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Thomas Barrett - One of the best experts on this subject based on the ideXlab platform.
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rescue of a chimeric rinderpest virus with the nucleocapsid protein derived from peste des petits ruminants virus use as a marker vaccine
Journal of General Virology, 2007Co-Authors: Satya Parida, M Mahapatra, Sai Kumar, Subash C Das, Michael D Baron, John R Anderson, Thomas BarrettAbstract:The nucleocapsid (N) protein of all Morbilliviruses has a highly conserved central region that is thought to interact with and encapsidate the viral RNA. The C-terminal third of the N protein is highly variable among Morbilliviruses and is thought to be located on the outer surface and to be available to interact with other viral proteins such as the phosphoprotein, the polymerase protein and the matrix protein. Using reverse genetics, a chimeric rinderpest virus (RPV)/peste-des-petits-ruminants virus (PPRV) was rescued in which the RPV N gene open reading frame had been replaced with that of PPRV (RPV–PPRN). The chimeric virus maintained efficient replication in cell culture. Cattle vaccinated with this chimeric vaccine showed no adverse reaction and were protected from subsequent challenge with wild-type RPV, indicating it to be a safe and efficacious vaccine. The carboxyl-terminal variable region of the rinderpest N protein was cloned and expressed in Escherichia coli. The expressed protein was used to develop an indirect ELISA that could clearly differentiate between RPV- and PPRV-infected animals. The possibility of using this virus as a marker vaccine in association with a new diagnostic ELISA in the rinderpest eradication programme is discussed.
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Full genome sequence of peste des petits ruminants virus, a member of the Morbillivirus genus.
Virus Research, 2005Co-Authors: Dalan Bailey, Aykut Ozkul, Pradyot Dash, Thomas BarrettAbstract:Peste des petits ruminants virus (PPRV) causes an acute febrile illness in small ruminant species, mostly sheep and goats. PPRV is a member of the Morbillivirus genus which includes measles, rinderpest (cattle plague), canine distemper, phocine distemper and the Morbilliviruses found in whales, porpoises and dolphins. Full length genome sequences for these Morbilliviruses are available and reverse genetic rescue systems have been developed for the viruses of terrestrial mammals, with the exception of PPRV. This paper presents the first published full length genome sequence for PPRV. The genome was found to be consistent with the rule-of-six and open reading frames (ORFs) were identified that encoded the eight proteins characteristic of Morbilliviruses. At the nucleotide (nt) level, the full length genome of PPRV was most similar to that of rinderpest, the other ruminant morbillivirus. However, at the protein level five of the six structural proteins and the V protein showed a greater similarity to the dolphin morbillivirus (DMV) while only the C and L proteins showed a high relationship to rinderpest.
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sequence analysis of the phosphoprotein gene of peste des petits ruminants ppr virus editing of the gene transcript
Virus Research, 2003Co-Authors: M Mahapatra, Adama Diallo, Berhe G Egziabher, Thomas BarrettAbstract:The gene encoding the phosphoprotein of the vaccine strain of Peste des petits ruminants (PPR) virus (Nigeria 75/1 vaccine strain) has been cloned and its nucleotide sequence been determined. This gene is 1655 nucleotides long and encodes two overlapping open reading frames (ORFs). Translation from the first AUG would produce a polypeptide of 509 amino acid residues with a predicted molecular mass of 54.9 kDa, the longest of the published morbillivirus P proteins. Translation from the second AUG would produce a protein of 177 amino acid residues with a predicted molecular mass of 20.3 kDa, analogous to the C proteins of other Morbilliviruses. Evidence was found for the production of two types of P mRNA transcript, one a faithful transcript of the gene and the other with an extra G residue inserted at position 751. Translation from the first AUG of this second mRNA would produce a protein of 298 amino acids, with a predicted molecular mass 32.3 kDa, analogous to the V protein produced by other Morbilliviruses. Sequences of the predicted P, C and V proteins were compared with those of the other morbillivirus sequences available to date. The P protein was found to be the most poorly conserved of the morbillivirus proteins, the amino acid identity ranging from 54% in case of Canine distemper virus (CDV) to 60% in the case of the Dolphin morbillivirus (DMV).
