EBV belongs to human gamma-herpesviruses which are able to establish latency in lymphocyte. About more than 95% of adults are carriers of the virus. A common disease caused by EBV is mononucleosis. Besides, EBV can transform and cause cancer. Every year, there are 200,000 new cases of cancer and more than 140,000 deaths worldwide. Two major targets of The virus are B-lymphocytes and epithelial cells. Epstein-Barr virus has two stages in its life cycle; latency and lytic replications.
Latent EBV pass through three latency phases (1). latency III, the virus infects a resting B-cell. The virus encodes a protein to induce the B-cell to proliferate. latency II, the virus gradually shuts off its genes, at last enter to latency I. Functions of …show more content…
The innate responses induce many proinflammatory factors which serve as an antiviral immune such as tumor necrosis factor alpha, interferon gamma (3). Latent Infection of Epstein-Barr virus induces secretion of several inflammatory factors, meanwhile lytic infections avoid the antiviral inflammatory response. Furthermore, it has been proposed that lytic proteins of herpesviruses a key role in avoiding host immune responses, including disruption of interferon signaling. For example, cytomegalovirus, EBV, and Varicella-Zoster virus inhibit IFN-γ-induced MHC class II expression. In addition, Kaposi's sarcoma-associated herpesvirus avoid the immune responses by encoding proteins which interfere with interferon signal transduction and subsequent gene transactivation …show more content…
BZLF1 binds to the promoter of TNF-⍺ and prevents NF-B activation. However, there was a decrease in EBV replication after the introduction of a ⧍ 207-210 mutation in BZLF1 (5). Moreover, previous studies demonstrated that BZLF1 Required both the Transactivation Domain and DNA Binding Domain to inhibition of IFN-ᵞ Signaling through STAT1. IFN-γ also was unable to induce MHC Class II Expression in a cell with BZLF1 (4). Additional studies showed that deletion of region 177 to 203 and particularly 27bp in BZLF1 which is near the Transactivation Domain, played an important role in responsiveness to anti-Ig
Latent EBV pass through three latency phases (1). latency III, the virus infects a resting B-cell. The virus encodes a protein to induce the B-cell to proliferate. latency II, the virus gradually shuts off its genes, at last enter to latency I. Functions of …show more content…
The innate responses induce many proinflammatory factors which serve as an antiviral immune such as tumor necrosis factor alpha, interferon gamma (3). Latent Infection of Epstein-Barr virus induces secretion of several inflammatory factors, meanwhile lytic infections avoid the antiviral inflammatory response. Furthermore, it has been proposed that lytic proteins of herpesviruses a key role in avoiding host immune responses, including disruption of interferon signaling. For example, cytomegalovirus, EBV, and Varicella-Zoster virus inhibit IFN-γ-induced MHC class II expression. In addition, Kaposi's sarcoma-associated herpesvirus avoid the immune responses by encoding proteins which interfere with interferon signal transduction and subsequent gene transactivation …show more content…
BZLF1 binds to the promoter of TNF-⍺ and prevents NF-B activation. However, there was a decrease in EBV replication after the introduction of a ⧍ 207-210 mutation in BZLF1 (5). Moreover, previous studies demonstrated that BZLF1 Required both the Transactivation Domain and DNA Binding Domain to inhibition of IFN-ᵞ Signaling through STAT1. IFN-γ also was unable to induce MHC Class II Expression in a cell with BZLF1 (4). Additional studies showed that deletion of region 177 to 203 and particularly 27bp in BZLF1 which is near the Transactivation Domain, played an important role in responsiveness to anti-Ig