Silver Nanoparticles (AgNPs) & Epstein-Barr Virus Research

Epstein-Barr virus (EBV), also known as human herpesvirus 4 (HHV-4), infects more than 90% of the global adult population and is etiologically linked to approximately 200,000 cancer cases per year worldwide. Despite its ubiquity and its role in malignancies ranging from Burkitt lymphoma and nasopharyngeal carcinoma to Hodgkin lymphoma and gastric carcinoma, there are currently no specific antiviral therapies targeting EBV. Silver nanoparticles (AgNPs) have emerged as a promising area of research, demonstrating two powerful mechanisms against EBV-associated disease: direct virucidal destruction of viral particles and selective killing of latently infected cancer cells through reactive oxygen species (ROS)-induced lytic reactivation.

This article reviews the current scientific evidence for AgNP activity against EBV, drawing from peer-reviewed research in virology, nanomedicine, and oncology.

Table of Contents

1. Epstein-Barr Virus: The Hidden Oncogenic Threat
2. EBV-Associated Cancers & Disease Burden
3. Latency vs. Lytic Cycle: Why It Matters for Therapy
4. AgNPs Selectively Kill EBV-Infected Cancer Cells
5. ROS Generation & Autophagy: The Mechanistic Basis
6. Direct Virion Destruction by Silver Nanoparticles
7. Silver vs. Gold Nanoparticles Against EBV
8. Nanoparticle Size, Shape & Surface Functionalization
9. Broader Herpesvirus Antiviral Context
10. Lytic Induction Therapy: AgNPs in the Treatment Landscape
11. Nanomedicine Approaches to EBV Treatment
12. Safety Considerations & Limitations
13. Future Directions
14. References & Research Papers
15. Connections
16. Featured Videos

1. Epstein-Barr Virus: The Hidden Oncogenic Threat

Epstein-Barr virus is a member of the gamma-herpesvirus family, discovered in 1964 by Michael Anthony Epstein and Yvonne Barr. It was the first human virus directly linked to cancer. EBV establishes lifelong latent infection in B lymphocytes after primary infection, which typically occurs in childhood (often asymptomatic) or adolescence (causing infectious mononucleosis in approximately 25–50% of cases).

Key Facts About EBV

• Global prevalence: Over 90–95% of adults worldwide are seropositive for EBV
• Transmission: Primarily through saliva; also via blood transfusion, organ transplantation, and sexual contact
• Latency: After primary infection, EBV persists in memory B cells for life, evading immune clearance through sophisticated immune evasion strategies
• Oncogenic potential: EBV is classified as a Group 1 carcinogen by the International Agency for Research on Cancer (IARC)
• No specific antiviral: Unlike herpes simplex virus (HSV), for which acyclovir is effective, there is no targeted antiviral therapy proven to eliminate latent EBV or treat EBV-associated malignancies

2. EBV-Associated Cancers & Disease Burden

EBV is responsible for approximately 1.5% of all human cancers and 1.8% of all cancer-related deaths worldwide, accounting for an estimated 239,700–357,900 new cases and 137,900–208,700 deaths annually. The virus drives malignancy through multiple latency programs that promote cell proliferation, inhibit apoptosis, and evade immune surveillance.

Major EBV-Associated Malignancies

• Burkitt Lymphoma: EBV-positive in approximately 59% of cases globally, rising to 76.5% in Sub-Saharan Africa where endemic Burkitt lymphoma is the most common childhood cancer
• Nasopharyngeal Carcinoma (NPC): Nearly 100% EBV-positive; highly prevalent in Southern China and Southeast Asia with incidence rates of 20–30 per 100,000
• Hodgkin Lymphoma: EBV detected in 30–40% of classical Hodgkin lymphoma cases worldwide
• Gastric Carcinoma: Approximately 10% of all gastric cancers worldwide are EBV-associated, representing roughly 75,000 cases annually
• Post-Transplant Lymphoproliferative Disorder (PTLD): The most common malignancy in transplant recipients, driven by EBV reactivation under immunosuppression
• NK/T-Cell Lymphoma: Virtually always EBV-positive, an aggressive extranodal lymphoma most common in Asia and Latin America
• Diffuse Large B-Cell Lymphoma (DLBCL): EBV-positive variant, particularly common in elderly and immunocompromised patients

Non-Malignant EBV-Associated Diseases

• Infectious mononucleosis: Acute primary EBV infection affecting adolescents and young adults
• Multiple sclerosis: Strong epidemiological evidence links prior EBV infection to a 32-fold increased risk of MS
• Chronic active EBV infection: A rare, life-threatening condition of persistent EBV replication
• Oral hairy leukoplakia: EBV-driven epithelial lesion in immunocompromised patients

3. Latency vs. Lytic Cycle: Why It Matters for Therapy

Understanding EBV’s dual lifecycle is essential to appreciating why silver nanoparticles represent a uniquely valuable therapeutic strategy.

