Table 1: Mechanism of viral inhibition and exacerbation induced by resveratrol on different viruses.

VirusMode of propagationMechanism of resveratrol actionEffects on viral infectionReferences

Influenza virusMDCK cellsBlock nuclear-cytoplasmic translocation of viral ribonucleoproteinsDecrease in the expression of late viral proteins related to inhibition of protein kinase C associated pathways[30]

Epstein-Barr virus(i) Raji cells
(ii) Mice
(iii) P3HR1 cells
(iv) Burkitt’s lymphoma cell
(v) Human B-cells
(i) Inhibition of early antigen induction
(ii) Inhibition of early genes expression of lytic proteins
(iii) Inhibition of lytic gene expression and viral particle production
(iv) Inhibition of protein synthesis and reduction of ROS production and transcription of factors NF-κβ and AP1
(v) Downregulation of antiapoptotic proteins: Mc1 and survivin
(vi) Suppression of NF-κβ, STAT-3, miR-155, and miR-34a signaling
(i) Reduce papilloma production
(ii) Inhibition of viral transcription
(iii) Prevents transformation of EBV
[31]
[12]
[32]
[11]

Herpes simplex virus(i) Vero and MRC-5 cells
(ii) Mice
(iii) Mice
(iv) HeLa, Vero, and H1299 cells
(v) Vero cells
(i) Decreased production of early viral protein ICP4
(ii) Inhibition of interphase phase and prevention of virus reactivation
(iii) Rapid and transient release of reactive oxygen species
(iv) Reduction of mRNA of ICP0, ICP4, ICP8, and HSV-1 DNA polymerase
(v) Reduction of mRNA of glycoprotein C and HSV late gene
(i) Reduction in viral yields
(ii) Suppression of development of cutaneous lesions
(iii) Prevented development of extravaginal lesions
(iv) Inhibition of HSV replication through ROS generation
(v) Inhibition of viral transcription and DNA synthesis
[15]
[16]
[14]
[13]
[33]

Respiratory syncytial virus(i) Mice
(ii) Lung epithelial cell
(iii) Mice
(iv) Mice
(v) Mice
(i) Control of toll-like receptor 3 expression, inhibition of TRIF signaling, and induction of M2 receptor
(ii) Inhibition of viral induced toll-like receptor domain and TANK binding kinase 1 protein expression
(iii) Increased SARM and decreased TRIF expression
(i) Reduction in inflammation and levels of interferon-gamma
(ii) Partial reduction in viral replication and decreased production of interleukin-6
(iii) Enhanced interferon-gamma expression and airway inflammatory response
(iv) Decreased level of inflammatory cells and interferon-gamma
(v) Increased TNF-α, IFN-γ, and IL-2 production
[9]
[7]
[6]
[34]
[8]
[5]

Human immunodeficiency virus (HIV-1)Primary peripheral blood lymphocytesInhibition of DNA synthesis in NL4-3 clone with mutant M184V RTInhibition of HIV-1 strain replication[18]

Varicella zoster virusMRC-5 cellReduction in synthesis of protein and mRNA levels of IE62Decrease in viral production[10]

Enterovirus (EV 71)Rhabdosarcoma cell lineInhibition of synthesis of viral protein 1 and phosphorylation of proinflammatory cytokinesInhibition of IL-6 and IFN-γ in infected cells[35]

Duck enteritis virus (DEV)Duck embryo fibroblastSuppression of nucleic acid replication, viral capsid formation, and viral early protein expressionInhibition of DEV in host cells[36]

Human metapneumonia virus (hMPV)Alveolar type 2 cancerous cell lineSuppression of NF-κβ and interferon regulatory factor (IRF-3)Inhibition of viral replication and reduction in cellular oxidative damage and proinflammatory mediators[37]

African swine fever virus (ASFV)Vero cellInhibition of early and late viral protein synthesis and virion formationReduced viral DNA replication resulting in 98–100% reduction in viral titers[38]

Human rhinovirus (HRV-16)HeLa cell and nasal epithelia (ex vivo)Reversion of HRV-induced expression of ICAM-1Exhibited high dose-dependent antiviral activity against HRV, leading to reduction in secretion of IL-6, IL-8, and RANTES[39]

Cytomegalovirus Human embryonic lung fibroblast (HEL 299)(i) Prevention of production of immediate-early, early, and late viral proteins
(ii) Reduced viral induced activation of epidermal growth factor receptor, phosphatidylinositol-3-kinase signaling, and NF-κ and Sp1 transcription factor activation
Decreased viral replication[40]

Hepatitis C virusOR6 cells(i) Dose-dependently enhanced HCV viral RNA replication
(ii) Reversed antiviral effects of ribavirin and interferon
Increased viral RNA replication[4]

Theiler’s murine encephalomyelitis virus (TMEV)Mice Significantly exacerbated demyelination and inflammation without neuroprotection in the central nervous system(i) Exacerbated clinical signs and histological findings in TMEV infected mice
(ii) Resulted in a twofold increase in IL-17 and a twofold decrease in IFN-γ
[19]