Lethal Canine Distemper Virus Outbreak in Cynomolgus Monkeys in Japan in 2008

Sakai, Kouji; Nagata, Noriyo; Ami, Yasushi; Seki, Fumio; Suzaki, Yuriko; Iwata‐Yoshikawa, Naoko; Suzuki, Tadaki; Fukushi, Shuetsu; Mizutani, Tetsuya; Yoshikawa, Tomoki; Otsuki, Noriyuki; Kurane, Ichiro; Komase, Katsuhiro; Yamaguchi, Ryoji; Hasegawa, Hideki; Saijo, Masayuki; Takeda, Makoto; Morikawa, Shigeru

doi:10.1128/jvi.02419-12

Cited by 120 publications

(134 citation statements)

References 21 publications

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“…Post-PPRV eradication, the world's cattle, sheep and goat populations would lack cross-protective immunity to morbillivirus infection. Canine distemper virus (CDV), a virus with an almost global distribution, is capable of causing significant disease in a broad range of hosts, including non-human primates [84,85]. CDV can rapidly adapt to use the human form of the morbillivirus receptor (SLAMF1) in vitro [86], raising concerns about the ease with which these viruses can effectively jump hosts.…”

Section: Examining the Potential For Inter-species (And Zoonotic) Tramentioning

confidence: 99%

Future research to underpin successful peste des petits ruminants virus (PPRV) eradication

Baron

Diop

Njeumi

et al. 2017

Journal of General Virology

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Peste des petits ruminants virus (PPRV) is a significant pathogen of small ruminants and is prevalent in much of Africa, the Near and Middle East and Asia. Despite the availability of an efficacious and cheap live-attenuated vaccine, the virus has continued to spread, with its range stretching from Morocco in the west to China and Mongolia in the east. Some of the world's poorest communities rely on small ruminant farming for subsistence and the continued endemicity of PPRV is a constant threat to their livelihoods. Moreover, PPRV's effects on the world's population are felt broadly across many economic, agricultural and social situations. This far-reaching impact has prompted the Food and Agriculture Organization of the United Nations (FAO) and the World Organisation for Animal Health (OIE) to develop a global strategy for the eradication of this virus and its disease. PPRV is a morbillivirus and, given the experience of these organizations in eradicating the related rinderpest virus, the eradication of PPRV should be feasible. However, there are many critical areas where basic and applied virological research concerning PPRV is lacking. The purpose of this review is to highlight areas where new research could be performed in order to guide and facilitate the eradication programme. These areas include studies on disease transmission and epidemiology, the existence of wildlife reservoirs and the development of next-generation vaccines and diagnostics. With the support of the international virology community, the successful eradication of PPRV can be achieved.

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Section: Examining the Potential For Inter-species (And Zoonotic) Tramentioning

confidence: 99%

Future research to underpin successful peste des petits ruminants virus (PPRV) eradication

Baron

Diop

Njeumi

et al. 2017

Journal of General Virology

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“…Recently, however, CDV outbreaks have emerged in a variety of mammals, including nonhuman primates, and showed high mortality rates (11,(13)(14)(15). The repeated lethal CDV outbreaks in monkeys in recent years clearly demonstrate that CDV is now a real threat for monkeys (11). Our concern is the potential risk of CDV infection in humans (16), since SLAM and nectin-4 both show high homology in their amino acid sequences between monkeys and humans (11).…”

mentioning

confidence: 99%

“…The repeated lethal CDV outbreaks in monkeys in recent years clearly demonstrate that CDV is now a real threat for monkeys (11). Our concern is the potential risk of CDV infection in humans (16), since SLAM and nectin-4 both show high homology in their amino acid sequences between monkeys and humans (11). Indeed, MV can spread and cause a measles-like illness in monkeys (17)(18)(19)(20)(21)(22).…”

mentioning

confidence: 99%

“…On the other hand, nectin-4, another morbillivirus receptor (8)(9)(10), is highly conserved in its amino acid sequence among different mammals and, thus, may play only a minor role in determining the host specificity of morbilliviruses (11,12). Recently, however, CDV outbreaks have emerged in a variety of mammals, including nonhuman primates, and showed high mortality rates (11,(13)(14)(15). The repeated lethal CDV outbreaks in monkeys in recent years clearly demonstrate that CDV is now a real threat for monkeys (11).…”

mentioning

confidence: 99%

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Canine Distemper Virus Associated with a Lethal Outbreak in Monkeys Can Readily Adapt To Use Human Receptors

Sakai

Yoshikawa

Seki

et al. 2013

J Virol

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A canine distemper virus (CDV) strain, CYN07-dV, associated with a lethal outbreak in monkeys, used human signaling lymphocyte activation molecule as a receptor only poorly but readily adapted to use it following a P541S substitution in the hemagglutinin protein. Since CYN07-dV had an intrinsic ability to use human nectin-4, the adapted virus became able to use both human immune and epithelial cell receptors, as well as monkey and canine ones, suggesting that CDV can potentially infect humans.

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“…Among the morbilliviruses, the human pathogen measles virus (MeV) is still responsible for over 120,000 fatalities annually (1), whereas canine distemper virus (CDV) causes high mortality and morbidity not only in dogs but also in an ever increasing spectrum of wild aquatic and terrestrial carnivores (2)(3)(4).…”

mentioning

confidence: 99%

Molecular Determinants Defining the Triggering Range of Prefusion F Complexes of Canine Distemper Virus

Avila

Alves

Khosravi

et al. 2014

J Virol

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The morbillivirus cell entry machinery consists of a fusion (F) protein trimer that refolds to mediate membrane fusion following receptor-induced conformational changes in its binding partner, the tetrameric attachment (H) protein. To identify molecular determinants that control F refolding, we generated F chimeras between measles virus (MeV) and canine distemper virus (CDV). We located a central pocket in the globular head domain of CDV F that regulates the stability of the metastable, prefusion conformational state of the F trimer. Most mutations introduced into this "pocket'" appeared to mediate a destabilizing effect, a phenotype associated with enhanced membrane fusion activity. Strikingly, under specific triggering conditions (i.e., variation of receptor type and H protein origin), some F mutants also exhibited resistance to a potent morbillivirus entry inhibitor, which is known to block F triggering by enhancing the stability of prefusion F trimers. Our data reveal that the molecular nature of the F stimulus and the intrinsic stability of metastable prefusion F both regulate the efficiency of F refolding and escape from smallmolecule refolding blockers. IMPORTANCEWith the aim to better characterize the thermodynamic basis of morbillivirus membrane fusion for cell entry and spread, we report here that the activation energy barrier of prefusion F trimers together with the molecular nature of the triggering "stimulus" (attachment protein and receptor types) define a "triggering range," which governs the initiation of the membrane fusion process. A central "pocket" microdomain in the globular F head contributes substantially to the regulation of the conformational stability of the prefusion complexes. The triggering range also defines the mechanism of viral escape from entry inhibitors and describes how the cellular environment can affect membrane fusion efficiency.

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Lethal Canine Distemper Virus Outbreak in Cynomolgus Monkeys in Japan in 2008

Cited by 120 publications

References 21 publications

Future research to underpin successful peste des petits ruminants virus (PPRV) eradication

Future research to underpin successful peste des petits ruminants virus (PPRV) eradication

Canine Distemper Virus Associated with a Lethal Outbreak in Monkeys Can Readily Adapt To Use Human Receptors

Molecular Determinants Defining the Triggering Range of Prefusion F Complexes of Canine Distemper Virus

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