scholarly journals The Trafficking of Viral Immune Evasion Protein m4/gp34 and MHC class I complexes is Facilitated by Another Viral Gene m168 in Murine Cytomegalovirus Infections

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Xiuju Lu ◽  
Kathy Cho ◽  
Ann Hill
Keyword(s):  
Mhc Class I ◽  
Immune Evasion ◽  
Class I ◽  
Murine Cytomegalovirus ◽  
Viral Gene ◽  
Viral Immune Evasion ◽  
Cytomegalovirus Infections

scholarly journals Processing and Presentation of Murine Cytomegalovirus pORFm164-Derived Peptide in Fibroblasts in the Face of All Viral Immunosubversive Early Gene Functions

2002 ◽  
Vol 76 (12) ◽  
pp. 6044-6053 ◽  
Author(s):  
Rafaela Holtappels ◽  
Natascha K. A. Grzimek ◽  
Christian O. Simon ◽  
Doris Thomas ◽  
Doris Dreis ◽  
...  
Keyword(s):  
T Cells ◽  
Mhc Class I ◽  
Immune Evasion ◽  
Cd8 T Cells ◽  
Early Gene ◽  
Class I ◽  
Murine Cytomegalovirus ◽  
Viral Gene ◽  
Immune Recognition ◽  
Bottom Line

ABSTRACT CD8 T cells are the principal effector cells in the resolution of acute murine cytomegalovirus (mCMV) infection in host organs. This undoubted antiviral and protective in vivo function of CD8 T cells appeared to be inconsistent with immunosubversive strategies of the virus effected by early (E)-phase genes m04, m06, and m152. The so-called immune evasion proteins gp34, gp48, and gp37/40, respectively, were found to interfere with peptide presentation at different steps in the major histocompatibility complex (MHC) class I pathway of antigen processing and presentation in fibroblasts. Accordingly, they were proposed to prevent recognition and lysis of infected fibroblasts by cytolytic T lymphocytes (CTL) during the E phase of viral gene expression. We document here that the previously identified MHC class I Dd-restricted antigenic peptide 257AGPPRYSRI265 encoded by gene m164 is processed as well as presented for recognition by m164-specific CTL during the E and late phases of viral replication in the very same cells in which the immunosubversive viral proteins are effectual in preventing the presentation of processed immediate-early 1 (m123-exon 4) peptide 168YPHFMPTNL176. Thus, while immunosubversion is a reality, these mechanisms are apparently not as efficient as the term immune evasion implies. The pORFm164-derived peptide is the first noted peptide that constitutively escapes the immunosubversive viral functions. The most important consequence is that even the concerted action of all immunosubversive E-phase proteins eventually fails to prevent immune recognition in the E phase. The bottom-line message is that there exists no immune evasion of mCMV in fibroblasts.

New insights into the structure of the MHC class I peptide-loading complex and mechanisms of TAP inhibition by viral immune evasion proteins

2019 ◽  
Vol 113 ◽  
pp. 103-114 ◽  
Author(s):  
Patrique Praest ◽  
A. Manuel Liaci ◽  
Friedrich Förster ◽  
Emmanuel J.H.J. Wiertz
Keyword(s):  
Mhc Class I ◽  
Immune Evasion ◽  
Class I ◽  
Viral Immune Evasion ◽  
Peptide Loading

Viral immune evasion: Lessons in MHC class I antigen presentation

2015 ◽  
Vol 27 (2) ◽  
pp. 125-137 ◽  
Author(s):  
Michael L. van de Weijer ◽  
Rutger D. Luteijn ◽  
Emmanuel J.H.J. Wiertz
Keyword(s):  
Antigen Presentation ◽  
Mhc Class I ◽  
Immune Evasion ◽  
Class I ◽  
Viral Immune Evasion ◽  
Mhc Class I Antigen

scholarly journals MHC Class I Cross-Presentation by Dendritic Cells Counteracts Viral Immune Evasion

2012 ◽  
Vol 3 ◽  
Author(s):  
Katrin Nopora ◽  
Caroline A. Bernhard ◽  
Christine Ried ◽  
Alejandro A. Castello ◽  
Kenneth M. Murphy ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Mhc Class I ◽  
Immune Evasion ◽  
Class I ◽  
Cross Presentation ◽  
Viral Immune Evasion

scholarly journals The Multiple Immune-Evasion Genes of Murine Cytomegalovirus Are Not Redundant

2001 ◽  
Vol 194 (7) ◽  
pp. 967-978 ◽  
Author(s):  
Daniel G. Kavanagh ◽  
Marielle C. Gold ◽  
Markus Wagner ◽  
Ulrich H. Koszinowski ◽  
Ann B. Hill
Keyword(s):  
Antigen Presentation ◽  
Mhc Class I ◽  
Cytotoxic T Lymphocytes ◽  
Immune Evasion ◽  
Surface Expression ◽  
Class I ◽  
Murine Cytomegalovirus ◽  
Histocompatibility Complex ◽  
Golgi Compartment ◽  
Partial Retention

