Wild-type Measles Virus Infection Upregulates Poliovirus Receptor-Related 4 and Causes Apoptosis in Brain Endothelial Cells by Induction of Tumor Necrosis Factor-Related Apoptosis-lnducing Ligand

Abdullah, Hani’ah; Brankin, Brenda; Brady, Clare; Cosby, S. L.

doi:10.1097/nen.0b013e31829a26b6

Cited by 19 publications

(15 citation statements)

References 52 publications

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“…Nectin-4 can greatly contribute to the CDV invasion into the CNS, since meningeal cells, ependymal cells, and epithelia of choroid plexus express nectin-4. However, in this study, the expression of nectin-4 in cerebral endothelial cells was not up-regulated after CDV infection which was inconsistent with the previous study in measles virus (MV) infection 33 . Abdullah et al 33 observed that nectin-4 was up-regulated in MV-infected human cerebral endothelial cells in vitro .…”

Section: Discussioncontrasting

confidence: 99%

“…However, in this study, the expression of nectin-4 in cerebral endothelial cells was not up-regulated after CDV infection which was inconsistent with the previous study in measles virus (MV) infection 33 . Abdullah et al 33 observed that nectin-4 was up-regulated in MV-infected human cerebral endothelial cells in vitro . It is suggested that MV infection of brain endothelial cells allows efficient virus production and likely allows virus invasion into the brain parenchyma in immunocompromised hosts.…”

Section: Discussioncontrasting

confidence: 99%

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Expression of canine distemper virus receptor nectin-4 in the central nervous system of dogs

Pratakpiriya

Teh

Radtanakatikanon

et al. 2017

Sci Rep

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Canine distemper virus (CDV) exhibits lymphotropic, epitheliotropic, and neurotropic nature, and causes a severe systemic infection in susceptible animals. Initially, signaling lymphocyte activation molecule (SLAM) expressed on immune cells has been identified as a crucial cellular receptor for CDV. Currently, nectin-4 expressed in epithelia has been shown to be another receptor for CDV. Our previous study demonstrated that neurons express nectin-4 and are infected with CDV. In this study, we investigated the distribution pattern of nectin-4 in various cell types in the canine central nervous system and showed its relation to CDV infection to further clarify the pathology of disease. Histopathological, immunohistochemical and immunofluorescent analyses were done using formalin-fixed paraffin-embedded tissues of CDV-infected dogs. Dual staining of nectin-4 and CDV antigen or nectin-4 and brain cell markers was performed. Nectin-4 was detected in ependymal cells, epithelia of choroid plexus, meningeal cells, neurons, granular cells, and Purkinje’s cells. CDV antigens were detected in these nectin-4-positive cells, further suggesting contribution of nectin-4 for the CDV neurovirulence. On the other hand, astrocytes did not express nectin-4, although they were frequently infected with CDV. Since astrocytes are negative for SLAM expression, they must express an unidentified CDV receptor, which also contributes to CDV neurovirulence.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussioncontrasting

confidence: 99%

Expression of canine distemper virus receptor nectin-4 in the central nervous system of dogs

Pratakpiriya

Teh

Radtanakatikanon

et al. 2017

Sci Rep

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“…More recently PVRL4 (also known as nectin 4) has been identified as a receptor for MV [22], [23], CDV [24] and PPRV [16] on the basal surface of epithelial cells. We have also shown that PVRL4 is up-regulated in human brain endothelial cells by MV infection [25]. It is not known if PDV also uses this receptor.…”

Section: Introductionmentioning

confidence: 73%

Use of SLAM and PVRL4 and Identification of Pro-HB-EGF as Cell Entry Receptors for Wild Type Phocine Distemper Virus

