated variant change the interferon-alpha response? | CRISPR knock-in of the variant with interferon-alpha readouts |
| Where and when is a protein expressed during the interferon-alpha response? | Tagged knock-in cell model for imaging and proteomics |
| Does overexpression of a suppressor gene block the interferon-alpha response? | Overexpression cell model with interferon-alpha stimulation |
| Which genes are essential for interferon-alpha responsiveness? | CRISPR library screening with interferon-alpha selection |
How to Study the cellular response to interferon-alpha Process
| Method | What It Measures | Typical Application |
|---|---|---|
| RNA sequencing | Gene expression changes after interferon-alpha stimulation | Identifying transcriptional programs in GO:0035457 |
| Immune cell functional assays | CD8+ T cell and NK cell function after interferon-alpha exposure | Testing therapy response modifiers in chronic hepatitis B |
| Plasmacytoid dendritic cell quantification | Recovery of blood plasmacytoid dendritic cells during interferon-alpha treatment | Correlating cellular response with clinical response |
| Viral replication assays | Viral replication under interferon-alpha treatment | Testing viral interference with GO:0035457 |
| Genotype comparison assays | Responsiveness of different viral isolates to interferon-alpha | Studying genotype-specific interferon-alpha response |
| Stress challenge experiments | Interferon-alpha response under physiological stress | Characterizing context-dependent regulation |
| B cell-dependent immune assays | Anti-HBV cellular immune response requiring B cells | Testing B cell dependence of interferon-alpha effects |
| Cell-type comparison assays | Divergent interferon-alpha responses across cell types | Comparing microglia and astrocytes |
Transcriptomic profiling of the interferon-alpha response
RNA sequencing is a direct way to measure the gene expression changes that define GO:0035457. Because the term includes changes in gene expression as a result of an interferon-alpha stimulus, transcriptomic profiling of cells before and after interferon-alpha treatment can identify the genes and pathways that are activated or repressed. This approach is especially informative when comparing cell types, as microglia and astrocytes show divergent responses to interferon-alpha, and when comparing viral genotypes, as shown for hepatitis D virus isolates.
Immune cell functional assays
Functional assays are needed to connect the cellular response to interferon-alpha with immune cell behavior. In chronic hepatitis B, the response to interferon-alpha therapy correlates with recovery of blood plasmacytoid dendritic cells, and taurocholic acid inhibits the response by impairing CD8+ T and NK cell function. Assays that measure CD8+ T cell and NK cell function after interferon-alpha stimulation can therefore be used to test whether a gene or treatment modifies GO:0035457. B cell-dependent anti-HBV cellular immune responses can also be measured to assess the role of B cells in this process.
Viral infection and replication readouts
Because viruses can suppress or delay the interferon-alpha response, infection models are valuable for studying GO:0035457. SARS-CoV-2 replication is promoted when interferon-alpha and interferon-gamma responses are suppressed through Huwe1-mediated Miz1 degradation, and Crimean-Congo hemorrhagic fever virus delays activation of the innate immune response. Measuring viral replication alongside interferon-alpha response markers allows researchers to determine whether a gene or treatment alters the cellular response and whether that change affects viral fitness.
Stress and physiological context experiments
The cellular response to interferon-alpha can be influenced by physiological context. The interferon-alpha response of pigs to weaning stress has been characterized, showing that stress can be a variable in this process. Experiments that combine a physiological stressor with interferon-alpha stimulation can reveal context-dependent regulation of GO:0035457. Such studies are useful for understanding how real-world conditions modify the cellular response.
How CRISPR Can Be Used to Study GO:0035457 cellular response to interferon-alpha
Knockout
CRISPR knockout is used to test whether a candidate gene is required for the cellular response to interferon-alpha. By deleting a gene and then stimulating cells with interferon-alpha, researchers can measure changes in gene expression, secretion, or immune cell function that define GO:0035457. For example, knocking out a suppressor such as Huwe1 could be used to test whether interferon-alpha and interferon-gamma responses are restored in a SARS-CoV-2 infection model. Knockout models are also useful for testing receptor and signaling components that initiate the response.
Point Mutation
CRISPR point mutation allows precise testing of specific residues or variants in genes involved in the cellular response to interferon-alpha. This is valuable when a disease-associated variant is suspected to alter interferon-alpha responsiveness, as suggested by genotype-specific differences in hepatitis D virus responsiveness to interferon-alpha treatment. Point mutation models can also be used to dissect signaling steps in the interferon-alpha response without fully deleting the gene.
Knock-in
CRISPR knock-in can introduce a variant, a reporter, or a tag into a gene involved in the cellular response to interferon-alpha. Tagged knock-in models enable imaging and proteomic tracking of proteins during the interferon-alpha response. Variant knock-in models allow researchers to test whether a specific sequence change alters the cellular response, which is relevant for interpreting genotype-specific interferon-alpha responsiveness. Knock-in approaches are also useful for building reporter cell lines that report on GO:0035457 activity.
Overexpression
CRISPR overexpression can be used to test whether increasing the level of a gene product enhances or suppresses the cellular response to interferon-alpha. For example, overexpression of a suppressor such as Huwe1 or Miz1 could be used to test whether interferon-alpha and interferon-gamma responses are reduced and SARS-CoV-2 replication is promoted. Overexpression models complement knockout models by providing gain-of-function evidence for a gene's role in GO:0035457.