Latent Infection

In latency, EBV expresses only a minimal set of genes (latency programs I, II, or III) that maintain the viral genome as an episome within host cells. Latently infected cells are largely invisible to the immune system and resistant to conventional antiviral drugs like acyclovir and ganciclovir, which target only lytic replication enzymes. This is the state that drives EBV-associated cancers — the virus keeps infected cells proliferating while avoiding immune detection.

Lytic Replication

The lytic cycle is initiated by expression of the master regulator BZLF1 (also called Zta or ZEBRA), which triggers a cascade of viral gene expression leading to production of new virions and ultimately cell death. During lytic replication, EBV-encoded kinases — thymidine kinase (TK) and BGLF4 protein kinase — become active and can convert nucleoside analogues like ganciclovir into their cytotoxic forms.

The Therapeutic Paradox

The most dangerous aspect of EBV — latent infection driving cancer — is precisely the state that is most resistant to treatment. This has led researchers to pursue lytic induction therapy: deliberately triggering the latent-to-lytic switch in EBV-infected cancer cells, which both exposes them to antiviral drugs and triggers natural cell death pathways. Silver nanoparticles have been shown to accomplish exactly this through ROS-mediated mechanisms.

4. AgNPs Selectively Kill EBV-Infected Cancer Cells

The landmark 2019 study by Wan, Tai et al., published in Cell Death & Disease, demonstrated that silver nanoparticles exhibit preferential cytotoxicity against EBV- and KSHV-latently infected cells compared to their uninfected counterparts. This selectivity is a critical finding because it suggests a therapeutic window that could spare normal cells while targeting virus-driven cancers.

Key Experimental Findings

• Nanoparticle specifications: 25 nm spherical PVP-coated silver nanoparticles were optimal; smaller particles (5 nm, 25 nm) showed stronger cytotoxicity than larger particles (100 nm, 200 nm)
• EBV cell lines tested: B95.8, LCL (lymphoblastoid cell lines), and Akata-EBV cells, compared against uninfected Akata and BJAB controls
• Selective toxicity: CC50 values were consistently lower for virus-infected cells versus uninfected counterparts
• Dose response: 5 µg/mL AgNPs reduced infected cell viability to below 50% at 48 hours
• Normal cell safety: Primary peripheral blood mononuclear cells (PBMCs) maintained greater than 80% viability even at 15 µg/mL for 72 hours
• Colony formation: Dramatic reduction in colony formation of EBV-positive LCL cells compared to controls

In Vivo Evidence

In a xenograft mouse model using NOD/SCID mice bearing BCBL1-Luc tumors (KSHV-positive), intraperitoneal injection of 0.2 mg AgNPs every 3 days for 3 doses showed:

• Bioluminescent tumor signals reduced to near-undetectable levels in responsive mice by day 21
• Moderate overall growth inhibition compared to PBS controls
• Greater efficacy in mice with smaller initial tumor burdens
• The authors noted that limited nanoparticle accumulation in target tissues may have reduced in vivo efficacy compared to the dramatic in vitro results

5. ROS Generation & Autophagy: The Mechanistic Basis

The selective cytotoxicity of silver nanoparticles against EBV-infected cells is driven by a cascade of interconnected cellular events centered on reactive oxygen species and autophagy.