Both human cytomegaloviruses (HCMVs) and murine cytomegaloviruses (MCMVs) encode multiple genes that interfere with antigen presentation by major histocompatibility complex (MHC) class I, and thus protect infected targets from lysis by virus-specific cytotoxic T lymphocytes (CTLs). HCMV has been shown to encode four such genes and MCMV to encode two. MCMV m152 blocks the export of class I from a pre-Golgi compartment, and MCMV m6 directs class I to the lysosome for degradation. A third MCMV gene, m4, encodes a glycoprotein which is expressed at the cell surface in association with class I. Here we here show that m4 is a CTL-evasion gene which, unlike previously described immune-evasion genes, inhibited CTLs without blocking class I surface expression. m152 was necessary to block antigen presentation to both Kb- and Db-restricted CTL clones, while m4 was necessary to block presentation only to Kb-restricted clones. m152 caused complete retention of Db, but only partial retention of Kb, in a pre-Golgi compartment. Thus, while m152 effectively inhibited Db-restricted CTLs, m4 was required to completely inhibit Kb-restricted CTLs. We propose that cytomegaloviruses encode multiple immune-evasion genes in order to cope with the diversity of class I molecules in outbred host populations.

Autophagy mediates transporter associated with antigen processing-independent presentation of viral epitopes through MHC class I pathway

Blood ◽  
2012 ◽  
Vol 120 (5) ◽  
pp. 994-1004 ◽  
Author(s):  
Siok-Keen Tey ◽  
Rajiv Khanna
Keyword(s):  
Endoplasmic Reticulum ◽  
Mhc Class I ◽  
Immune Evasion ◽  
Antigen Processing ◽  
Secretory Pathway ◽  
Proteasomal Degradation ◽  
Class I ◽  
Acid Stability ◽  
Peptide Epitopes ◽  
Viral Immune Evasion

Abstract The endogenous presentation of the majority of viral epitopes through MHC class I pathway is strictly dependent on the transporter associated with antigen processing (TAP) complex, which transfers the peptide products of proteasomal degradation into the endoplasmic reticulum. A small number of epitopes can be presented through the TAP-independent pathway, the precise mechanism for which remains largely unresolved. Here we show that TAP-independent presentation can be mediated by autophagy and that this process uses the vacuolar pathway and not the conventional secretory pathway. After macroautophagy, the antigen is processed through a proteasome-independent pathway, and the peptide epitopes are loaded within the autophagolysosomal compartment in a process facilitated by the relative acid stability of the peptide-MHC interaction. Despite bypassing much of the conventional MHC class I pathway, the autophagy-mediated pathway generates the same epitope as that generated through the conventional pathway and thus may have a role in circumventing viral immune evasion strategies that primarily target the conventional pathway.

scholarly journals Mechanisms of virus immune evasion lead to development from chronic inflammation to cancer formation associated with human papillomavirus infection

2012 ◽  
Vol 6 (2) ◽  
pp. 17 ◽  
Author(s):  
Masachika Senba ◽  
Naoki Mori
Keyword(s):  
Immune Response ◽  
Human Papillomavirus ◽  
Immune System ◽  
Tumor Suppressor ◽  
Chronic Inflammation ◽  
Mhc Class I ◽  
Immune Evasion ◽  
Latency Period ◽  
Class I ◽  
Presentation Pathway

Human papillomavirus (HPV) has developed strategies to escape eradication by innate and adaptive immunity. Immune response evasion has been considered an important aspect of HPV persistence, which is the main contributing factor leading to HPV-related cancers. HPV-induced cancers expressing viral oncogenes E6 and E7 are potentially recognized by the immune system. The major histocompatibility complex (MHC) class I molecules are patrolled by natural killer cells and CD8<sup>+</sup> cytotoxic T lymphocytes, respectively. This system of recognition is a main target for the strategies of immune evasion deployed by viruses. The viral immune evasion proteins constitute useful tools to block defined stages of the MHC class I presentation pathway, and in this way HPV avoids the host immune response. The long latency period from initial infection to persistence signifies that HPV evolves mechanisms to escape the immune response. It has now been established that there are oncogenic mechanisms by which E7 binds to and degrades tumor suppressor Rb, while E6 binds to and inactivates tumor suppressor p53. Therefore, interaction of p53 and pRb proteins can give rise to an increased immortalization and genomic instability. Overexpression of NF-kB in cervical and penile cancers suggests that NF-kB activation is a key modulator in driving chronic inflammation to cancer. HPV oncogene-mediated suppression of NF-kB activity contributes to HPV escape from the immune system. This review focuses on the diverse mechanisms of the virus immune evasion with HPV that leads to chronic inflammation and cancer.

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