scholarly journals Variation Profile of the Orthotospovirus Genome

Pathogens ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 521 ◽  
Author(s):  
Deepti Nigam ◽  
Hernan Garcia-Ruiz

Orthotospoviruses are plant-infecting members of the family Tospoviridae (order Bunyavirales), have a broad host range and are vectored by polyphagous thrips in a circulative-propagative manner. Because diverse hosts and vectors impose heterogeneous selection constraints on viral genomes, the evolutionary arms races between hosts and their pathogens might be manifested as selection for rapid changes in key genes. These observations suggest that orthotospoviruses contain key genetic components that rapidly mutate to mediate host adaptation and vector transmission. Using complete genome sequences, we profiled genomic variation in orthotospoviruses. Results show that the three genomic segments contain hypervariable areas at homologous locations across species. Remarkably, the highest nucleotide variation mapped to the intergenic region of RNA segments S and M, which fold into a hairpin. Secondary structure analyses showed that the hairpin is a dynamic structure with multiple functional shapes formed by stems and loops, contains sites under positive selection and covariable sites. Accumulation and tolerance of mutations in the intergenic region is a general feature of orthotospoviruses and might mediate adaptation to host plants and insect vectors.

2019 ◽  
Author(s):  
Michael A. Martin ◽  
Drishti Kaul ◽  
Gene S. Tan ◽  
Christopher W. Woods ◽  
Katia Koelle

AbstractThe rapid evolution of influenza is an important contributing factor to its high worldwide incidence. The emergence and spread of genetic point mutations has been thoroughly studied both within populations and within individual hosts. In addition, influenza viruses are also known to generate genomic variation during their replication in the form of defective viral genomes (DVGs). These DVGs are formed by internal deletions in at least one gene segment that render them incapable of replication without the presence of wild-type virus. DVGs have previously been identified in natural human infections and may be associated with less severe clinical outcomes. These studies have not been able to address how DVG populations evolve in vivo in individual infections due to their cross-sectional design. Here we present an analysis of DVGs present in samples from two longitudinal influenza A H3N2 human challenge studies. We observe the generation of DVGs in almost all subjects. Although the genetic composition of DVG populations was highly variable, identical DVGs were observed both between multiple samples within single hosts as well as between hosts. Most likely due to stochastic effects, we did not observe clear instances of selection for specific DVGs or for shorter DVGs over the course of infection. Furthermore, DVG presence was not found to be associated with peak viral titer or peak symptom scores. Our analyses highlight the diversity of DVG populations within a host over the course of infection and the apparent role that genetic drift plays in their population dynamics.ImportanceThe evolution of influenza virus, in terms of single nucleotide variants and the reassortment of gene segments, has been studied in detail. However, influenza is known to generate defective viral genomes (DVGs) during replication, and little is known about how these genomes evolve both within hosts and at the population level. Studies in animal models have indicated that prophylactically or therapeutically administered DVGs can impact patterns of disease progression. However, the formation of naturally-occurring DVGs, their evolutionary dynamics, and their contribution to disease severity in human hosts is not well understood. Here, we identify the formation of de novo DVGs in samples from human challenge studies throughout the course of infection. We analyze their evolutionary trajectories, revealing the important role of genetic drift in shaping DVG populations during acute infections with well-adapted viral strains.


2012 ◽  
Vol 86 (18) ◽  
pp. 10239-10239 ◽  
Author(s):  
Sanna Sillankorva ◽  
Andrew M. Kropinski ◽  
Joana Azeredo

The broad-host-range lyticPseudomonasphage Φ-S1 possess a 40,192 bp double-stranded DNA (dsDNA) genome of 47 open reading frames (ORFs) and belongs to the familyPodoviridae, subfamilyAutographivirinae, genusT7likevirus.


2019 ◽  
Vol 3 (2) ◽  
pp. 438
Author(s):  
Fakhrurrazi M. Yunus ◽  
Amira Luthfiani

Such rapid development of science and technology lately resulted in such rapid changes in the social life of the human culture, one of which is medical field. But although there has been no progress there may be some problems that have not been solved by human beings, such as the discovery of drugs or a potent bidder to cure deadly diseases such AS AIDS, cancer, and other malignant diseases. These deadly diseases are a reason for someone to end his life from having to endure a long time ill one of them by asking for family assistance to end his life, which in medicine is called euthanasia. This research aims to determine how the position of passive euthanasia and birthright position for applicants of euthanasia passive according to Islamic law when viewed in terms of maqāṣid al-Syarī'ah. This research is done by collecting the library materials in the form of books, encyclopedia, and scientific works related to this discussion. The results of this study gave the answer that stopping the treatment, or releasing the organ and respiratory aids from the sick or euthanasia passive the law may but only in the case of the sick suffer the death of the brainstem. Because while using these tools is contrary to sharia teachings among them, postponing the management of dead and its funeral without emergency reasons, postponing the division of inheritance and resigning the time of his wife. Therefore, the birthright position for the heir or the family that asks or plea for passive euthanasia is not hindered by the heir. Because the passive euthanasia in this case is not classified as an act of murder.