Reactive Oxygen Species (ROS) Pathway

1. AgNPs enter cells through endocytosis and release silver ions (Ag+) within the acidic endosomal/lysosomal compartment
2. ROS generation: Both the nanoparticles and released ions catalyze production of superoxide anion (O₂⁻), hydrogen peroxide (H₂O₂), and hydroxyl radicals (•OH)
3. Lytic reactivation trigger: ROS activates transcription of BZLF1 (EBV) and RTA (KSHV) — the master lytic switch genes — in a dose-dependent manner
4. Confirmation: Treatment with N-acetylcysteine (NAC), a ROS scavenger, blocked both ROS generation and viral lytic reactivation, confirming the causal relationship

Autophagy Induction

• AgNPs triggered accumulation of LC3B-II (an autophagy marker) and reduction of SQSTM1/p62, confirming active autophagic flux
• Chloroquine treatment confirmed that autophagy was actively proceeding, not blocked
• Autophagy is a known trigger of EBV lytic reactivation and contributes to the selective killing mechanism

Why Virus-Infected Cells Are More Vulnerable

EBV-latently infected cells exist in a precarious metabolic state. They already maintain higher baseline levels of oxidative stress due to the metabolic demands of viral latency programs. The additional ROS burden imposed by AgNPs pushes these cells past a critical threshold that:

• Tips the balance from latency to lytic replication
• Triggers mitochondrial dysfunction and apoptotic pathways
• Activates autophagy-mediated cell death
• Overwhelms the already-strained antioxidant defense systems of infected cells

Uninfected cells, with lower baseline oxidative stress and no latent viral genome to reactivate, can better tolerate the same AgNP concentrations.

6. Direct Virion Destruction by Silver Nanoparticles

Beyond killing infected cells, silver nanoparticles can directly destroy free viral particles, preventing new infections. This dual mechanism — killing infected cells while neutralizing extracellular virus — is a significant therapeutic advantage.

Mechanism of Virion Destruction

• Physical disruption: Transmission electron microscopy (TEM) revealed that AgNPs physically alter virion morphology — capsids that were normally spherical (100–200 nm) became swollen and flattened after incubation with just 0.2 µg/mL AgNPs
• Envelope damage: AgNPs interact with the viral lipid envelope, compromising its structural integrity
• Non-glycoprotein mechanism: Importantly, AgNPs did not impair virion-cell binding through glycoprotein interference, suggesting the mechanism involves direct physical damage to the viral particle rather than blocking receptor-ligand interactions
• Sub-cytotoxic activity: Viral blocking occurred at concentrations as low as 0.6 µg/mL — well below concentrations that cause cellular toxicity

Evidence from EBV-Specific Studies

The 2022 study published in the Microbiological Journal tested 5–20 nm silver and gold nanoparticles stabilized with different capping agents against EBV in P3HR-1 lymphoblastoid cell cultures. Key findings:

• Citrate-stabilized silver nanoparticles proved most effective, inhibiting EBV replication by up to 70%
• Nanoparticles stabilized with tryptophan and citrate showed low toxicity, with cell viability maintained at 65–100%
• Electron microscopy confirmed physical damage to EBV virions after just 2 hours of contact with gold nanoparticles
• The stabilizing agent (capping chemistry) significantly influenced antiviral effectiveness

7. Silver vs. Gold Nanoparticles Against EBV

The comparative study of metal nanoparticles against EBV provides important insights into why silver outperforms gold for antiviral applications:

Silver Nanoparticles (AgNPs)

• Inhibited EBV replication by up to 70%
• Citrate-buffered formulations were most effective
• Effective across a broader concentration range
• Multiple mechanisms of action (ROS, direct virucidal, lytic induction)
• Sustained ion release provides prolonged antiviral activity

Gold Nanoparticles (AuNPs)

• Reduced EBV DNA by a maximum of only 16%
• Effective only at very low concentrations (0.00001 µg/mL), with a paradoxical dose-dependent effect
• Demonstrated physical damage to virion particles via electron microscopy
• Generally better biocompatibility but significantly weaker antiviral activity
• May have complementary roles in diagnostic applications due to unique optical properties

Why Silver Outperforms Gold

The superior antiviral activity of silver nanoparticles is attributed to:

• Ion release: AgNPs continuously release Ag+ ions that have intrinsic antimicrobial and antiviral properties; gold nanoparticles are chemically inert and do not release bioactive ions
• ROS generation: Silver is far more potent at generating reactive oxygen species through Fenton-like reactions
• Surface reactivity: Silver’s higher chemical reactivity enables stronger interactions with viral envelope proteins and lipids
• Dual mechanism: Silver uniquely combines direct virucidal activity with the ability to trigger lytic reactivation in latently infected cells

8. Nanoparticle Size, Shape & Surface Functionalization

The antiviral efficacy of silver nanoparticles is critically dependent on their physical and chemical characteristics. Research across multiple herpesvirus studies has identified optimal parameters.