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rinderpest virus rpv iscom vaccine induces protection in cattle against virulent rpv challenge
Vaccine, 2001Co-Authors: Hiroshi Kamata, Kazuya Yamanouchi, Kazue Ohishi, M S Shaila, Ellena Hulskotte, Albert D M E Osterhaus, Kenjiro Inui, Thomas BarrettAbstract:Rinderpest virus (RPV), a member of genus Morbillivirus in the family Paramyxoviridae, causes an acute and often fatal disease in cattle and other large ruminants. A subunit rinderpest vaccine consisting of an immune-stimulating complex (ISCOM) incorporating the RPV haemaggulutinin (H) protein, was examined for its ability to induce protective immunity in cattle, the natural host of RPV. All of four cattle vaccinated with the ISCOM vaccine survived challenge with virulent virus. Three were solidly protected, showing no clinical signs of infection, while the fourth animal developed only mild and transient symptoms. Virus neutralizing antibodies were produced at a significant level in all vaccinated cattle. These results indicate that this ISCOM vaccine is effective in producing protective immunity in cattle and should be a suitable means of delivering glycoprotein antigens from other Morbilliviruses.
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Morbillivirus infections, with special emphasis on Morbilliviruses of carnivores.
Veterinary Microbiology, 1999Co-Authors: Thomas BarrettAbstract:Morbilliviruses infections cause significant mortality in human beings and animals. Measles virus is responsible for up to two million childhood deaths annually in the developing world, while rinderpest and peste des petits ruminants cause severe epizootics in domestic and wild ruminants in areas of the world where they remain endemic. Canine distemper virus (CDV) is a cause of fatal disease in many species of carnivores. Distemper is controlled by vaccination in domestic dogs and farmed mink, but it may be impossible to eradicate the virus because of its global distribution and wide variety of susceptible host species, which includes both freshwater and marine seals. Research is currently under way to develop new recombinant vaccines, since the currently available live attenuated vaccines for CDV are not safe for use for all species and many valuable zoo animals need to be protected from CDV. New Morbilliviruses with potentially disastrous ecological consequences for marine mammals have been discovered in the past decade; phocid distemper virus (PDV) in seals and the cetacean morbillivirus (CMV) has been found in dolphins, whales and porpoises. Reverse transcription, coupled with the polymerase chain reaction (RT/PCR) and nucleic acid sequencing, has been used to characterise the Morbilliviruses and has given insights into the evolution of this virus genus.
Thomas P Lipscomb - One of the best experts on this subject based on the ideXlab platform.
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Dispatches Molecular Genetic Evidence of a Novel Morbillivirus in a Long-Finned Pilot Whale (Globicephalus melas)
2013Co-Authors: Thomas G. Fanning, R. B. Moeller, S. E. Kodsi, M. G. Mense, Amy E Krafft, Thomas P LipscombAbstract:A long-finned pilot whale with morbilliviral disease was stranded in New Jersey. An immunohistochemical stain demonstrated morbilliviral antigen. Reverse transcriptasepolymerase chain reaction for morbillivirus P and N genes was positive. Novel sequences most closely related to, but distinct from, those of dolphin and porpoise Morbilliviruses suggest that this virus may represent a third member of the cetacean morbillivirus group. In the last 12 years, newly recognized members of the morbillivirus family have caused many deaths among marine mammals, specifically cetaceans and pinnipeds (1). The first recognized marine mammal morbilliviral epizootic occurred in 1987-88 along the Atlantic coast of the United States (2,3). More than half the in-shore population of bottlenose dolphins (Tursiops truncatus) may have died. In 1988, thousands of harbor seals (Phoca vitulina) (4) and small numbers of harbor porpoises (Phocoena phocoena) (5) died in morbilliviral epizootics in northwestern Europe. A separate epizootic claimed thousands of striped dolphins (Stenella coeruleoalba) in the western Mediterranean (6). In 1993-94, another bottlenose dolphin epizootic occurred in the Gulf of Mexico (7,8). Recently, morbilliviral infection has been reported in cetaceans in the Pacific (9). Viruses have been cultured from animals from some of the epizootics, and novel marine mammal Morbilliviruses have been recognized. Two cetacean Morbilliviruses have been identified and named porpoise morbillivirus (PMV) and dolphin morbillivirus (DMV). PMV was isolated from harbor porpoises that died along the Irish coast. DMV was first identified in striped dolphins from the Mediterranean (10)
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Molecular genetic evidence of a novel morbillivirus in a long-finned pilot whale (Globicephalus melas).
