Bovine herpesvirus-1 infection affects the peptide transport activity in bovine cells

Hinkley, Susanne; Hill, Ann B.; Srikumaran, Subramaniam

doi:10.1016/s0168-1702(97)00128-7

Cited by 68 publications

(48 citation statements)

References 35 publications

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“…For example, the murine ␥ 2 -herpesvirus, MHV-68, encodes an MK3 protein with the ability to target TAP for ubiquitination and proteosomal degradation (30). Interestingly, the recently identified ␣-herpesvirus BHV-1-encoded inhibitor of TAP uses a combination of the two mechanisms by locking the TAP transporter in a translocation-incompetent state as well as by inducing degradation of its components (27,45).…”

Section: Discussionmentioning

confidence: 99%

Impaired Transporter Associated with Antigen Processing-Dependent Peptide Transport during Productive EBV Infection

Ressing

Keating

Leeuwen

et al. 2005

The Journal of Immunology

103

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Human herpesviruses, including EBV, persist for life in infected individuals. During the lytic replicative cycle that is required for the production of infectious virus and transmission to another host, many viral Ags are expressed. Especially at this stage, immune evasion strategies are likely to be advantageous to avoid elimination of virus-producing cells. However, little is known about immune escape during productive EBV infection because no fully permissive infection model is available. In this study, we have developed a novel strategy to isolate populations of cells in an EBV lytic cycle based on the expression of a reporter gene under the control of an EBV early lytic cycle promoter. Thus, induction of the viral lytic cycle in transfected EBV+ B lymphoma cells resulted in concomitant reporter expression, allowing us, for the first time, to isolate highly purified cell populations in lytic cycle for biochemical and functional studies. Compared with latently infected B cells, cells supporting EBV lytic cycle displayed down-regulation of surface HLA class I, class II, and CD20, whereas expression levels of other surface markers remained unaffected. Moreover, during lytic cycle peptide transport into the endoplasmic reticulum, was reduced to <30% of levels found in latent infection. Because steady-state levels of TAP proteins were unaffected, these results point toward EBV-induced interference with TAP function as a specific mechanism contributing to the reduced levels of cell surface HLA class I. Our data implicate that EBV lytic cycle genes encode functions to evade T cell recognition, thereby creating a window for the generation of viral progeny.

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Section: Discussionmentioning

confidence: 99%

Impaired Transporter Associated with Antigen Processing-Dependent Peptide Transport during Productive EBV Infection

Ressing

Keating

Leeuwen

et al. 2005

The Journal of Immunology

103

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“…The latter is known to decrease host defence amongst others by diminishing the activities of T lymphocytes, B lymphocytes, monocytes and macrophages [24,67] and by interfering with the host's antigen presentation machinery to evade the host's immune response in vivo [74,134]. Moreover, it has been shown that leukocyte exposure to inflammatory cytokines released in response to BHV-1 infection (interleukin-1 beta, interleukin-8, tumour necrosis factor alpha and interferon gamma) can modulate the migration and functional activation of bovine leukocytes [26,105,106].…”

Section: Molecular Synergies With Other Pathogensmentioning

confidence: 99%

How Mannheimia haemolytica defeats host defence through a kiss of death mechanism

2005

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-Mannheimia haemolytica induced pneumonias are only observed in goats, sheep and cattle. The bacterium produces several virulence factors,whose principal ones are lipopolysaccharide and leukotoxin. The latter is cytotoxic only for ruminant leukocytes, a phenomenon that is correlated with its ability to bind and interact with the ruminant β2-integrin Lymphocyte Function-associated Antigen 1. This paper globally reviews all the information available on host-pathogen interactions underlying respiratory mannheimiosis (formerly pasteurellosis), from the stable and the Petri dish to the biochemical cascade of events triggered by the leukotoxin inside ruminant leukocytes. One conclusion can be made: the most widespread cattle respiratory disease with the most important impact on beef production worldwide, is probably due to a tiny ruminant-specific focal variation in the CD18-and/or CD11a-expressing genes.

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“…43 In addition, several other viruses, such as the bovine herpesvirus-1, pseudorabies virus and the murine g-herpesvirus 68 (MHV-68), are able to block TAP function. [44][45][46][47] Interestingly, MHV-68 has been shown to degrade TAP and, to a lesser extent, tpn, thereby abrogating both efficient peptide transport and peptide loading onto MHC class I molecules. 47 In contrast, the latent membrane protein LMP1 of EBV uniquely induces TAP expression in BL cell lines.…”

Section: Defects In Tap Expression And/or Functionmentioning

confidence: 99%

Molecular mechanisms of HLA class I antigen abnormalities following viral infection and transformation

Seliger

Ritz

Ferrone

2005

Intl Journal of Cancer

112

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In humans as in other animal species, CD81 cytotoxic T lymphocytes (CTLs) play an important if not the major role in controlling virus-infected and malignant cell growth. The interactions between CD81 T cells and target cells are mediated by human leukocyte antigen (HLA) class I antigens loaded with viral and tumor antigen-derived peptides along with costimulatory receptor/ligand stimuli. Thus, to escape from CD8 1 T-cell recognition and destruction, viruses and tumor cells have developed strategies to inhibit the expression and/or function of HLA class I antigens. In contrast, cells with downregulated MHC class I surface expression can be recognized by NK cells, although NK cell-mediated lysis could be abrogated by the expression of inhibiting NK cell receptors. This review discusses the molecular mechanisms utilized by viruses to inhibit the formation, transport and/or expression of HLA class I antigen/peptide complexes on the cell surface. The knowledge about viral interference with MHC class I antigen presentation is not only crucial to understand the pathogenesis of viral diseases, but contributes also to the design of novel strategies to counteract the escape mechanisms utilized by viruses. These investigations may eventually lead to the development of effective immunotherapies to control viral infections and virus-associated malignant diseases. ' 2005 Wiley-Liss, Inc.

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Bovine herpesvirus-1 infection affects the peptide transport activity in bovine cells

Cited by 68 publications

References 35 publications

Impaired Transporter Associated with Antigen Processing-Dependent Peptide Transport during Productive EBV Infection

Impaired Transporter Associated with Antigen Processing-Dependent Peptide Transport during Productive EBV Infection

How Mannheimia haemolytica defeats host defence through a kiss of death mechanism

Molecular mechanisms of HLA class I antigen abnormalities following viral infection and transformation

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