2021 ◽  
Author(s):  
Chakradhar Mattupalli ◽  
Jason Shiller ◽  
Prasanna Kankanala ◽  
Nick D Krom ◽  
Stephen Marek ◽  
...  

Phymatotrichopsis omnivora is a destructive plant pathogen causing root rot disease of alfalfa, cotton, pecan, grape, and many other important dicotyledonous species. A member of the family Rhizinaceae, in the class Pezizomycetes, P. omnivora is a soilborne ascomycete fungus that is difficult to maintain in culture, currently genetically intractable, and for which there are no publicly available genomic resources. We have generated draft genome sequences of four P. omnivora isolates obtained from cotton and alfalfa, growing in Texas and Oklahoma, USA. These genome sequences will provide new insights into the biology of the fungus, including the factors responsible for its broad host range and pathogenicity.


PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0242362
Author(s):  
Xin Feng ◽  
Rui-lian Lai ◽  
Min-xia Gao ◽  
Wen-guang Chen ◽  
Ru-jian Wu ◽  
...  

Two distinct closterovirus-like genome sequences (termed AdV-1 v1 and v2) were identified in Actinidia chinensis var. deliciosa ‘Miliang-1’ that had no disease symptoms using high-throughput sequencing. Using overlapping reverse transcription-polymerase chain reaction and rapid amplification of cDNA ends, the genomic sequences of AdV-1 v1 and v2 were confirmed as 17,646 and 18,578 nucleotides in length, respectively. The two complete genomes contained 9 and 15 open reading frames, respectively, coding for proteins having domains typical of Closteroviridae, such as RNA-dependent RNA polymerase (RdRp), heat shock protein 70 homolog (HSP70h) and coat protein (CP). Sequence analysis showed that the amino acid sequences of RdRp, HSP70h, and CP of the two variants exhibited high similarity (> 80%), while their genomic organization was somewhat different. This suggested that the two viral genomes identified here are variants of the family Closteroviridae in a single kiwifruit host. Furthermore, phylogenetic relationship analysis revealed that the two variants had a closer relationship with the unclassified virus Persimmon virus B (PeVB) and Actinidia virus 1 (AcV-1) than with other members of the family Closteroviridae, as did their genomic organization. It is speculated that the two variants, together with PeVB and AcV-1 belong to a new subfamily of Closteroviridae.


1999 ◽  
Vol 65 (1) ◽  
pp. 117-125 ◽  
Author(s):  
Roeland C. H. J. Van Ham ◽  
David Martínez-Torres ◽  
Andrés Moya ◽  
Amparo Latorre

ABSTRACT Buchnera aphidicola is an obligate intracellular symbiont of aphids. One of its proposed functions is the synthesis of essential amino acids, nutrients required by aphids but deficient in their diet of plant phloem sap. The genetic organization of the tryptophan pathway in Buchnera from proliferous aphids of the family Aphididae has previously been shown to reflect a capacity to overproduce this essential amino acid (C.-Y. Lai, L. Baumann, and P. Baumann, Proc. Natl. Acad. Sci. USA 91:3819–3823, 1994). This involved amplification of the genes for the first enzyme in the pathway, anthranilate synthase (TrpEG), on a low-copy-number plasmid. Here we report on the finding and molecular characterization of TrpEG-encoding plasmids in Buchnera from aphids of the distantly related family Pemphigidae. Buchnera fromTetraneura caerulescens contained a 3.0-kb plasmid (pBTc2) that carried a single copy of trpEG and resembledtrpEG plasmids of Buchnera from the Aphididae. The second plasmid (pBPs2), isolated from Buchnera ofPemphigus spyrothecae, contained a different replicon. It consisted of a putative origin of replication containing iterons and an open reading frame, designated repAC, which showed a high similarity to the gene encoding the replication initiation protein RepA of the RepA/C replicon from the broad-host-range IncA/C group of plasmids. The plasmid population was heterogeneous with respect to the number of tandem repeats of a 1.8-kb unit carryingrepAC1 , trpG, and remnants of trpE. The two principal forms consisted of either five or six copies of this repeat and a single-copy region carryingrepAC2 , the putative origin of replication, andtrpE. The unexpected finding of elements of the RepA/C replicon in previously characterized trpEG plasmids fromBuchnera of the Aphididae suggests that a replacement of replicons has occurred during the evolution of these plasmids, which may point to a common ancestry for all Buchnera trpEGamplifications.


Blood ◽  
2000 ◽  
Vol 96 (4) ◽  
pp. 1443-1448 ◽  
Author(s):  
Elisabetta Castoldi ◽  
Paolo Simioni ◽  
Michael Kalafatis ◽  
Barbara Lunghi ◽  
Daniela Tormene ◽  
...  