Emerging Infectious Diseases, 2000Co-Authors: Mark M. Tsai, T. J. Atkin, Thomas G. Fanning, R. B. Moeller, S. E. Kodsi, M. G. Mense, Amy E Krafft, Thomas P LipscombAbstract:: A long-finned pilot whale with morbilliviral disease was stranded in New Jersey. An immunohistochemical stain demonstrated morbilliviral antigen. Reverse transcriptase-polymerase chain reaction for morbillivirus P and N genes was positive. Novel sequences most closely related to, but distinct from, those of dolphin and porpoise Morbilliviruses suggest that this virus may represent a third member of the cetacean morbillivirus group.
A.d.m.e. Osterhaus - One of the best experts on this subject based on the ideXlab platform.
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Is Dolphin Morbillivirus Virulent for White-Beaked Dolphins (Lagenorhynchus albirostris)?
Veterinary pathology, 2014Co-Authors: C. E. Van Elk, Thierry Jauniaux, Geoffrey Foster, Sjoukje Hiemstra, P.r.w.a Van Run, J. Meerbeek, A.d.m.e. Osterhaus, Thijs KuikenAbstract:The virulence of Morbilliviruses for toothed whales (odontocetes) appears to differ according to host species. In 4 species of odontocetes, Morbilliviruses are highly virulent, causing large-scale epizootics with high mortality. In 8 other species of odontocetes, including white-beaked dolphins (Lagenorhynchus albirostris), Morbilliviruses have been found as an incidental infection. In these species, the virulence of Morbilliviruses is not clear. Therefore, the admission of 2 white-beaked dolphins with morbillivirus infection into a rehabilitation center provided a unique opportunity to investigate the virulence of morbillivirus in this species. By phylogenetic analysis, the Morbilliviruses in both animals were identified as a dolphin morbillivirus (DMV) most closely related to that detected in a white-beaked dolphin in Germany in 2007. Both animals were examined clinically and pathologically. Case No. 1 had a chronic neural DMV infection, characterized by polioencephalitis in the cerebrum and morbillivirus antigen expression limited to neurons and glial cells. Surprisingly, no nervous signs were observed in this animal during the 6 months before death. Case No. 2 had a subacute systemic DMV infection, characterized by interstitial pneumonia, leucopenia, lymphoid depletion, and DMV antigen expression in mononuclear cells and syncytia in the lung and in mononuclear cells in multiple lymphoid organs. Cause of death was not attributed to DMV infection in either animal. DMV was not detected in 2 contemporaneously stranded white-beaked dolphins. Stranding rate did not increase in the region. These results suggest that DMV is not highly virulent for white-beaked dolphins.
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is dolphin morbillivirus virulent for white beaked dolphins lagenorhynchus albirostris
Veterinary Pathology, 2014Co-Authors: Thierry Jauniaux, Geoffrey Foster, Marco W G Van De Bildt, C. E. Van Elk, Sjoukje Hiemstra, P.r.w.a Van Run, J. Meerbeek, A.d.m.e. Osterhaus, Thijs KuikenAbstract:The virulence of Morbilliviruses for toothed whales (odontocetes) appears to differ according to host species. In 4 species of odontocetes, Morbilliviruses are highly virulent, causing large-scale epizootics with high mortality. In 8 other species of odontocetes, including white-beaked dolphins (Lagenorhynchus albirostris), Morbilliviruses have been found as an incidental infection. In these species, the virulence of Morbilliviruses is not clear. Therefore, the admission of 2 white-beaked dolphins with morbillivirus infection into a rehabilitation center provided a unique opportunity to investigate the virulence of morbillivirus in this species. By phylogenetic analysis, the Morbilliviruses in both animals were identified as a dolphin morbillivirus (DMV) most closely related to that detected in a white-beaked dolphin in Germany in 2007. Both animals were examined clinically and pathologically. Case No. 1 had a chronic neural DMV infection, characterized by polioencephalitis in the cerebrum and morbillivirus antigen expression limited to neurons and glial cells. Surprisingly, no nervous signs were observed in this animal during the 6 months before death. Case No. 2 had a subacute systemic DMV infection, characterized by interstitial pneumonia, leucopenia, lymphoid depletion, and DMV antigen expression in mononuclear cells and syncytia in the lung and in mononuclear cells in multiple lymphoid organs. Cause of death was not attributed to DMV infection in either animal. DMV was not detected in 2 contemporaneously stranded white-beaked dolphins. Stranding rate did not increase in the region. These results suggest that DMV is not highly virulent for white-beaked dolphins.
