About: Programmed −2/−1 Ribosomal Frameshifting in Simarteriviruses: an Evolutionarily Conserved Mechanism

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Programmed −2/−1 Ribosomal Frameshifting in Simarteriviruses: an Evolutionarily Conserved Mechanism
Creator	Brierley, Ian Wang, Tao Li, Yanhua Fang, Ying Napthine, Sawsan Cai, Yingyun Yan, Xingyu Firth, Andrew Kuhn, Jens
Source	PMC
abstract	The −2/−1 programmed ribosomal frameshifting (−2/−1 PRF) mechanism in porcine reproductive and respiratory syndrome virus (PRRSV) leads to the translation of two additional viral proteins, nonstructural protein 2TF (nsp2TF) and nsp2N. This −2/−1 PRF mechanism is transactivated by a viral protein, nsp1β, and cellular poly(rC) binding proteins (PCBPs). Critical elements for −2/−1 PRF, including a slippery sequence and a downstream C-rich motif, were also identified in 11 simarteriviruses. However, the slippery sequences (XXXUCUCU instead of XXXUUUUU) in seven simarteriviruses can only facilitate −2 PRF to generate nsp2TF. The nsp1β of simian hemorrhagic fever virus (SHFV) was identified as a key factor that transactivates both −2 and −1 PRF, and the universally conserved Tyr111 and Arg114 in nsp1β are essential for this activity. In vitro translation experiments demonstrated the involvement of PCBPs in simarterivirus −2/−1 PRF. Using SHFV reverse genetics, we confirmed critical roles of nsp1β, slippery sequence, and C-rich motif in −2/−1 PRF in SHFV-infected cells. Attenuated virus growth ability was observed in SHFV mutants with impaired expression of nsp2TF and nsp2N. Comparative genomic sequence analysis showed that key elements of −2/−1 PRF are highly conserved in all known arteriviruses except equine arteritis virus (EAV) and wobbly possum disease virus (WPDV). Furthermore, −2/−1 PRF with SHFV PRF signal RNA can be stimulated by heterotypic nsp1βs of all non-EAV arteriviruses tested. Taken together, these data suggest that −2/−1 PRF is an evolutionarily conserved mechanism employed in non-EAV/-WPDV arteriviruses for the expression of additional viral proteins that are important for viral replication. IMPORTANCE Simarteriviruses are a group of arteriviruses infecting nonhuman primates, and a number of new species have been established in recent years. Although these arteriviruses are widely distributed among African nonhuman primates of different species, and some of them cause lethal hemorrhagic fever disease, this group of viruses has been undercharacterized. Since wild nonhuman primates are historically important sources or reservoirs of human pathogens, there is concern that simarteriviruses may be preemergent zoonotic pathogens. Thus, molecular characterization of simarteriviruses is becoming a priority in arterivirology. In this study, we demonstrated that an evolutionarily conserved ribosomal frameshifting mechanism is used by simarteriviruses and other distantly related arteriviruses for the expression of additional viral proteins. This mechanism is unprecedented in eukaryotic systems. Given the crucial role of ribosome function in all living systems, the potential impact of the in-depth characterization of this novel mechanism reaches beyond the field of virology.
has issue date	2019-07-30(xsd:dateTime)
bibo:doi	10.1128/jvi.00370-19
bibo:pmid	31167906
has license	cc-by
sha1sum (hex)	870c8d63bfe7cbede0c0779b7991b8296dfede1c
schema:url	https://doi.org/10.1128/jvi.00370-19
resource representing a document's title	Programmed −2/−1 Ribosomal Frameshifting in Simarteriviruses: an Evolutionarily Conserved Mechanism
has PubMed Central identifier	PMC6675879
has PubMed identifier	31167906
schema:publication	J Virol
resource representing a document's body	covid:870c8d63bfe7cbede0c0779b7991b8296dfede1c#body_text
is schema:about of	named entity 'Comparative' named entity 'viral' named entity 'PRF' named entity 'In vitro' named entity 'conserved' named entity 'factor' named entity 'EAV' named entity 'key' named entity 'mechanism' named entity 'NONSTRUCTURAL PROTEIN' named entity 'INFECTED' named entity 'SEQUENCE ANALYSIS' named entity 'CRITICAL' named entity 'ATTENUATED' named entity 'ADDITIONAL' named entity 'GROWTH ABILITY' named entity 'EXPERIMENTS' named entity 'REVERSE GENETICS' named entity 'SIMIAN HEMORRHAGIC FEVER VIRUS' named entity 'MECHANISM' covid:arg/870c8d63bfe7cbede0c0779b7991b8296dfede1c named entity 'CELLULAR' named entity 'EXCEPT' named entity 'CONSERVED' named entity 'NON-' named entity 'EXPRESSION' named entity 'PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS' named entity 'GENERATE' named entity 'EMPLOYED' named entity 'RIBOSOMAL' named entity 'CONSERVED' named entity 'MECHANISM' named entity 'POSSUM' named entity 'ELEMENTS' named entity 'SEQUENCES' named entity 'PRF' named entity 'DOWNSTREAM' named entity 'GENOMIC SEQUENCE' named entity 'AA1' named entity 'POLY' named entity 'TAKEN' named entity 'KNOWN' named entity 'ARTERIVIRUSES' named entity 'MOTIF' named entity 'THESE' named entity 'ROLES' named entity 'VIRAL PROTEIN' named entity 'PROTEIN ' named entity 'KEY' named entity 'EQUINE ARTERITIS VIRUS' named entity 'INCLUDING' named entity 'MUTANTS' named entity 'TESTED' named entity 'INVOLVEMENT' named entity 'TRANSLATION' named entity 'DATA' named entity 'STIMULATED' named entity 'BINDING PROTEINS' named entity 'IN VITRO TRANSLATION' named entity 'FACTOR' named entity 'SEQUENCE' named entity 'CONFIRMED' named entity 'RICH' named entity 'IDENTIFIED' named entity 'HIGHLY' named entity 'AA2' named entity 'IMPORTANT' named entity 'USING' named entity 'SEVEN' named entity 'VIRAL PROTEINS' named entity 'NSP1' named entity 'ACTIVITY' named entity 'SIGNAL'

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