et al. 2014

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Signalling lymphocyte activation molecule (SLAM) has been identified as an immune cell receptor for the morbilliviruses, measles (MV), canine distemper (CDV), rinderpest and peste des petits ruminants (PPRV) viruses, while CD46 is a receptor for vaccine strains of MV. More recently poliovirus like receptor 4 (PVRL4), also known as nectin 4, has been identified as a receptor for MV, CDV and PPRV on the basolateral surface of polarised epithelial cells. PVRL4 is also up-regulated by MV in human brain endothelial cells. Utilisation of PVRL4 as a receptor by phocine distemper virus (PDV) remains to be demonstrated as well as confirmation of use of SLAM. We have observed that unlike wild type (wt) MV or wtCDV, wtPDV strains replicate in African green monkey kidney Vero cells without prior adaptation, suggesting the use of a further receptor. We therefore examined candidate molecules, glycosaminoglycans (GAG) and the tetraspan proteins, integrin β and the membrane bound form of heparin binding epithelial growth factor (proHB-EGF),for receptor usage by wtPDV in Vero cells. We show that wtPDV replicates in Chinese hamster ovary (CHO) cells expressing SLAM and PVRL4. Similar wtPDV titres are produced in Vero and VeroSLAM cells but more limited fusion occurs in the latter. Infection of Vero cells was not inhibited by anti-CD46 antibody. Removal/disruption of GAG decreased fusion but not the titre of virus. Treatment with anti-integrin β antibody increased rather than decreased infection of Vero cells by wtPDV. However, infection was inhibited by antibody to HB-EGF and the virus replicated in CHO-proHB-EGF cells, indicating use of this molecule as a receptor. Common use of SLAM and PVRL4 by morbilliviruses increases the possibility of cross-species infection. Lack of a requirement for wtPDV adaptation to Vero cells raises the possibility of usage of proHB-EGF as a receptor in vivo but requires further investigation.

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“…Interestingly, Trail − / − mice are unable to clear an IAV infection as well as wild-type mice, and Trail − / − mice are more susceptible to death from immunopathology after IAV infection (Brincks et al, 2008; Brincks et al, 2011). Additional data report increased TRAIL expression after infection with Dengue virus, hepatitis virus, human immunodeficiency virus, measles virus, respiratory syncytial virus, and West Nile virus contributes to both viral clearance and immunopathology (Bem et al, 2010; Stegmann et al, 2010; van Grevenynghe et al, 2011; Barblu et al, 2012; Shrestha et al, 2012; Abdullah et al, 2013; Gandini et al, 2013; Gras et al, 2013; Werner et al, 2013; Brost et al, 2014; Limonta et al, 2014). …”

Section: Immunotherapy Involving Trail Receptor Agonists In Non-camentioning

confidence: 98%

Therapeutic applications of TRAIL receptor agonists in cancer and beyond

Amarante-Mendes

Griffith

2015

Pharmacology & Therapeutics

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TRAIL/Apo-2L is a member of the TNF superfamily first described as an apoptosis-inducing cytokine in 1995. Similar to TNF and Fas ligand, TRAIL induces apoptosis in caspase-dependent manner following TRAIL death receptor trimerization. Because tumor cells were shown to be particularly sensitive to this cytokine while normal cells/tissues proved to be resistant along with being able to synthesize and release TRAIL, it was rapidly appreciated that TRAIL likely served as one of our major physiologic weapons against cancer. In line with this, a number of research laboratories and pharmaceutical companies have attempted to exploit the ability of TRAIL to kill cancer cells by developing recombinant forms of TRAIL or TRAIL receptor agonists (e.g., receptor-specific mAb) for therapeutic purposes. In this review article we will describe the biochemical pathways used by TRAIL to induce different cell death programs. We will also summarize the clinical trials related to this pathway and discuss possible novel uses of TRAIL-related therapies. In recent years, the physiological importance of TRAIL has expanded beyond being a tumoricidal molecule to one critical for a number of clinical settings — ranging from infectious disease and autoimmunity to cardiovascular anomalies. We will also highlight some of these conditions where modulation of the TRAIL/TRAIL receptor system may be targeted in the future.

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Wild-type Measles Virus Infection Upregulates Poliovirus Receptor-Related 4 and Causes Apoptosis in Brain Endothelial Cells by Induction of Tumor Necrosis Factor-Related Apoptosis-lnducing Ligand

Cited by 19 publications

References 52 publications

Expression of canine distemper virus receptor nectin-4 in the central nervous system of dogs

Expression of canine distemper virus receptor nectin-4 in the central nervous system of dogs

Use of SLAM and PVRL4 and Identification of Pro-HB-EGF as Cell Entry Receptors for Wild Type Phocine Distemper Virus

Therapeutic applications of TRAIL receptor agonists in cancer and beyond

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