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dolphin and porpoise Morbilliviruses are genetically distinct from phocine distemper virus
Virology, 1993Co-Authors: Thomas Barrett, Ilona Visser, L Mamaev, L Goatley, M F Van Bressem, A.d.m.e. OsterhausAbstract:The Morbilliviruses recently isolated from two cetacean species in the North and Mediterranean Seas have been shown to differ from phocine distemper virus isolated from European seals using monoclonal antibodies. We have identified a "universal" morbillivirus primer set, based on highly conserved regions of the morbillivirus phosphoprotein (P) gene and used this to amplify a region surrounding the RNA editing site from all known members of the group. Sequence analysis of this region of the gene shows that the dolphin and porpoise viruses are related but quite different from all other members of the group, forming a distinct lineage more closely related to the ruminant Morbilliviruses than to the carnivore viruses.
Veronika Von Messling - One of the best experts on this subject based on the ideXlab platform.
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canine distemper virus spread and transmission to naive ferrets selective pressure on signaling lymphocyte activation molecule dependent entry
Journal of Virology, 2018Co-Authors: Bevan Sawatsky, Roberto Cattaneo, Veronika Von MesslingAbstract:Upon infection, Morbilliviruses such as measles virus, rinderpest virus, and canine distemper virus (CDV) initially target immune cells via the signaling lymphocyte activation molecule (SLAM) before spreading to respiratory epithelia through the adherens junction protein nectin-4. However, the roles of these receptors in transmission from infected to naive hosts have not yet been formally tested. To experimentally addressing this question, we established a model of CDV contact transmission between ferrets. We show here that transmission of wild-type CDV sometimes precedes the onset of clinical disease. In contrast, transmission was not observed in most animals infected with SLAM- or nectin-4-blind CDVs, even though all animals infected with the nectin-4-blind virus developed sustained viremia. There was an unexpected case of transmission of a nectin-4-blind virus, possibly due to biting. Another unprecedented event was transient viremia in an infection with a SLAM-blind virus. We identified three compensatory mutations within or near the SLAM-binding surface of the attachment protein. A recombinant CDV expressing the mutated attachment protein regained the ability to infect ferret lymphocytes in vitro, but its replication was not as efficient as that of wild-type CDV. Ferrets infected with this virus developed transient viremia and fever, but there was no transmission to naive contacts. Our study supports the importance of epithelial cell infection and of sequential CDV H protein interactions first with SLAM and then nectin-4 receptors for transmission to naive hosts. It also highlights the in vivo selection pressure on the H protein interactions with SLAM.IMPORTANCE Morbilliviruses such as measles virus, rinderpest virus, and canine distemper virus (CDV) are highly contagious. Despite extensive knowledge of how Morbilliviruses interact with their receptors, little is known about how those interactions influence viral transmission to naive hosts. In a ferret model of CDV contact transmission, we showed that sequential use of the signaling lymphocytic activation molecule (SLAM) and nectin-4 receptors is essential for transmission. In one animal infected with a SLAM-blind CDV, we documented mild viremia due to the acquisition of three compensatory mutations within or near the SLAM-binding surface. The interaction, however, was not sufficient to cause disease or sustain transmission to naive contacts. This work confirms the sequential roles of SLAM and nectin-4 in morbillivirus transmission and highlights the selective pressure directed toward productive interactions with SLAM.
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morbillivirus experimental animal models measles virus pathogenesis insights from canine distemper virus
Viruses, 2016Co-Authors: Renata Da Fontoura Budaszewski, Veronika Von MesslingAbstract:Morbilliviruses share considerable structural and functional similarities. Even though disease severity varies among the respective host species, the underlying pathogenesis and the clinical signs are comparable. Thus, insights gained with one morbillivirus often apply to the other members of the genus. Since the Canine distemper virus (CDV) causes severe and often lethal disease in dogs and ferrets, it is an attractive model to characterize morbillivirus pathogenesis mechanisms and to evaluate the efficacy of new prophylactic and therapeutic approaches. This review compares the cellular tropism, pathogenesis, mechanisms of persistence and immunosuppression of the Measles virus (MeV) and CDV. It then summarizes the contributions made by studies on the CDV in dogs and ferrets to our understanding of MeV pathogenesis and to vaccine and drugs development.
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Membrane fusion-mediated autophagy induction enhances morbillivirus cell-to-cell spread.
