scholarly journals Immune evasion proteins gpUS2 and gpUS11 of human cytomegalovirus incompletely protect infected cells from CD8 T cell recognition

Virology ◽  
2009 ◽  
Vol 391 (1) ◽  
pp. 5-19 ◽  
Author(s):  
K. Besold ◽  
M. Wills ◽  
B. Plachter
2010 ◽  
Vol 91 (8) ◽  
pp. 2040-2048 ◽  
Author(s):  
Siok-Keen Tey ◽  
Felicia Goodrum ◽  
Rajiv Khanna

Recent studies have shown that long-term persistence of human cytomegalovirus (HCMV) in mononuclear cells of myeloid lineage is dependent on the UL138 open reading frame, which promotes latent infection. Although T-cell recognition of protein antigens from all stages of lytic HCMV infection is well established, it is not clear whether proteins expressed during latent HCMV infection can also be recognized. This study conducted an analysis of T-cell response towards proteins associated with HCMV latency. Ex vivo analysis of T cells from healthy virus carriers revealed a dominant CD8+ T-cell response to the latency-associated pUL138 protein, which recognized a non-canonical 13 aa epitope in association with HLA-B*3501. These pUL138-specific T cells displayed a range of memory phenotypes that were in general less differentiated than that previously described in T cells specific for HCMV lytic antigens. Antigen-presentation assays revealed that endogenous pUL138 could be presented efficiently by HCMV-infected cells. However, T-cell recognition of pUL138 was dependent on newly synthesized protein, with little presentation from stable, long-lived protein. These data demonstrate that T cells targeting latency-associated protein products exist, although HCMV may limit the presentation of latent proteins, thereby restricting T-cell recognition of latently infected cells.


2004 ◽  
Vol 72 (5) ◽  
pp. 3059-3062 ◽  
Author(s):  
Alberto Diaz-Quiñonez ◽  
Natalia Martin-Orozco ◽  
Armando Isibasi ◽  
Vianney Ortiz-Navarrete

ABSTRACT We report the identification of two peptides from Salmonella OmpC porin that can bind to major histocompatibility complex class I Kb molecules and are targets of cytotoxic T lymphocytes from Salmonella-infected mice. These peptides are conserved in gram-negative bacterial porins and are the first Salmonella porin-specific epitopes described for possible CD8+-T-cell elimination of infected cells.


2014 ◽  
Vol 10 (8) ◽  
pp. e1004322 ◽  
Author(s):  
Laura L. Quinn ◽  
Jianmin Zuo ◽  
Rachel J. M. Abbott ◽  
Claire Shannon-Lowe ◽  
Rosemary J. Tierney ◽  
...  

Blood ◽  
2009 ◽  
Vol 114 (19) ◽  
pp. 4128-4137 ◽  
Author(s):  
Allen K. L. Cheung ◽  
David J. Gottlieb ◽  
Bodo Plachter ◽  
Sandra Pepperl-Klindworth ◽  
Selmir Avdic ◽  
...  

AbstractThe capacity of human cytomegalovirus (HCMV) to establish and maintain a latent infection from which it can later reactivate ensures its widespread distribution in the population, but the mechanisms enabling maintenance of latency in the face of a robust immune system are poorly understood. We examined the role of the HCMV UL111A gene, which encodes homologs of the immunosuppressive cytokine interleukin-10 in the context of latent infection of myeloid progenitor cells. A UL111A deletion virus was able to establish, maintain, and reactivate from experimental latency in a manner comparable with parental virus, but major histocompatibility complex class II levels increased significantly on the surfaces of cells infected with the deletion virus. Importantly, there was an increase in both allogeneic and autologous peripheral blood mononuclear cells and CD4+ T-cell responses to UL111A deletion virus-infected myeloid progenitors, indicating that loss of the capacity to express viral interleukin-10 during latency results in latently infected cells becoming more readily recognizable by a critical arm of the immune response. The detection of a viral gene that suppresses CD4+ T-cell recognition of latently infected cells identifies an immune evasion strategy that probably enhances the capacity of HCMV to persist in a latent state within the human host.


Hepatology ◽  
2021 ◽  
Author(s):  
Adrian Kuipery ◽  
Juan Diego Sanchez Vasquez ◽  
Aman Mehrotra ◽  
Jordan J. Feld ◽  
Harry L. A. Janssen ◽  
...  

2019 ◽  
Vol 70 (1) ◽  
pp. e51
Author(s):  
Christine Y.L. Tham ◽  
Janine Kah ◽  
Anthony Tan ◽  
Alessandro Loglio ◽  
Camille Sureau ◽  
...  

Cell Reports ◽  
2019 ◽  
Vol 27 (1) ◽  
pp. 142-153.e4 ◽  
Author(s):  
Blandine Monel ◽  
Annmarie McKeon ◽  
Pedro Lamothe-Molina ◽  
Priya Jani ◽  
Julie Boucau ◽  
...  

Viruses ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 1363
Author(s):  
Giuseppina Maria Elena Colomba ◽  
Noemi Urone ◽  
Vito di Marco ◽  
Donatella Ferraro

Therapies for HCV care could change the prevalence and the geographic distribution of genotypes due to differences in Sustained Virologic Response (SVR). In this scenario, uncommon genotypes/subtypes, such as genotype 4, could spread from high-risk groups, replacing genotypes eradicated by antiviral drugs. Genotype eradication is also strongly influenced by the CD8+ T cell response. In this study, the genetic variability in HCV genotype 4 strains obtained from a cohort of 67 patients naïve to DAA therapy was evaluated. We found that the presence of resistance-associated substitutions (RAS) was able to affect drug responses. Next, using a prediction tool, viral mutations were identified by their ability, or lack thereof, to reduce the binding affinity with HLA, which affects T cell recognition. The Bayesian coalescent analysis suggested two different circulation clusters, one in risk groups (IDUs and MSM) and the other due to migration flows, dated to 1940 and 1915, respectively. Most of the RAS overlapped with HLA and a lack of binding mutations was observed in 96% of strains. This study describes the introduction of HCV genotype 4 in a region of the Mediterranean basin and evaluates how HCV genotype 4’s genetic variability could affect the response of antiviral drugs and CD8+ T cell recognition.


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