Size Effects

• Optimal antiviral range: 2–25 nm particles show maximal antiviral efficacy across herpesvirus studies
• EBV-specific: 25 nm PVP-coated AgNPs were optimal in the Wan et al. (2019) study; 5 nm particles also showed strong activity
• Size-toxicity trade-off: Ultra-small particles (<10 nm) show the highest antiviral activity but also the greatest cytotoxicity risk
• Enveloped virus general finding: Nanoparticles ≤10 nm display superior activity against enveloped viruses at 1–10 ppm concentrations

Surface Functionalization Strategies

• PVP (polyvinylpyrrolidone): Used in the landmark EBV study; provides colloidal stability and biocompatibility
• Citrate: Most effective stabilizer in the comparative metal nanoparticle EBV study; enhances dispersion and cellular uptake
• Tannic acid: Demonstrated potent anti-herpesvirus activity; blocks viral attachment and entry while activating immune cytokine production
• EGCG (epigallocatechin gallate): Green tea polyphenol coating that boosts HSV inhibition and immune cell recruitment
• Lactoferrin: Protein coating that strengthens immune modulation against herpesvirus infections
• Tryptophan: Amino acid stabilizer tested in EBV studies; showed low cytotoxicity but less antiviral potency than citrate

Shape Considerations

• Spherical nanoparticles are the most studied and best characterized for antiviral applications
• Triangular nanoplates and nanorods may offer different surface area-to-volume ratios, potentially affecting activity
• Shape influences cellular uptake pathways and intracellular distribution

9. Broader Herpesvirus Antiviral Context

EBV belongs to the herpesvirus family, and findings from AgNP research against other herpesviruses provide valuable mechanistic context and support for EBV-specific applications.

Herpes Simplex Virus (HSV-1 & HSV-2)

• Tannic acid-modified AgNPs (13, 33, 46 nm) reduced HSV-2 infectivity both in vitro and in vivo
• Blocked viral attachment by 40–80% and viral penetration with approximately 80% efficiency
• Mycosynthesized AgNPs (4–13 nm) demonstrated 80–90% inhibition of HSV-1
• Pre-treatment prevention proved superior to post-infection intervention
• Polyurethane-incorporated AgNPs achieved complete loss of HSV infectivity in topical applications

KSHV (Kaposi’s Sarcoma-Associated Herpesvirus)

• Studied alongside EBV in the Wan et al. (2019) research as both are oncogenic gamma-herpesviruses
• AgNPs showed even stronger selective toxicity against KSHV-infected cells (BCBL-1, BCP1, iSLK-KSHV)
• Virion destruction confirmed by TEM showing capsid deformation
• In vivo efficacy demonstrated in KSHV xenograft mouse model

Common Mechanisms Across Herpesviruses

The consistent antiviral mechanisms observed across the herpesvirus family include:

1. Disruption of the viral lipid envelope common to all herpesviruses
2. Interference with viral attachment and entry machinery
3. ROS-mediated reactivation of latent herpesviruses (EBV, KSHV)
4. Inhibition of viral DNA replication through multiple pathways
5. Immune system stimulation through cytokine and chemokine induction

10. Lytic Induction Therapy: AgNPs in the Treatment Landscape

The ability of silver nanoparticles to trigger EBV lytic reactivation places them within the broader therapeutic strategy known as lytic induction therapy (also called cytolytic virus activation or CLVA) — one of the most promising approaches for EBV-associated malignancies.

How Lytic Induction Therapy Works

1. Induce lytic switch: A drug or agent triggers expression of BZLF1, forcing EBV from latency into the lytic cycle
2. Viral kinase expression: Lytic replication activates EBV-encoded thymidine kinase (TK) and BGLF4 protein kinase
3. Prodrug conversion: These viral kinases convert the antiviral prodrug ganciclovir (GCV) into its cytotoxic triphosphate form
4. Selective cell death: The activated ganciclovir kills dividing cells — but only those expressing the viral kinases, providing tumor-selective cytotoxicity
5. Bystander effect: Phosphorylated ganciclovir diffuses to neighboring cells through gap junctions, killing adjacent tumor cells even if not all are virally reactivated