Journal of Virology, 2012Co-Authors: Sébastien Delpeut, Penny A Rudd, Patrick Labonté, Veronika Von MesslingAbstract:In the context of viral infections, autophagy induction can be beneficial or inhibitory. Within the Paramyxoviridae family, only Morbilliviruses have been investigated and are reported to induce autophagy. Here we show that Morbilliviruses rapidly induce autophagy and require this induction for efficient cell-to-cell spread. Coexpression of both glycoproteins in cells expressing one of the cellular receptors was required for autophagy induction, and LC3 punctum formation, indicative of autophagy, was mainly observed in syncytia. A similar correlation between syncytium formation and autophagy induction was also observed for other paramyxovirus glycoproteins, suggesting that membrane fusion-mediated autophagy may be common among paramyxoviruses and possibly other enveloped viruses.
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region between the canine distemper virus m and f genes modulates virulence by controlling fusion protein expression
Journal of Virology, 2008Co-Authors: Danielle E Anderson, Veronika Von MesslingAbstract:Morbilliviruses, including measles and canine distemper virus (CDV), are nonsegmented, negative-stranded RNA viruses that cause severe diseases in humans and animals. The transcriptional units in their genomes are separated by untranslated regions (UTRs), which contain essential transcription and translation signals. Due to its increased length, the region between the matrix (M) protein and fusion (F) protein open reading frames is of particular interest. In measles virus, the entire F 5′ region is untranslated, while several start codons are found in most other Morbilliviruses, resulting in a long F protein signal peptide (Fsp). To characterize the role of this region in morbillivirus pathogenesis, we constructed recombinant CDVs, in which either the M-F UTR was replaced with that between the nucleocapsid (N) and phosphoprotein (P) genes, or 106 Fsp residues were deleted. The Fsp deletion alone had no effect in vitro and in vivo. In contrast, substitution of the UTR was associated with a slight increase in F gene and protein expression. Animals infected with this virus either recovered completely or experienced prolonged disease and death due to neuroinvasion. The combination of both changes resulted in a virus with strongly increased F gene and protein expression and complete attenuation. Taken together, our results provide evidence that the region between the morbillivirus M and F genes modulates virulence through transcriptional control of the F gene expression.
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tropism illuminated lymphocyte based pathways blazed by lethal morbillivirus through the host immune system
Proceedings of the National Academy of Sciences of the United States of America, 2004Co-Authors: Veronika Von Messling, Dragana Milosevic, Roberto CattaneoAbstract:The immunosuppressive properties of Morbilliviruses including measles and canine distemper virus (CDV) are well known, but the host cells supporting infection are poorly characterized. To identify these cells, a recombinant CDV expressing green fluorescent protein was produced by reverse genetics based on a wild-type strain lethal for ferrets. This recombinant virus fully retained virulence and blazed three lymphocyte-based pathways through the immune system of its host: first, it infected rapidly and massively circulating B and T cells; second, it took over and damaged secondary lymphatic organs including spleen, lymph nodes, and gut-associated and mucosal lymphoid tissues; third, it infected most thymocytes. In contrast, replication in epithelial cells was initially not detectable, but substantial before host death. Thus, CDV initially infects lymphocytes and massively replicates therein, thereby causing immunosuppression and preparing systemic invasion and host escape.
Fumio Seki - One of the best experts on this subject based on the ideXlab platform.
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computational analysis reveals a critical point mutation in the n terminal region of the signaling lymphocytic activation molecule responsible for the cross species infection with canine distemper virus
Molecules, 2021Co-Authors: Yuta Yamamoto, Fumio Seki, Hiroaki Tokiwa, Shogo Nakano, Yasuteru Shigeta, Sohei Ito, Makoto TakedaAbstract:Infection of hosts by Morbilliviruses is facilitated by the interaction between viral hemagglutinin (H-protein) and the signaling lymphocytic activation molecule (SLAM). Recently, the functional importance of the n-terminal region of human SLAM as a measles virus receptor was demonstrated. However, the functional roles of this region in the infection process by other Morbilliviruses and host range determination remain unknown, partly because this region is highly flexible, which has hampered accurate structure determination of this region by X-ray crystallography. In this study, we analyzed the interaction between the H-protein from canine distemper virus (CDV-H) and SLAMs by a computational chemistry approach. Molecular dynamics simulations and fragment molecular orbital analysis demonstrated that the unique His28 in the N-terminal region of SLAM from Macaca is a key determinant that enables the formation of a stable interaction with CDV-H, providing a basis for CDV infection in Macaca. The computational chemistry approach presented should enable the determination of molecular interactions involving regions of proteins that are difficult to predict from crystal structures because of their high flexibility.
