Subversion of Host Defense Mechanisms by Adenoviruses

Burgert, Hans‐Gerhard; Ruzsics, Zsolt; Obermeier, Sandra; Hilgendorf, Annette; Windheim, Mark; Elsing, A.

doi:10.1007/978-3-642-59421-2_16

Cited by 105 publications

(124 citation statements)

References 200 publications

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“…16,17 Furthermore, HadVinfected cells may escape from recognition by the immune system through several mechanisms. 18 Evidence has been obtained that recovery of immunity after SCT is essential for the elimination of HAdV infection. The first indication was a case report in which a severe HAdV infection resolved in a patient after infusion of donor lymphocytes (DLI).…”

Section: Immunity and Hadv Infectionmentioning

confidence: 99%

Adenovirus infection in children after allogeneic stem cell transplantation: diagnosis, treatment and immunity

Tol

Claas

Heemskerk

et al. 2005

Bone Marrow Transplant

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Summary:Human adenoviruses (HAdV) are a frequent cause of potentially fatal infections in patients after allogeneic stem cell transplantation, especially in children. Monitoring of serum/plasma by real-time quantitative PCR is a sensitive tool for the recognition of patients at risk of a potentially fatal infection and for the evaluation of the efficacy of treatment. Data from a retrospective study and from a prospective study demonstrate that recovery of immunity after transplantation is essential for the elimination of HAdV infection. The feasibility of several approaches for the manipulation of immunity in the immunocompromised host to prevent a fatal course of the infection is discussed. Bone Marrow Transplantation (2005) 35, S73-S76.

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Section: Immunity and Hadv Infectionmentioning

confidence: 99%

Adenovirus infection in children after allogeneic stem cell transplantation: diagnosis, treatment and immunity

Tol

Claas

Heemskerk

et al. 2005

Bone Marrow Transplant

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“…This limits the infection and is one of the major mechanisms the host immune system utilized for virus clearance. Adenovirus evolved several genes to antagonize this process (Burgert et al, 2002). Adenoviral E1B-19kD blocks TNF-mediated apoptosis mainly by binding to Bax and Bak, both of which belong to proapoptotic Bcl-2 family.…”

Section: Viral Mutants That Interfere With the Tnf Signaling Pathwaymentioning

confidence: 99%

“…Apart from E1B-19kD, several other adenoviral genes are capable of blocking TNF-induced cell death. Adenoviral E3B contains receptor internalization and degradation (RID) complex and E3-14.7, both of which have important functions in immunomodulation (Burgert et al, 2002). The RID complex, composed of RIDa (10.4 kDa) and RIDb (14.5 kDa), localizes to the plasma membrane and intracellular vesicles.…”

Section: Viral Mutants That Interfere With the Tnf Signaling Pathwaymentioning

confidence: 99%

Viruses with deletions in antiapoptotic genes as potential oncolytic agents

Liu

Kirn

2005

Oncogene

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“…HPV infection results in physical degradation of p53 through binding of p53 to the viral E6 protein (Mantovani and Banks, 2001). Adenoviral infection leads to p53 inactivation via the p53-binding viral protein, E1b (McCormick, 2000;Burgert et al, 2002). For both types of viruses, any deficiency in p53 inactivation strongly suppresses viral replication due to a rapid apoptotic response in the host cells.…”

Section: Introductionmentioning

confidence: 99%

Mycoplasma infection suppresses p53, activates NF-κB and cooperates with oncogenic Ras in rodent fibroblast transformation

et al. 2008

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Prokaryotes of the genus Mycoplasma are the smallest cellular organisms that persist as obligate extracellular parasites. Although mycoplasma infection is known to be associated with chromosomal instability and can promote malignant transformation, the mechanisms underlying these phenomena remain unknown. Since persistence of many cellular parasites requires suppression of apoptosis in host cells, we tested the effect of mycoplasma infection on the activity of the p53 and nuclear factor (NF)-jB pathways, major mechanisms controlling programmed cell death. To monitor the activity of p53 and NF-jB in mycoplasma-infected cells, we used a panel of reporter cell lines expressing the bacterial b-galactosidase gene under the control of p53-or NF-jB-responsive promoters. Cells incubated with media conditioned with different species of mycoplasma showed constitutive activation of NF-jB and reduced activation of p53, common characteristics of the majority of human tumor cells, with M. arginini having the strongest effect among the species tested. Moreover, mycoplasma infection reduced the expression level and inducibility of an endogenous p53-responsive gene, p21 waf1 , and inhibited apoptosis induced by genotoxic stress. Infection with M. arginini made rat and mouse embryo fibroblasts susceptible to transformation with oncogenic H-Ras, whereas mycoplasma-free cells underwent irreversible p53-dependent growth arrest. Mycoplasma infection was as effective as shRNA-mediated knockdown of p53 expression in making rodent fibroblasts permissive to Rasinduced transformation. These observations indicate that mycoplasma infection plays the role of a p53-suppressing oncogene that cooperates with Ras in cell transformation and suggest that the carcinogenic and mutagenic effects of mycoplasma might be due to inhibition of p53 tumor suppressor function by this common human parasite.

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Subversion of Host Defense Mechanisms by Adenoviruses

Cited by 105 publications

References 200 publications

Adenovirus infection in children after allogeneic stem cell transplantation: diagnosis, treatment and immunity

Adenovirus infection in children after allogeneic stem cell transplantation: diagnosis, treatment and immunity

Viruses with deletions in antiapoptotic genes as potential oncolytic agents

Mycoplasma infection suppresses p53, activates NF-κB and cooperates with oncogenic Ras in rodent fibroblast transformation

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