(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
(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
(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
(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
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