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measles virus hemagglutinin protein establishes a specific interaction with the extreme n terminal region of human signaling lymphocytic activation molecule to enhance infection
Frontiers in Microbiology, 2020Co-Authors: Fumio Seki, Kazue Ohishi, Tadashi Maruyama, Yuta Yamamoto, Hideo Fukuhara, Katsumi Maenaka, Hiroaki Tokiwa, Makoto TakedaAbstract:Measles virus (MV) is a human pathogen that is classified in the genus Morbillivirus in the family Paramyxoviridae together with several non-human animal Morbilliviruses. They cause severe systemic infections by using signaling lymphocytic activation molecule (SLAM) and poliovirus receptor-like 4 expressed on immune and epithelial cells, respectively, as receptors. The viral hemagglutinin (H) protein is responsible for the receptor-binding. Previously determined structures of MV-H and SLAM complexes revealed a major binding interface between the SLAM V domain and MV-H with four binding components (sites 1-4) in the interface. We studied the MV-H and human SLAM (hSLAM) complex structure in further detail by in silico analyses and determined missing regions or residues in the previously determined complex structures. These analyses showed that, in addition to sites 1-4, MV-H establishes a unique interaction with the extreme N-terminal region (ExNTR) of hSLAM. The first principles calculation-based fragment molecular orbital computation method revealed that methionine at position 29 (hSLAM-Met29) is the key residue for the interaction. hSLAM-Met29 was predicted to establish a CH-π interaction with phenylalanine at position 549 of MV-H (MVH-Phe549). A cell-cell fusion assay showed that the hSLAM-Met29 and MVH-Phe549 interaction is important for hSLAM-dependent MV membrane fusion. Furthermore, Jurkat cell lines expressing hSLAM with or without Met29 and recombinant MV possessing the H protein with or without Phe549 showed that the hSLAM-Met29 and MVH-Phe549 interaction enhanced hSLAM-dependent MV infection by ~10-fold. We speculate that in the evolutionary history of Morbilliviruses, this interaction may have contributed to MV adaptation to humans because this interaction is unique for MV and only MV uses hSLAM efficiently among Morbilliviruses.
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Phocine distemper virus uses phocine and other animal SLAMs as a receptor but not human SLAM.
Microbiology and Immunology, 2020Co-Authors: Fumio Seki, Kazue Ohishi, Tadashi MaruyamaAbstract:Morbilliviruses use the signaling lymphocyte activation molecule (SLAM) as a receptor to infect their hosts. Seals are almost the only animal species that show apparent infection with phocine distemper virus (PDV). Seal SLAM functioned as a PDV receptor. However, dolphin- and dog-SLAM molecules, but not human SLAM, were also fully functional PDV receptors. These data suggest that the host range of PDV is not simply determined by its SLAM usage. However, human nonsusceptibility to PDV infection may be at least partly attributable to the inability of PDV to use human SLAM as a receptor.
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Marine Morbilliviruses: Diversity and Interaction with Signaling Lymphocyte Activation Molecules
Viruses, 2019Co-Authors: Kazue Ohishi, Tadashi Maruyama, Fumio SekiAbstract:Epidemiological reports of phocine distemper virus (PDV) and cetacean morbillivirus (CeMV) have accumulated since their discovery nearly 30 years ago. In this review, we focus on the interaction between these marine Morbilliviruses and their major cellular receptor, the signaling lymphocyte activation molecule (SLAM). The three-dimensional crystal structure and homology models of SLAMs have demonstrated that 35 residues are important for binding to the morbillivirus hemagglutinin (H) protein and contribute to viral tropism. These 35 residues are essentially conserved among pinnipeds and highly conserved among the Caniformia, suggesting that PDV can infect these animals, but are less conserved among cetaceans. Because CeMV can infect various cetacean species, including toothed and baleen whales, the CeMV-H protein is postulated to have broader specificity to accommodate more divergent SLAM interfaces and may enable the virus to infect seals. In silico analysis of viral H protein and SLAM indicates that each residue of the H protein interacts with multiple residues of SLAM and vice versa. The integration of epidemiological, virological, structural, and computational studies should provide deeper insight into host specificity and switching of marine Morbilliviruses.