scholarly journals A novel RNA mycovirus in a hypovirulent isolate of the plant pathogen Diaporthe ambigua

2000 ◽  
Vol 81 (12) ◽  
pp. 3107-3114 ◽  
Author(s):  
O. Preisig ◽  
N. Moleleki ◽  
W. A. Smit ◽  
B. D. Wingfield ◽  
M. J. Wingfield

Hypovirulent isolates of the fruit tree fungal pathogen Diaporthe ambigua have previously been shown to harbour a double-stranded (ds)RNA genetic element of about 4 kb. In this study, we established the complete cDNA sequence of this dsRNA, which represents a replicative form of a positive-strand RNA virus that we have named D. ambigua RNA virus (DaRV). The nucleotide sequence of the genome is 4113 bp and has a GC content of 53%. Two large ORFs are present in the same reading frame. They are most probably translated by readthrough of a UAG stop codon in the central part of the genome. The longest possible translation product (p125) has a predicted molecular mass of about 125 kDa. A significant homology can be found to the non-structural proteins of carmoviruses of the positive-strand RNA virus family Tombusviridae. These proteins also include the conserved RNA-dependent RNA polymerase (RDRP) domain. In contrast to the genome organization of these plant viruses, no ORF is present at the 3′ end of the DaRV genome that encodes a coat protein. Therefore, it is proposed that DaRV is not encapsidated but that it occurs as RNA–RDRP complexes and/or that it might be associated with cell membranes. Interestingly, six putative transmembrane helices are predicted in the N-terminal part of p56 (translation product of the first ORF, N-terminal part of p125), which might direct and anchor the viral complex to membranes. DaRV is a mycovirus with a unique genome organization and has a distant relationship to the plant virus family Tombusviridae.

Viruses ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 66 ◽  
Author(s):  
Krin Mann ◽  
Hélène Sanfaçon

Many plant viruses express their proteins through a polyprotein strategy, requiring the acquisition of protease domains to regulate the release of functional mature proteins and/or intermediate polyproteins. Positive-strand RNA viruses constitute the vast majority of plant viruses and they are diverse in their genomic organization and protein expression strategies. Until recently, proteases encoded by positive-strand RNA viruses were described as belonging to two categories: (1) chymotrypsin-like cysteine and serine proteases and (2) papain-like cysteine protease. However, the functional characterization of plant virus cysteine and serine proteases has highlighted their diversity in terms of biological activities, cleavage site specificities, regulatory mechanisms, and three-dimensional structures. The recent discovery of a plant picorna-like virus glutamic protease with possible structural similarities with fungal and bacterial glutamic proteases also revealed new unexpected sources of protease domains. We discuss the variety of plant positive-strand RNA virus protease domains. We also highlight possible evolution scenarios of these viral proteases, including evidence for the exchange of protease domains amongst unrelated viruses.


mSystems ◽  
2021 ◽  
Author(s):  
Rohit Verma ◽  
Sandhini Saha ◽  
Shiv Kumar ◽  
Shailendra Mani ◽  
Tushar Kanti Maiti ◽  
...  

Replication of a positive-strand RNA virus involves an RNA-protein complex consisting of viral genomic RNA, host RNA(s), virus-encoded proteins, and host proteins. Dissecting out individual components of the replication complex will help decode the mechanism of viral replication. 5′ and 3′ UTRs in positive-strand RNA viruses play essential regulatory roles in virus replication.


mBio ◽  
2016 ◽  
Vol 7 (6) ◽  
Author(s):  
Diede Oudshoorn ◽  
Barbara van der Hoeven ◽  
Ronald W. A. L. Limpens ◽  
Corrine Beugeling ◽  
Eric J. Snijder ◽  
...  

ABSTRACTInfection with nidoviruses like corona- and arteriviruses induces a reticulovesicular network of interconnected endoplasmic reticulum (ER)-derived double-membrane vesicles (DMVs) and other membrane structures. This network is thought to accommodate the viral replication machinery and protect it from innate immune detection. We hypothesized that the innate immune response has tools to counteract the formation of these virus-induced replication organelles in order to inhibit virus replication. Here we have investigated the effect of type I interferon (IFN) treatment on the formation of arterivirus-induced membrane structures. Our approach involved ectopic expression of arterivirus nonstructural proteins nsp2 and nsp3, which induce DMV formation in the absence of other viral triggers of the interferon response, such as replicating viral RNA. Thus, this setup can be used to identify immune effectors that specifically target the (formation of) virus-induced membrane structures. Using large-scale electron microscopy mosaic maps, we found that IFN-β treatment significantly reduced the formation of the membrane structures. Strikingly, we also observed abundant stretches of double-membrane sheets (a proposed intermediate of DMV formation) in IFN-β-treated samples, suggesting the disruption of DMV biogenesis. Three interferon-stimulated gene products, two of which have been reported to target the hepatitis C virus replication structures, were tested for their possible involvement, but none of them affected membrane structure formation. Our study reveals the existence of a previously unknown innate immune mechanism that antagonizes the viral hijacking of host membranes. It also provides a solid basis for further research into the poorly understood interactions between the innate immune system and virus-induced replication structures.IMPORTANCEViruses with a positive-strand RNA genome establish a membrane-associated replication organelle by hijacking and remodeling intracellular host membranes, a process deemed essential for their efficient replication. It is unknown whether the cellular innate immune system can detect and/or inhibit the formation of these membrane structures, which could be an effective mechanism to delay viral RNA replication. In this study, using an expression system that closely mimics the formation of arterivirus replication structures, we show for the first time that IFN-β treatment clearly reduces the amount of induced membrane structures. Moreover, drastic morphological changes were observed among the remaining structures, suggesting that their biogenesis was impaired. Follow-up experiments suggested that host cells contain a hitherto unknown innate antiviral mechanism, which targets this common feature of positive-strand RNA virus replication. Our study provides a strong basis for further research into the interaction of the innate immune system with membranous viral replication organelles.


Virology ◽  
2011 ◽  
Vol 409 (2) ◽  
pp. 175-188 ◽  
Author(s):  
Zhi Zhou ◽  
Nan Wang ◽  
Sara E. Woodson ◽  
Qingming Dong ◽  
Jie Wang ◽  
...  

Uirusu ◽  
2003 ◽  
Vol 53 (1) ◽  
pp. 53-53
Author(s):  
Paul Ahlquist ◽  
Michael Schwartz ◽  
Jianbo Chen ◽  
Michael Janda ◽  
Johan den Boon ◽  
...  

2021 ◽  
Vol 6 (1) ◽  
pp. 1-2
Author(s):  
Tahir Sultan Shamsi ◽  
◽  
Mehjabeen Imam ◽  

Covid-19 pandemic plagued this world since the beginning of 2020 AD. It is caused by a new positive-strand RNA virus of coronaviridae family [1]. It causes Coronavirus disease 2019 (hence the name COVID-19). It is a contagious disease predominantly causes severe acute respiratory syndrome, hence the name SARS-CoV-2. It started from Wuhan, China, in December 2019. Since then, it has spread globally. It is reported to be a new virus therefore it’s properties, pathogenesis, virulence, immunogenicity, variants, and how will host body will react to this virus was unknown. Despite of 22 months since this virus started to spread worldwide, researchers and clinicians continued to learn about it on daily basis. Newer information about it poured in daily in scientific journals as well as in print / electronic media. Mostly, newer information continued to negate earlier information. Social media disinformation continued to confuse the masses.


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