Reorganization and expansion of the nidoviral family Arteriviridae

Kuhn, Jens H.; Lauck, Michael; Bailey, Adam L.; Щетинин, А. М.; Vishnevskaya, Tatyana V.; Bào, Yīmíng; Ng, Terry Fei Fan; LeBreton, Matthew; Schneider, Bradley S.; Gillis, Amethyst; Tamoufé, Ubald; Diffo, Joseph Le Doux; Takuo, Jean Michel; Kondov, Nikola O.; Coffey, Lark L.; Wolfe, Nathan; Delwart, Eric; Clawson, Anna N.; Postnikova, Elena; Bollinger, Laura; Lackemeyer, Matthew G.; Radoshitzky, Sheli R.; Palacios, Gustavo; Wada, Jiro; Shevtsova, Z V; Jahrling, Peter B.; Лапин, Б. А.; Дерябин, П Г; Dunowska, Magdalena; Alkhovsky, Sergey V.; Rogers, Jeffrey; Friedrich, Thomas C.; O’Connor, David H.; Goldberg, Tony L.

doi:10.1007/s00705-015-2672-z

Cited by 278 publications

(198 citation statements)

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“…PRRSV is a small, enveloped virus with a single-stranded RNA genome of positive polarity, which is grouped in the family Arterivirdae [1–3]. Due to the high degree of genetic diversity, PRRSV was recently divided into two species: PRRSV-1 (formerly European genotype 1) and PRRSV-2 (formerly North American genotype 2) [4, 5]. Extensive genetic differences do exist not only between but also within the two species leading to the sub-classification into at least three European subtypes [6].…”

Section: Introductionmentioning

confidence: 99%

Emergence of a virulent porcine reproductive and respiratory syndrome virus (PRRSV) 1 strain in Lower Austria

Sinn

Klingler²,

Lamp

et al. 2016

Porc Health Manag

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BackgroundIn spring 2015, an outbreak of porcine reproductive and respiratory syndrome (PRRS) struck Lower Austria caused by a PRRS virus (PRRSV) strain spreading rapidly among both previously PRRSV negative and vaccinated pig herds. This case report describes the first well-documented emergence of the PRRSV strain responsible for this outbreak.Case presentationA PRRSV seronegative piglet-producing farm in Lower Austria encountered losses in foetuses and suckling piglets of up to 90 %; clinical signs in sows and nursery piglets included fever and reduced feed intake. Additionally, high percentages of repeat breeders and losses of up to 40 % in nursery piglets occurred. An infection with PRRSV was suggested by the detection of antibodies by enzyme linked immunosorbent assay and confirmed by quantitative real time PCR. The underlying PRRSV strain, termed AUT15-33, was isolated by passage on porcine alveolar macrophages, partially sequenced (ORF2-7) and grouped as PRRSV-1, subtype 1. In phylogenetic analysis of the genome region coding for the structural proteins, ORF2-7, AUT15-33 clustered with Belgian strains but identities were as low as 88 %. In contrast, analysis of ORF7 sequences revealed a close relationship to Croatian strains from 2012 with an identity of 94 – 95 %.ConclusionsIn the year following the outbreak, the same PRRSV strain was identified repeatedly in different regions of Austria. It can be speculated that the new strain has novel advantageous properties.

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Section: Introductionmentioning

confidence: 99%

Emergence of a virulent porcine reproductive and respiratory syndrome virus (PRRSV) 1 strain in Lower Austria

Sinn

Klingler²,

Lamp

et al. 2016

Porc Health Manag

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“…These two viruses were subsequently named Kibale red colobus viruses 1 and 2 (KRCV-1 and -2) (10,11). KRCV-1 has not been detected in any other primate species of African or Asian origin besides red colobus monkeys, either in captivity or in the wild, despite screens of captive macaques and wild nonhuman primates from Kibale National Park.…”

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confidence: 99%

“…KRCV-1 has not been detected in any other primate species of African or Asian origin besides red colobus monkeys, either in captivity or in the wild, despite screens of captive macaques and wild nonhuman primates from Kibale National Park. However, additional highly divergent simian arteriviruses have recently been discovered in apparently healthy wild red-tailed monkeys (Cercopithecus ascanius) (12), yellow baboons (Papio cynocephalus) (13), hybrid kinda ϫ grayfooted-chacma baboons (Papio kindae ϫ Papio ursinus griseipes) (14), malbroucks (Chlorocebus cynosuros), African green monkeys (Chlorocebus aethiops) (15), vervet monkeys (Chlorocebus pygerythrus) (15), and De Brazza's monkeys (Cercopithecus neglectus) (10), indicating that these viruses are widespread among African monkeys. We recently analyzed samples collected during three separate SHF outbreaks that occurred in captive macaque colonies in the 1960s and late 1980s.…”

