Pages that link to "Q39753081"
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The following pages link to The lytic cycle of Epstein-Barr virus is associated with decreased expression of cell surface major histocompatibility complex class I and class II molecules (Q39753081):
Displaying 34 items.
- De novo infection with rhesus monkey rhadinovirus leads to the accumulation of multiple intranuclear capsid species during lytic replication but favors the release of genome-containing virions (Q30311978) (← links)
- The Epstein-Barr virus G-protein-coupled receptor contributes to immune evasion by targeting MHC class I molecules for degradation (Q33396983) (← links)
- Stage-specific inhibition of MHC class I presentation by the Epstein-Barr virus BNLF2a protein during virus lytic cycle (Q33474804) (← links)
- Interferon regulatory factor 7 is negatively regulated by the Epstein-Barr virus immediate-early gene, BZLF-1 (Q33908810) (← links)
- The interplay between Epstein-Barr virus and the immune system: a rationale for adoptive cell therapy of EBV-related disorders (Q34166602) (← links)
- The Epstein-Barr virus BZLF1 protein inhibits tumor necrosis factor receptor 1 expression through effects on cellular C/EBP proteins (Q34291099) (← links)
- Latent membrane protein 1 inhibits Epstein-Barr virus lytic cycle induction and progress via different mechanisms. (Q34532370) (← links)
- Epstein-Barr virus immediate-early protein BZLF1 inhibits tumor necrosis factor alpha-induced signaling and apoptosis by downregulating tumor necrosis factor receptor 1 (Q34553626) (← links)
- Terminal differentiation into plasma cells initiates the replicative cycle of Epstein-Barr virus in vivo (Q34553645) (← links)
- Epstein-Barr virus Zta-induced immunomodulators from nasopharyngeal carcinoma cells upregulate interleukin-10 production from monocytes (Q35077651) (← links)
- TAP-independent antigen presentation on MHC class I molecules: lessons from Epstein–Barr virus (Q35111423) (← links)
- Inhibition of heavy chain and beta2-microglobulin synthesis as a mechanism of major histocompatibility complex class I downregulation during Epstein-Barr virus replication (Q35635291) (← links)
- Host shutoff during productive Epstein-Barr virus infection is mediated by BGLF5 and may contribute to immune evasion (Q35652539) (← links)
- HLA Allele E*01:01 Is Associated with a Reduced Risk of EBV-Related Classical Hodgkin Lymphoma Independently of HLA-A*01/*02. (Q35742269) (← links)
- The Epstein-Barr Virus Lytic Protein BZLF1 as a Candidate Target Antigen for Vaccine Development (Q35815850) (← links)
- Interference with T cell receptor–HLA-DR interactions by Epstein–Barr virus gp42 results in reduced T helper cell recognition (Q36161320) (← links)
- Control of Epstein-Barr virus infection in vitro by T helper cells specific for virion glycoproteins. (Q36228567) (← links)
- Herpesvirus interference with major histocompatibility complex class II-restricted T-cell activation (Q36641746) (← links)
- Viral proteins interfering with antigen presentation target the major histocompatibility complex class I peptide-loading complex (Q37151597) (← links)
- Immune responses to Epstein-Barr virus: molecular interactions in the virus evasion of CD8+ T cell immunity (Q37652046) (← links)
- Immune Evasion by Epstein-Barr Virus (Q38597254) (← links)
- Reduced humoral immunity and atypical cell-mediated immunity in response to vaccination in cows naturally infected with bovine leukemia virus (Q39173906) (← links)
- (-)-Epigallocatechin-3-gallate inhibition of Epstein-Barr virus spontaneous lytic infection involves ERK1/2 and PI3-K/Akt signaling in EBV-positive cells (Q39238849) (← links)
- Epstein-Barr virus regulates STAT1 through latent membrane protein 1. (Q39736747) (← links)
- Cellular factors associated with latency and spontaneous Epstein-Barr virus reactivation in B-lymphoblastoid cell lines. (Q39740136) (← links)
- The DNase of gammaherpesviruses impairs recognition by virus-specific CD8+ T cells through an additional host shutoff function (Q40033016) (← links)
- The switch from latent to productive infection in epstein-barr virus-infected B cells is associated with sensitization to NK cell killing. (Q40213261) (← links)
- Two alternate strategies for innate immunity to Epstein-Barr virus: One using NK cells and the other NK cells and γδ T cells. (Q40216780) (← links)
- BZLF1, an Epstein-Barr virus immediate-early protein, induces p65 nuclear translocation while inhibiting p65 transcriptional function (Q40508322) (← links)
- Cooperation between Epstein-Barr virus immune evasion proteins spreads protection from CD8+ T cell recognition across all three phases of the lytic cycle (Q41807836) (← links)
- Natural killer cell education in mice with single or multiple major histocompatibility complex class I molecules (Q41926180) (← links)
- Cytotoxic CD4+ T cell responses to EBV contrast with CD8 responses in breadth of lytic cycle antigen choice and in lytic cycle recognition (Q42066029) (← links)
- CD8+ immunodominance among Epstein-Barr virus lytic cycle antigens directly reflects the efficiency of antigen presentation in lytically infected cells (Q42282904) (← links)
- Tonsillar homing of Epstein-Barr virus-specific CD8+ T cells and the virus-host balance (Q42938727) (← links)