Morbilliviruses Use Signaling Lymphocyte Activation Molecules (CD150) as Cellular Receptors

Tatsuo, Hironobu; Ono, Nobuyuki; Yanagi, Yusuke

doi:10.1128/jvi.75.13.5842-5850.2001

Cited by 305 publications

(297 citation statements)

References 45 publications

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“…Asterisks (*) correspond to significant (P,0.05) differences between the DK91-infected and mock-inoculated mink; g indicate significant differences involving the Snyder Hill-infected mink. CDV has been found to be linked closely to SLAM recognition and constitutes a virulence determinant (Condack et al, 2007;Tatsuo et al, 2001;von Messling et al, 2006). We found a rapid and unexpectedly extensive virus invasion of lymphocytes in the mildly virulent wildtype infections.…”

Section: Discussionmentioning

confidence: 67%

“…Thus, accumulating evidence strongly links immunosuppression and lymphopenia not only to direct effects following infection and subsequent destruction of signalling lymphocytic activating molecule (SLAM)-positive immune cells and precursor cells in the acute phase of the infections, but also to indirect effects modulating the host innate and adaptive immune systems (Cruz et al, 2006;Devaux et al, 2008;Heaney et al, 2005;Karp et al, 1996;Schlender et al, 1996;Tatsuo et al, 2001;von Messling et al, 2006). The relative impact on virulence of the different mechanisms modulating the immune system in vivo is, however, not yet clarified.…”

Section: Introductionmentioning

confidence: 99%

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Lymphotropism and host responses during acute wild-type canine distemper virus infections in a highly susceptible natural host

Nielsen

Søgaard

Jensen

et al. 2009

Journal of General Virology

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The mechanisms behind the in vivo virulence of immunosuppressive wild-type morbillivirus infections are still not fully understood. To investigate lymphotropism and host responses, we have selected the natural host model of canine distemper virus (CDV) infection in mink. This model displays multisystemic infection, similar to measles virus and rinderpest virus infections in their susceptible natural hosts. The wild-type CDVs investigated provoked marked virulence differences, inducing mild versus marked to severe acute disease. The mildly virulent wild-type virus induced transient lymphopenia, despite the development of massive infection of peripheral blood mononuclear cells (PBMCs) exceeding that determined for the highly virulent wild-type virus, indicating an inverse relationship between acute virulence and the extent of viraemia in the investigated wild-type viruses. Single-cell cytokine production in PBMCs was investigated throughout the acute infections. We observed Th1-and Th2-type cytokine responses beginning in the prodromal phase, and late inflammatory responses were shared between the wild-type infections. INTRODUCTIONMorbilliviruses are lymphotrophic and induce multisystemic infections in their highly susceptible natural hosts, causing disease with high morbidity and mortality worldwide. Members of the genus Morbillivirus within the family Paramyxoviridae include Measles virus (MV) of primates, Canine distemper virus (CDV) of carnivores and Rinderpest virus (RPV) of cloven-hoofed animals. Natural infections by all of these share common features, including lymphopenia and inhibition of lymphocyte proliferation in the acute phase (Griffin, 2007;Heaney et al., 2002;von Messling et al., 2003;Yanagi et al., 2006). Although live vaccines have effectively reduced the incidence of disease, the highly contagious morbilliviruses are still a major problem in human and veterinary medicine (Greene & Appel, 2006;Rima & Duprex, 2006). Like MV and RPV, CDV causes a typical acute infection characterized by virus replication in cells of the lymphoid system, with subsequent spread to tissues throughout the body. Acute clinical morbillivirus disease often takes a fatal course in highly susceptible natural hosts such as young dogs, mink and ferrets due to the highly multisystemic virulence, which includes central nervous system (CNS) involvement and profound immunosuppression, favouring opportunistic secondary pathogens (Appel, 1969;Blixenkrone-Møller, 1989;Kauffman et al., 1982;von Messling et al., 2006). Despite the clinically relevant immunosuppression, another hallmark of virulent morbillivirus infections is the induction of efficient and lifelong humoral and cellular immunity in hosts that eventually survive and appear to clear the virus (Appel et al., 1982;Griffin, 2007).The molecular events behind morbillivirus-induced perturbation of the immune system have been studied extensively and, based on in vitro studies, several mechanisms have been proposed to be involved (Heaney et al., 2002;Schneider-Schaulies & Dittme...