Conventional Lytic Inducers

• Histone deacetylase inhibitors: Sodium butyrate, valproic acid, vorinostat
• Chemotherapy agents: Gemcitabine, doxorubicin (but not 5-azacytidine, cis-platinum, or 5-fluorouracil)
• Rituximab + dexamethasone: Synergistic lytic induction in EBV-positive B-cell lymphomas
• Radiation therapy: Can activate lytic EBV replication in combination with chemical inducers

Emerging mRNA-Based Approach

A 2024 study in Nature Communications demonstrated lipid nanoparticle-encapsulated mRNA encoding a synthetic BZLF1-targeted transcriptional activator (mTZ3-LNP) that more efficiently activates EBV lytic gene expression than conventional chemical inducers. When combined with ganciclovir, this yielded highly selective cytotoxic effects against EBV-positive tumor cells.

Where AgNPs Fit In

Silver nanoparticles offer several advantages over conventional lytic inducers:

• Multi-mechanism action: AgNPs simultaneously induce lytic reactivation, generate cytotoxic ROS, trigger autophagy, and directly destroy extracellular virions — conventional inducers typically only trigger the lytic switch
• Inherent selectivity: AgNPs show higher toxicity to infected cells at baseline, even before considering lytic induction effects
• Combination potential: AgNPs could be paired with ganciclovir for a triple-mechanism attack: AgNP-mediated lytic induction + ganciclovir prodrug activation + direct AgNP cytotoxicity
• Infection prevention: Unlike other lytic inducers, AgNPs also block primary infection by destroying virions, potentially preventing viral spread from lysed tumor cells

11. Nanomedicine Approaches to EBV Treatment

Silver nanoparticles represent one arm of a broader nanomedicine revolution targeting EBV. Understanding the full landscape provides context for where AgNPs fit among other nanoparticle-based strategies.

Targeted Drug Delivery Nanoparticles

Surface-modified nanoparticles can specifically recognize and bind to EBV-infected cells, delivering therapeutic payloads such as antivirals or immunomodulators directly to viral targets. This approach minimizes systemic toxicity while maximizing local drug concentrations at the tumor site.

Iron Oxide Nanoparticles

Researchers have proposed leveraging iron oxide nanoparticles for EBV applications, combining magnetic targeting capabilities with potential therapeutic and diagnostic functions (theranostics).

Hybrid Platforms

Silver nanoparticle cores with surface-conjugated EBV-targeting ligands could combine direct antiviral activity with targeted delivery, broadening the therapeutic toolkit for the 90%+ of the population already carrying EBV.

12. Safety Considerations & Limitations

While the research on AgNPs against EBV is promising, significant safety and translational challenges must be acknowledged.

Cytotoxicity Window

• In vitro antimicrobial/antiviral concentrations (5–15 µg/mL) can overlap with cytotoxic ranges for mammalian cells
• Primary PBMCs showed good tolerance (>80% viability at 15 µg/mL), providing evidence for a therapeutic window
• PVP coating and other surface functionalizations significantly improve the safety profile
• The selectivity toward virus-infected cells provides an additional safety margin

In Vivo Limitations

• The mouse xenograft study showed only moderate tumor growth inhibition, likely due to limited nanoparticle accumulation in target tissues
• Nanoparticle biodistribution, pharmacokinetics, and clearance from the body remain incompletely characterized for systemic antiviral applications
• AgNPs accumulate in liver, spleen, and kidneys, raising concerns about organ toxicity at therapeutic doses
• Long-term effects of nanosilver exposure are not fully understood

Translational Barriers

• No clinical trials: As of 2025, no clinical trials specifically test AgNPs for EBV-associated disease
• Standardization: Variations in synthesis method, size, shape, surface coating, and stability produce dramatically different biological effects, making cross-study comparisons difficult
• Regulatory pathway: Systemic nanoparticle therapies face stringent regulatory requirements including comprehensive toxicology studies
• Manufacturing: GMP-grade production with batch-to-batch consistency remains a challenge, particularly for biogenic (green-synthesized) AgNPs

Important Caveats

• Most EBV-AgNP research is in vitro or early preclinical; human efficacy is unproven
• Silver nanoparticles are not the same as colloidal silver products sold as dietary supplements, which have different particle characteristics, lack standardization, and carry risks of argyria (irreversible skin discoloration)
• Self-treatment with uncharacterized silver products based on this research would be premature and potentially dangerous

13. Future Directions

The convergence of nanotechnology, virology, and oncology points toward several promising research avenues for AgNPs against EBV.