mentioning

confidence: 99%

Within-Host Evolution of Simian Arteriviruses in Crab-Eating Macaques

Moncla

Weiler²,

Barry³

et al. 2017

J Virol

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Simian arteriviruses are a diverse clade of viruses infecting captive and wild nonhuman primates. We recently reported that Kibale red colobus virus 1 (KRCV-1) causes a mild and self-limiting disease in experimentally infected crabeating macaques, while simian hemorrhagic fever virus (SHFV) causes lethal viral hemorrhagic fever. Here we characterize how these viruses evolved during replication in cell culture and in experimentally infected macaques. During passage in cell culture, 68 substitutions that were localized in open reading frames (ORFs) likely associated with host cell entry and exit became fixed in the KRCV-1 genome. However, we did not detect any strong signatures of selection during replication in macaques. We uncovered patterns of evolution that were distinct from those observed in surveys of wild red colobus monkeys, suggesting that these species may exert different adaptive challenges for KRCV-1. During SHFV infection, we detected signatures of selection on ORF 5a and on a small subset of sites in the genome. Overall, our data suggest that patterns of evolution differ markedly among simian arteriviruses and among host species.IMPORTANCE Certain RNA viruses can cross species barriers and cause disease in new hosts. Simian arteriviruses are a diverse group of related viruses that infect captive and wild nonhuman primates, with associated disease severity ranging from apparently asymptomatic infections to severe, viral hemorrhagic fevers. We infected nonhuman primate cell cultures and then crab-eating macaques with either simian hemorrhagic fever virus (SHFV) or Kibale red colobus virus 1 (KRCV-1) and assessed within-host viral evolution. We found that KRCV-1 quickly acquired a large number of substitutions in its genome during replication in cell culture but that evolution in macaques was limited. In contrast, we detected selection focused on SHFV ORFs 5a and 5, which encode putative membrane proteins. These patterns suggest that in addition to diverse pathogenic phenotypes, these viruses may also exhibit distinct patterns of within-host evolution both in vitro and in vivo.KEYWORDS evolution, simian arterivirus, simian hemorrhagic fever virus, virology, within-host diversity I n 1964, acute outbreaks of a highly lethal viral hemorrhagic fever caused by a previously unknown agent swept through captive nonhuman primate research facilities in the former Soviet Union and the United States (1-4). Although the origin and

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“…We also discovered two novel simian arteriviruses, which we named Drakensberg Mountain vervet virus (DMVV-1) and Zambian malbrouck virus (ZMbV-1). These viruses contained the additional ORFs characteristic of all simian arteriviruses discovered to date (34,35) and phylogenetically clustered with other simian arteriviruses (Fig. 1B).…”

Section: Virus Discoverymentioning

confidence: 88%

Arteriviruses, Pegiviruses, and Lentiviruses Are Common among Wild African Monkeys

Bailey

Lauck

Ghai

et al. 2016

J Virol

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Nonhuman primates (NHPs) are a historically important source of zoonotic viruses and are a gold-standard model for research on many human pathogens. However, with the exception of simian immunodeficiency virus (SIV) (family Retroviridae), the blood-borne viruses harbored by these animals in the wild remain incompletely characterized. Here, we report the discovery and characterization of two novel simian pegiviruses (family Flaviviridae) and two novel simian arteriviruses (family Arteriviridae) in wild African green monkeys from Zambia (malbroucks [Chlorocebus cynosuros]) and South Africa (vervet monkeys [Chlorocebus pygerythrus]). We examine several aspects of infection, including viral load, genetic diversity, evolution, and geographic distribution, as well as host factors such as age, sex, and plasma cytokines. In combination with previous efforts to characterize blood-borne RNA viruses in wild primates across sub-Saharan Africa, these discoveries demonstrate that in addition to SIV, simian pegiviruses and simian arteriviruses are widespread and prevalent among many African cercopithecoid (i.e., Old World) monkeys. IMPORTANCEPrimates are an important source of viruses that infect humans and serve as an important laboratory model of human virus infection. Here, we discover two new viruses in African green monkeys from Zambia and South Africa. In combination with previous virus discovery efforts, this finding suggests that these virus types are widespread among African monkeys. Our analysis suggests that one of these virus types, the simian arteriviruses, may have the potential to jump between different primate species and cause disease. In contrast, the other virus type, the pegiviruses, are thought to reduce the disease caused by human immunodeficiency virus (HIV) in humans. However, we did not observe a similar protective effect in SIV-infected African monkeys coinfected with pegiviruses, possibly because SIV causes little to no disease in these hosts.

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Reorganization and expansion of the nidoviral family Arteriviridae

Cited by 278 publications

References 50 publications

Emergence of a virulent porcine reproductive and respiratory syndrome virus (PRRSV) 1 strain in Lower Austria

Emergence of a virulent porcine reproductive and respiratory syndrome virus (PRRSV) 1 strain in Lower Austria

Within-Host Evolution of Simian Arteriviruses in Crab-Eating Macaques

Arteriviruses, Pegiviruses, and Lentiviruses Are Common among Wild African Monkeys

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