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Section: Discussionmentioning

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Lymphotropism and host responses during acute wild-type canine distemper virus infections in a highly susceptible natural host

Nielsen

Søgaard

Jensen

et al. 2009

Journal of General Virology

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“…For measles virus, a single amino acid substitution within the H gene is able to confer entry into different cell types in vitro (Hsu et al, 1998;Seki et al, 2006). The signaling lymphocyte activation molecule has long been proposed as a morbillivirus receptor (Tatsuo et al, 2001), and although exact virus:receptor interactions are unknown, it is now generally accepted that multiple receptors are utilized by these viruses (Fujita et al, 2007) and that this must have a significant effect on the potential for species-to-species transmission (von Messling et al, 2001). For CDV, it has been demonstrated that molecular adaptation at specific receptor-binding sites of the H gene is associated with the spread of this virus from dogs to novel noncanid hosts in the wild (McCarthy et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Epidemiology, Pathology, and Genetic Analysis of a Canine Distemper Epidemic in Namibia

Gowtage-Sequeira

Banyard

Barrett

et al. 2009

Journal of Wildlife Diseases

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ABSTRACT:Severe population declines have resulted from the spillover of canine distemper virus (CDV) into susceptible wildlife, with both domestic and wild canids being involved in the maintenance and transmission of the virus. This study (March 2001 to October 2003 collated case data, serologic, pathologic, and molecular data to describe the spillover of CDV from domestic dogs (Canis familiaris) to black-backed jackals (Canis mesomelas) during an epidemic on the Namibian coast. Antibody prevalence in jackals peaked at 74.1%, and the clinical signs and histopathologic observations closely resembled those observed in domestic dog cases. Viral RNA was isolated from the brain of a domestic dog from the outbreak area. Sequence data from the phosphoprotein (P) gene and the hemagglutinin (H) genes were used for phylogenetic analyses. The P gene sequence from the domestic dog shared 98% identity with the sequence data available for other CDV isolates of African carnivores. For the H gene, the two sequences available from the outbreak that decimated the lion population in Tanzania in 1994 were the closest match with the Namibian sample, being 94% identical across 1,122 base pairs (bp). Phylogenetic analyses based on this region clustered the Namibian sample with the CDV that is within the morbilliviruses. This is the first description of an epidemic involving black-backed jackals in Namibia, demonstrating that this species has the capacity for rapid and large-scale dissemination of CDV. This work highlights the threat posed to endangered wildlife in Namibia by the spillover of CDV from domestic dog populations. Very few sequence data are currently available for CDV isolates from African carnivores, and this work provides the first sequence data from a Namibian CDV isolate.

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“…Thus, members infect man: measles virus (MV); cattle: rinderpest virus (RPV); sheep and goats: peste des petits ruminants virus (PPRV); a wide range of carnivores: canine distemper virus (CDV); seals: phocine distemper virus (PDV); and porpoises and dolphins: cetacean morbillivirus (CeMV) [2]. As this review focuses on the involvement of these viruses in human disease, we can be very brief about RPV, PPRV, CeMV, and PDV, since in spite of their clear evolutionary relationship with MV and CDV and their potential to use the same cell surface receptors [3,4], they have not been implicated in any human disease. Domesticated animals infected with RPV or PPRV could potentially transmit very large doses of infectious virus to those who care for them.…”

Section: Introductionmentioning

confidence: 99%

Morbilliviruses and human disease

Rima

Duprex

2005

The Journal of Pathology

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Morbilliviruses are a group of viruses that belong to the family Paramyxoviridae. The most instantly recognizable member is measles virus (MV) and individuals acutely infected with the virus exhibit a wide range of clinical symptoms ranging from a characteristic mild selflimiting infection to death. Canine distemper virus (CDV) and rinderpest virus (RPV) cause a similar but distinctive pathology in dogs and cattle, respectively, and these, alongside experimental MV infection of primates, have been useful models for MV pathogenesis. Traditionally, viruses were identified because a distinctive disease was observed in man or animals; an infectious agent was subsequently isolated, cultured, and this could be used to recapitulate the disease in an experimentally infected host. Thus, satisfying Koch's postulates has been the norm. More recently, particularly due to the advent of exceedingly sensitive molecular biological assays, many researchers have looked for infectious agents in disease conditions for which a viral aetiology has not been previously established. For these cases, the modified Koch's postulates of Bradford Hill have been developed as criteria to link a virus to a specific disease. Only in a few cases have these conditions been fulfilled. Therefore, many viruses have over the years been definitely and tentatively linked to human diseases and in this respect the morbilliviruses are no different. In this review, human diseases associated with morbillivirus infection have been grouped into three broad categories: (1) those which are definitely caused by the infection; (2) those which may be exacerbated or facilitated by an infection; and (3) those which currently have limited, weak, unsubstantiated or no credible scientific evidence to support any link to a morbillivirus. Thus, an attempt has been made to clarify the published data and separate human diseases actually linked to morbilliviruses from those that are merely anecdotally associated.

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Morbilliviruses Use Signaling Lymphocyte Activation Molecules (CD150) as Cellular Receptors

Cited by 305 publications

References 45 publications

Lymphotropism and host responses during acute wild-type canine distemper virus infections in a highly susceptible natural host

Lymphotropism and host responses during acute wild-type canine distemper virus infections in a highly susceptible natural host

Epidemiology, Pathology, and Genetic Analysis of a Canine Distemper Epidemic in Namibia

Morbilliviruses and human disease

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