Near-Term Research Priorities

• AgNP + ganciclovir combination studies: Testing whether AgNP-induced lytic reactivation sensitizes EBV-positive tumors to ganciclovir in animal models
• Optimized formulations: Systematic comparison of different sizes, shapes, and surface coatings specifically against EBV-positive cell lines and tumor models
• Targeted delivery: Conjugating AgNPs with EBV-specific antibodies or peptides (e.g., anti-LMP1, anti-gp350) to enhance selective accumulation in EBV-infected cells
• Nasopharyngeal carcinoma models: Given that NPC is nearly 100% EBV-associated, it represents an ideal cancer type for AgNP therapeutic testing

Longer-Term Possibilities

• Theranostic platforms: Combining diagnostic imaging (fluorescent silver nanoclusters) with therapeutic antiviral activity
• Immunotherapy combinations: Using AgNPs alongside checkpoint inhibitors or EBV-specific T cell therapy to enhance anti-tumor immune responses
• Post-transplant applications: Preventing or treating PTLD in organ transplant recipients where EBV reactivation is a major concern
• Multiple sclerosis prevention: If the EBV-MS link is confirmed as causal, AgNP-based strategies to suppress EBV could have implications far beyond oncology
• AI-driven nanoparticle optimization: Machine learning approaches to predict optimal AgNP characteristics for maximum anti-EBV activity with minimum toxicity

14. References & Research Papers

Silver Nanoparticles & EBV/Herpesvirus Research

1. Wan C, Tai J, Zhang J, et al. Silver nanoparticles selectively induce human oncogenic γ-herpesvirus-related cancer cell death through reactivating viral lytic replication. Cell Death & Disease. 2019;10(6):392.
2. Effect of metal nanoparticles on EBV-associated cell culture. Microbiological Journal. 2022;84(5):30-39.
3. Antiviral nanomedicine-based approaches against Epstein-Barr virus infection. Current Treatment Options in Infectious Diseases. 2024.
4. Mosidze E, Franci G, Dell’Annunziata F, et al. Silver nanoparticle-mediated antiviral efficacy against enveloped viruses: a comprehensive review. Global Challenges. 2025.

EBV Lytic Induction Therapy

5. Wang Y, et al. Synthetic BZLF1-targeted transcriptional activator for efficient lytic induction therapy against EBV-associated epithelial cancers. Nature Communications. 2024;15:3729.
6. Feng WH, Hong G, Delecluse HJ, Kenney SC. Lytic induction therapy for Epstein-Barr virus-positive B-cell lymphomas. Journal of Virology. 2004;78(4):1893-1902.
7. Li H, et al. Therapies based on targeting Epstein-Barr virus lytic replication for EBV-associated malignancies. Cancer Science. 2018;109(7):2101-2108.

AgNPs Against Herpes Simplex Virus

8. Orlowski P, Tomaszewska E, Gniadek M, et al. Tannic acid modified silver nanoparticles show antiviral activity in herpes simplex virus type 2 infection. PLoS ONE. 2014;9(8):e104113.
9. Orlowski P, Kowalczyk A, Tomaszewska E, et al. Antiviral activity of tannic acid modified silver nanoparticles: potential to activate immune response in herpes genitalis. Viruses. 2018;10(10):524.

Silver Nanoparticle Antiviral Reviews

10. Silver nanoparticles: review of antiviral properties, mechanism of action and applications. International Journal of Molecular Sciences. 2023;24(5):4284.
11. Galdiero S, Falanga A, Vitiello M, et al. Silver nanoparticles as potential antiviral agents. Molecules. 2011;16(10):8894-8918.

EBV-Associated Cancer Burden

12. Khan G, Hashim MJ. Estimating the global burden of Epstein-Barr virus-related cancers. Journal of Cancer Research and Clinical Oncology. 2022;148:1819-1832.
13. The association of Epstein-Barr virus with cancer. Frontiers in Oncology. 2022;12:936128.

ROS & EBV Reactivation

14. Reactive oxygen species mediate Epstein-Barr virus reactivation by N-methyl-N’-nitro-N-nitrosoguanidine. PLoS Pathogens. 2013;9(12):e1003838.
15. Targeting the signaling in Epstein-Barr virus-associated diseases: mechanism, regulation, and clinical study. Signal Transduction and Targeted Therapy. 2021;6:15.

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