Abstract The study of the molecular bases of thrombophilia in a large family with 4 symptomatic members is reported. Three thrombophilic genetic components (FV R506Q, FV H1299R, and PT 20210G/A), all affecting the activity of the prothrombinase complex, were detected alone and in combination in various family members. In addition, a newly identified missense mutation (factor V [FV] Y1702C), causing FV deficiency, was also present in the family and appeared to enhance activated protein C (APC) resistance in carriers of FV R506Q or FV H1299R by abolishing the expression of the counterpart FV allele. The relationships between complex genotypes, coagulation laboratory findings, and clinical phenotypes were analyzed in the family. All symptomatic family members were carriers of combined defects and showed APC resistance and elevated F1 + 2 values. Evidence for the causative role of the FV Y1702C mutation, which affects a residue absolutely conserved in all 3 A domains of FV, factor VIII, and ceruloplasmin, relies on (1) the absolute cosegregation between the mutation and FV deficiency, both in the family and in the general population; (2) FV antigen and immunoblot studies indicating the absence of Y1702C FV molecules in plasma of carriers of the mutation, despite normal levels of the FV Y1702C messenger RNA; and (3) molecular modeling data that support a crucial role of the mutated residue in the A domain structure. These findings help to interpret the variable penetrance of thrombosis in thrombophilic families and to define the molecular bases of FV deficiency.


2015 ◽  
Vol 59 (8) ◽  
pp. 5073-5077 ◽  
Author(s):  
Ying-Min Huang ◽  
Lan-lan Zhong ◽  
Xue-Fei Zhang ◽  
Hang-tong Hu ◽  
Yu-qi Li ◽  
...  

ABSTRACTWe identified New Delhi metallo-β-lactamase (NDM-1)-producingCitrobacter freundiiGB032,Escherichia coliGB102, andAcinetobacter baumanniiGB661 in urine and stool samples from a single patient in China. Plasmid profiling and Southern blotting indicated thatblaNDM-1from GB032 and that from GB102 were likely located on the same plasmid, whileblaNDM-1from GB661 was located on a very large (>400-kb) plasmid. This case underscores the broad host range ofblaNDM-1and its potential to spread between members of the familyEnterobacteriaceaeandA. baumannii.


1978 ◽  
Vol 147 (4) ◽  
pp. 1280-1284 ◽  
Author(s):  
J Tung ◽  
PV O'Donnell ◽  
E Fleissner ◽  
EA Boyse

The family of glycoproteins called gp70 includes molecules that are the main constituent of murine C-type viral envelopes, and some that are expressed as mendelian constituents of thymocyte plasma membranes in the absence of virions. To investigate further the relation of viral gp70s to plasma- membrane gp70s we compared peptide maps of gp70s derived by immunoprecipitation from cells infected with chosen viruses and from various thymocytes and leukemiacells known to express one or more of three immunogenetically defined gp70 types: Glx-gp70, X-gp70, and O-gp70. Maps of gp70 from cultured cells infected with ecotropic and xenotropic viruses were distinguishable from one another, and in general resembled gp70 maps prepared directly from ecotropic and xenotropic virions respectively. Maps of gp70s immunoprecipitated from thymocytes of five mouse strains and from two A strain T-cell leukemias also fell into two distinguishable and generally corresponding patterns. Thus peptide-mapping substantiates earlier conclusions that viral gp70s and plasma-membrane gp70s inherited independently of virus-production are highly related or identical molecules. The gp70 maps of thymocytes from B6, B6-G(+IX), 129, and A mice formed a group resembling the map from cultured cells infected with xenotropic virus. Thymocytes from AKR mice, and the two A strain leukemias, gave gp70 maps conforming more to the second pattern, that of cultured cells infected with ecotropic virus. This second pattern probably comprises at least two gp70 types, one of which is X-gp70. Our data indicate that the G(IX)-gp70 and O-gp70 sub-species of gp70 expressed in the cell populations we have studied are coded by xenotropic viral genomes, and X-gp70 by ecotropic viral genomes.


2005 ◽  
Vol 69 (2) ◽  
pp. 262-291 ◽  
Author(s):  
David E. Levin

SUMMARY The yeast cell wall is a highly dynamic structure that is responsible for protecting the cell from rapid changes in external osmotic potential. The wall is also critical for cell expansion during growth and morphogenesis. This review discusses recent advances in understanding the various signal transduction pathways that allow cells to monitor the state of the cell wall and respond to environmental challenges to this structure. The cell wall integrity signaling pathway controlled by the small G-protein Rho1 is principally responsible for orchestrating changes to the cell wall periodically through the cell cycle and in response to various forms of cell wall stress. This signaling pathway acts through direct control of wall biosynthetic enzymes, transcriptional regulation of cell wall-related genes, and polarization of the actin cytoskeleton. However, additional signaling pathways interface both with the cell wall integrity signaling pathway and with the actin cytoskeleton to coordinate polarized secretion with cell wall expansion. These include Ca2+ signaling, phosphatidylinositide signaling at the plasma membrane, sphingoid base signaling through the Pkh1 and -2 protein kinases, Tor kinase signaling, and pathways controlled by the Rho3, Rho4, and Cdc42 G-proteins.


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