Structure-Guided Identification of a Nonhuman Morbillivirus with Zoonotic Potential

Abdullah, Nurshariza; Kelly, James; Graham, Stephen C.; Birch, Jamie; Gonçalves-Carneiro, Daniel; Mitchell, Tim; Thompson, Robin N; Lythgoe, Katrina A.; Logan, Nicola; Hosie, Margaret J.; Bavro, Vassiliy N.; Willett, Brian J.; Heaton, Michael P.; Bailey, Dalan

doi:10.1128/jvi.01248-18

Cited by 30 publications

(50 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The host traits of other species susceptible to PPRV-infection according to serological or virological evidence is still under investigation or unknown. We therefore suggest the terms "typical" hosts for domestic small ruminants and "atypical" hosts for other susceptible host species of PPRV, similar to Bataille, et al [29] and Abdullah, et al [30].…”

Section: Introductionsupporting

confidence: 63%

Camelids and Cattle Are Dead-End Hosts for Peste-des-Petits-Ruminants Virus

Schulz

Fast

Wernery

et al. 2019

Viruses

View full text Add to dashboard Cite

Peste-des-petits-ruminants virus (PPRV) causes a severe respiratory disease in small ruminants. The possible impact of different atypical host species in the spread and planed worldwide eradication of PPRV remains to be clarified. Recent transmission trials with the virulent PPRV lineage IV (LIV)-strain Kurdistan/2011 revealed that pigs and wild boar are possible sources of PPRV-infection. We therefore investigated the role of cattle, llamas, alpacas, and dromedary camels in transmission trials using the Kurdistan/2011 strain for intranasal infection and integrated a literature review for a proper evaluation of their host traits and role in PPRV-transmission. Cattle and camelids developed no clinical signs, no viremia, shed no or only low PPRV-RNA loads in swab samples and did not transmit any PPRV to the contact animals. The distribution of PPRV-RNA or antigen in lymphoid organs was similar in cattle and camelids although generally lower compared to suids and small ruminants. In the typical small ruminant hosts, the tissue tropism, pathogenesis and disease expression after PPRV-infection is associated with infection of immune and epithelial cells via SLAM and nectin-4 receptors, respectively. We therefore suggest a different pathogenesis in cattle and camelids and both as dead-end hosts for PPRV.

show abstract

Section: Introductionsupporting

confidence: 63%

Camelids and Cattle Are Dead-End Hosts for Peste-des-Petits-Ruminants Virus

Schulz

Fast

Wernery

et al. 2019

Viruses

View full text Add to dashboard Cite

show abstract

“…The commonly used estimate for the major epidemic probability when a pathogen first arrives in a host population [8,9,35,36,21,27,[29][30][31][32][33][34] can be derived by assuming that infections occur according to a branching process, making the assumptions that the susceptible population is large and that infection lineages arising from different infected hosts are independent. When a single infected host arrives in an otherwise susceptible population, the branching process estimate for the major epidemic probability is given by…”

Section: Standard Estimate (Stochastic Sis/sir Models)mentioning

confidence: 99%

“…The quantity in equation (1), and particularly the version in which I(0) = 1, is used extensively in the epidemiological modelling literature [8,9,21,[26][27][28][29][30][31][32][33][34][35]. It is increasingly used in real-time during emerging outbreaks.…”

Section: Introductionmentioning

confidence: 99%

Will an outbreak exceed available resources for control? Estimating the risk from invading pathogens using practical definitions of a severe epidemic

Thompson

Gilligan

Cunniffe

2019

Preprint

View full text Add to dashboard Cite

14Forecasting whether or not initial reports of disease will be followed by a major epidemic 15 is an important component of disease management. Most estimates of the probability of 16 a major epidemic involve assuming that infections occur according to a branching 17 process. Surprisingly, however, these calculations can be carried out without the factors 18 that differentiate a major epidemic from a minor outbreak ever being defined precisely. 19We assess potential implications of this lack of explicitness by considering the differences 20 between three practically relevant possible definitions of a major epidemic. Specifically, 21we consider a major epidemic as an outbreak in which: i) a large number of hosts are 22 infected simultaneously; ii) a large number of infections occur in total; and iii) disease 23 persists in the population for a long time. We calculate the probability of a major epidemic 24 under each of these definitions, initially considering the commonly used stochastic 25Susceptible-Infected-Susceptible model as a tractable case study allowing analytical 26 progress. We show how the probability of a major epidemic can either be similar to, or 27 very different from, the branching process estimate, depending on which definition of a 28 major epidemic is used. We also show, using other models, that this ambiguity continues 29 to hold in different epidemiological settings. In particular, we consider two additional 30 models: the stochastic Susceptible-Infected-Removed model, and a more complex host-31 vector model parameterised for Zika virus. Our work highlights how the precise definition 32 of a major epidemic must be considered carefully when estimating the risk posed by a 33 new outbreak. It also demonstrates that the precise definition of a major epidemic must 34 be tailored to the epidemiology of the host-pathogen system under consideration. 35 36 KEYWORDS 37 mathematical modelling; infectious disease epidemiology; major epidemic; forecasting 38 39 SHORT TITLE 40 Assessing the practically relevant risk of a major epidemic 41 42 AUTHOR SUMMARY 43When cases of disease are first reported in a new region or country, policy-makers must 44 decide if a disease control programme should be rolled out, as well as how to deploy 45 limited resources. Central to this assessment is understanding the risk of initial cases 46 generating a major epidemic as opposed to fading out as a minor outbreak in which only 47

show abstract

“…Ruminants Virus (PPRV), another morbilliviral agent closely related to RPV, following a single amino acid change within its hemagglutinin (H) antigen [20]. Still notably, also CDV has been shown to successfully infect primate species phylogenetically close to humans, with reports of viral transmission to non-human primates under both natural and experimental conditions, together with a proven CDV adaptation to SLAM/CD150-expressing human cells following a single amino acid substitution in the viral H protein [21][22][23].…”

Section: As a Matter Of Fact A Zoonotic Potential Has Been Recently mentioning

confidence: 99%

Cetacean morbillivirus, a journey from land to sea and vice versa

Guardo

Mazzariol

2019

Preprint

View full text Add to dashboard Cite

Cetacean Morbillivirus, the most relevant pathogen impacting the health and conservation of cetaceans worldwide, has shown in recent years an increased tendency to cross “interspecies barriers”, thereby giving rise to disease and mortality outbreaks in free-ranging dolphins and whales. The present “Opinion Article” deals with the evolutionary “trajectories” of this viral pathogen, likely originating from Rinderpest Virus, along with its "journey" from land to sea (and vice versa), mimicking that of cetaceans' terrestrial ancestors.

show abstract

Structure-Guided Identification of a Nonhuman Morbillivirus with Zoonotic Potential

Cited by 30 publications

References 59 publications

Camelids and Cattle Are Dead-End Hosts for Peste-des-Petits-Ruminants Virus

Camelids and Cattle Are Dead-End Hosts for Peste-des-Petits-Ruminants Virus

Will an outbreak exceed available resources for control? Estimating the risk from invading pathogens using practical definitions of a severe epidemic

Cetacean morbillivirus, a journey from land to sea and vice versa

Contact Info

Product

Resources

About