Diverse immune evasion strategies by human cytomegalovirus

Noriega, Vanessa M.; Redmann, Veronika; Gardner, Thomas J.; Tortorella, Domenico

doi:10.1007/s12026-012-8304-8

Cited by 111 publications

(90 citation statements)

References 141 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CMV is known to evade the immune system through a variety of mechanisms. There was still a risk of acute exacerbation of chronic bronchial CMV infection although the cellular immune function was normal or even increased (18)(19)(20)(21).…”

Section: Discussionmentioning

confidence: 99%

Bruton’s agammaglobulinemia in an adult male due to a novel mutation: a case report

Liu

et al. 2016

J. Thorac. Dis.

View full text Add to dashboard Cite

X-linked agammaglobulinemia (XLA) is caused by mutation in the gene coding for Bruton's tyrosine kinase (BTK), which impairs peripheral B cell maturation and hypogammaglobulinemia. In this report, we present a case of XLA in a 22-year-old adult male. Genetic testing revealed a novel mutation located at the conserved region (c.383T>C). The patient had a history of recurrent respiratory tract infection which eventually progressed to chronic type II respiratory failure. Several pathogenic bacteria were isolated on culture of respiratory secretions obtained on bronchoscopy. The patient improved on treatment with antibiotics.

show abstract

Section: Discussionmentioning

confidence: 99%

Bruton’s agammaglobulinemia in an adult male due to a novel mutation: a case report

Liu

et al. 2016

J. Thorac. Dis.

View full text Add to dashboard Cite

show abstract

“…Following primary infection, which is usually benign in immunocompetent individuals, CMV can establish latency in myeloid and endothelial cells and can periodically reactivate to an active infection (3). CMV disease is a major cause of morbidity and mortality in immunosuppressed patients, especially recipients of solid organ or bone marrow transplants, neonates, AIDS patients, cardiovascular disease patients, and the elderly (4)(5)(6).…”

mentioning

confidence: 99%

“…While viral membrane envelope proteins are known to play critical roles in the virus life cycle by permitting cellular attachment and fusion with the host membrane, many CMV glycoproteins perform additional roles by serving critical functions in immune evasion, both within and outside the cellular environment. We and others previously reviewed the elegant methods by which CMV "immune evasin" proteins dampen the anti-CMV immune response (3,(28)(29)(30). Therefore, in the sections below, we aim to highlight the critical and diverse roles of CMV-encoded virion envelope proteins and their "innate" ability to evade the immune response.…”

mentioning

confidence: 99%

Virion Glycoprotein-Mediated Immune Evasion by Human Cytomegalovirus: a Sticky Virus Makes a Slick Getaway

Gardner

Tortorella

2016

Microbiol Mol Biol Rev

Self Cite

View full text Add to dashboard Cite

SUMMARYThe prototypic herpesvirus human cytomegalovirus (CMV) exhibits the extraordinary ability to establish latency and maintain a chronic infection throughout the life of its human host. This is even more remarkable considering the robust adaptive immune response elicited by infection and reactivation from latency. In addition to the ability of CMV to exist in a quiescent latent state, its persistence is enabled by a large repertoire of viral proteins that subvert immune defense mechanisms, such as NK cell activation and major histocompatibility complex antigen presentation, within the cell. However, dissemination outside the cell presents a unique existential challenge to the CMV virion, which is studded with antigenic glycoprotein complexes targeted by a potent neutralizing antibody response. The CMV virion envelope proteins, which are critical mediators of cell attachment and entry, possess various characteristics that can mitigate the humoral immune response and prevent viral clearance. Here we review the CMV glycoprotein complexes crucial for cell attachment and entry and propose inherent properties of these proteins involved in evading the CMV humoral immune response. These include viral glycoprotein polymorphism, epitope competition, Fc receptor-mediated endocytosis, glycan shielding, and cell-to-cell spread. The consequences of CMV virion glycoprotein-mediated immune evasion have a major impact on persistence of the virus in the population, and a comprehensive understanding of these evasion strategies will assist in designing effective CMV biologics and vaccines to limit CMV-associated disease.

show abstract

“…However, early downregulation of MHC I was observed in infected cells, indicating that HCMV has developed means to subvert CTL recognition (Barnes & Grundy, 1992;Yamashita et al, 1993). Endoplasmic reticulum (ER)-resident viral proteins encoded in the genomic region from US2 to US11 have been found to be instrumental in this downmodulation (Jones et al, 1995;Noriega et al, 2012a). The glycoprotein (gp) US3 binds to MHC I molecules in the ER, leading to their retention (Ahn et al, 1996;Jones et al, 1996;Lee et al, 2000;Zhao & Biegalke, 2003).…”

Section: Introductionmentioning

confidence: 99%

Suppression of CD8+ T-cell recognition in the immediate-early phase of human cytomegalovirus infection

Hesse

Ameres

Besold

et al. 2013

Journal of General Virology

View full text Add to dashboard Cite

Human cytomegalovirus (HCMV) interferes with MHC class I-restricted antigen presentation and thereby reduces recognition by CD8 + T-cells. This interference is mediated primarily by endoplasmic reticulum-resident glycoproteins that are encoded in the US2-11 region of the viral genome. Such a suppression of recognition would be of particular importance immediately after infection, because several immunodominant viral antigens are already present in the cell in this phase. However, which of the evasion proteins gpUS2-11 interfere(s) with antigen presentation to CD8 + T-cells at this time of infection is not known. Here we address this question, using recombinant viruses (RV) that express only one of the immunoevasins gpUS2, gpUS3 or gpUS11. Infection with RV-US3 had only a limited impact on the presentation of peptides from the CD8 + T-cell antigens IE1 and pp65 under immediate-early (IE) conditions imposed by cycloheximide/ actinomycin D blocking. Unexpectedly, both RV-US2 and RV-US11 considerably impaired the recognition of IE1 and pp65 by CD8 + T-cells, and both US2 and, to a lesser extent, US11 were transcribed under IE conditions. Thus, gpUS2 and gpUS11 are key effectors of MHC class I immunoevasion immediately after HCMV infection.

show abstract

Diverse immune evasion strategies by human cytomegalovirus

Cited by 111 publications

References 141 publications

Bruton’s agammaglobulinemia in an adult male due to a novel mutation: a case report

Bruton’s agammaglobulinemia in an adult male due to a novel mutation: a case report

Virion Glycoprotein-Mediated Immune Evasion by Human Cytomegalovirus: a Sticky Virus Makes a Slick Getaway

Suppression of CD8+ T-cell recognition in the immediate-early phase of human cytomegalovirus infection

Contact Info

Product

Resources

About