How EDITGENE Supports cellular response to interferon-alpha Research
Researchers studying cellular response to interferon-alpha-related genes often need to determine whether a candidate gene is causally involved in the response or merely correlated with it. Building the right CRISPR cell model, whether a knockout, point mutation, knock-in, or overexpression line, is the decisive step that turns an association into a mechanistic finding. EDITGENE provides these models together with CRISPR library screening and bioinformatics support so that interferon-alpha response studies can move from hypothesis to publication-ready data.
Contact EDITGENE today to design your custom CRISPR model for cellular response to interferon-alpha research.
Frequently Asked Questions About cellular response to interferon-alpha
What is GO:0035457 cellular response to interferon-alpha?
GO:0035457 is a biological process ontology term describing any change in a cell's state or activity, such as movement, secretion, enzyme production, or gene expression, that occurs as a result of an interferon-alpha stimulus, where interferon-alpha is a type I interferon.
What genes are involved in the cellular response to interferon-alpha?
Genes and proteins experimentally linked to this process include interferon-alpha itself, type I interferon receptor components, signaling kinases, transcription factors, and regulators such as Huwe1 and Miz1, as well as immune cell markers studied in hepatitis B and COVID-19 research.
Why is the cellular response to interferon-alpha important in chronic hepatitis B?
Interferon-alpha facilitates an anti-HBV cellular immune response in a B cell-dependent manner, and impaired CD8+ T and NK cell responses to interferon-alpha are associated with poor therapy response in HBeAg-positive chronic hepatitis B.
How do viruses suppress the cellular response to interferon-alpha?
SARS-CoV-2 can suppress interferon-alpha and interferon-gamma responses through Huwe1-mediated Miz1 degradation, which promotes viral replication, and Crimean-Congo hemorrhagic fever virus delays activation of the innate immune response.
Is the cellular response to interferon-alpha different between cell types?
Yes. Microglia have a more extensive and divergent response to interferon-alpha compared with astrocytes, showing that the process is cell-type specific.
What is the difference between cellular response to interferon-alpha and response to type I interferon?
GO:0035457 is specifically anchored to interferon-alpha, a type I interferon, and captures cell-level changes after that stimulus, rather than the broader category of all type I interferon responses.
How is the cellular response to interferon-alpha studied experimentally?
Researchers use transcriptomic profiling, immune cell functional assays, viral replication assays, genotype comparison assays, and stress challenge experiments to measure the response.
Can CRISPR be used to study the cellular response to interferon-alpha?
Yes. CRISPR knockout, point mutation, knock-in, and overexpression models can be used to test whether a candidate gene is required for or modifies the cellular response to interferon-alpha.
What is the role of plasmacytoid dendritic cells in interferon-alpha treatment?
Recovery of blood plasmacytoid dendritic cells correlates with response to interferon-alpha treatment in children with chronic hepatitis B, making them a cellular marker of the response.
Does hepatitis D virus genotype affect interferon-alpha responsiveness?
Yes. Multimodal characterization of eight hepatitis D virus genotype isolates showed differences in responsiveness to interferon-alpha treatment.
Conclusion
GO:0035457, cellular response to interferon-alpha, is a precise biological process term for the cell-level changes triggered by interferon-alpha, a type I interferon. The literature shows that this response is central to antiviral immunity and therapy outcomes in chronic hepatitis B, hepatitis D, COVID-19, and Crimean-Congo hemorrhagic fever, and that it is shaped by cell type, viral genotype, metabolism, and physiological stress. Because the response can be measured through gene expression, immune cell function, and viral replication readouts, it is well suited to CRISPR-based mechanistic studies. For researchers, the practical path forward is to combine careful cell model design with context-aware readouts. Knockout, point mutation, knock-in, and overexpression models each answer a different causal question, and CRISPR library screening can identify new regulators of the response. EDITGENE supports this workflow with cell model generation, screening, and bioinformatics services tailored to cellular response to interferon-alpha research.
References
- 1. Zhong S et al.. 2022. Interferon α facilitates anti-HBV cellular immune response in a B cell-dependent manner.. Antiviral Res 207:105420 PMID: 36165866
- 2. Xun Z et al.. 2021. Taurocholic acid inhibits the response to interferon-α therapy in patients with HBeAg-positive chronic hepatitis B by impairing CD8(+) T and NK cell function.. Cell Mol Immunol 18(2):461-471 PMID: 33432062
- 3. Ding Y et al.. 2025. Multimodal characterization of the responsiveness of eight hepatitis D virus genotype isolates to interferon-alpha treatment.. J Virol 99(10):e0128025 PMID: 40965142
- 4. Arunagiri V et al.. 2024. Suppression of interferon α and γ response by Huwe1-mediated Miz1 degradation promotes SARS-CoV-2 replication.. Front Immunol 15:1388517 PMID: 39034993
- 5. Li W et al.. 2018. Microglia have a more extensive and divergent response to interferon-α compared with astrocytes.. Glia 66(10):2058-2078 PMID: 30051922
- 6. Andersson I et al.. 2008. Crimean-Congo hemorrhagic fever virus delays activation of the innate immune response.. J Med Virol 80(8):1397-404 PMID: 18551619
- 7. Zhang Z et al.. 2007. Response to interferon-alpha treatment correlates with recovery of blood plasmacytoid dendritic cells in children with chronic hepatitis B.. J Hepatol 47(6):751-9 PMID: 17920718
- 8. Razzuoli E et al.. 2011. Characterization of the interferon-α response of pigs to the weaning stress.. J Interferon Cytokine Res 31(2):237-47 PMID: 20950132
