Evidence for Host Jumping and Diversification of Marine Cephaloidophorid Gregarines (Apicomplexa) Between Two Distantly Related Animals, viz., Crustaceans and Salps

Protist ◽  
2021 ◽  
pp. 125822
Author(s):  
Kevin C. Wakeman ◽  
Shimpei Hiruta ◽  
Yusuke Kondo ◽  
Susumu Ohtsuka
Keyword(s):  
2012 ◽  
Vol 99 (3) ◽  
pp. 552-561 ◽  
Author(s):  
Ryan M. Kepler ◽  
Gi-Ho Sung ◽  
Yukio Harada ◽  
Kazuaki Tanaka ◽  
Eiji Tanaka ◽  
...  
Keyword(s):  

Coronaviruses ◽  
2021 ◽  
Vol 02 ◽  
Author(s):  
Akshay Uttarkar ◽  
Vidya Niranjan ◽  
Shivam Pandit ◽  
Srividya Subash

Background: SARS-nCOV-2 is a variant of the known SARS coronavirus family. The mutations in viruses are very rapid and can play a crucial role in the evolution or devolution of the organism. This has a direct impact on “host jumping” and pathogenicity of the virus. Objective: The study aims to understand the frequency of genomic variations that have occurred in the virus affecting the Indian sub-population. The impact of variations translating to proteins and its consequences affecting protein stability and interaction were studied. Method: Phylogenetic analysis of the 140 genomes from the India region was performed, followed by SNP and Indel analysis of both CDS and non-CDS regions. This effort was followed by a prediction of mutations occurring in 8 proteins of interest and the impact on protein stability and prospective drug interactions. Results: Genomes showed variability in origin, and major branches can be mapped to the 2002 outbreak of SARS. The mutation frequency in CDS regions showed that 241 C >T, 3037 C >T, 2836 C >T, and 6312 C >A occurred in 81.5 % of genomes mapping to major genes. Corresponding mutations were mapped to protein sequences. The effect of mutations occurring in spike glycoprotein, RNA dependent RNA polymerase, nsp8, nucleocapsid and 3c protease were also mapped. Conclusion: Whilst the mutations in spike glycoprotein showcased an increase in protein stability, the residues undergoing mutations were also a part of drug binding pockets for hydroxychloroquine. Mutations occurring in other proteins of interest were leading to a decrease in protein stability. The mutations were also a part of drug binding pockets for Favipiravir, Remdesivir and Dexamethasone. The work promotes the will to analyse larger datasets to understand mutation pattern globally.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Irene Righetto ◽  
Francesco Filippini

Host jump can result in deadly pandemic events when avian influenza A viruses broaden their host specificity and become able to infect mammals, including humans. Haemagglutinin—the major capsid protein in influenza A viruses—is subjected to high rate mutations, of which several occur at its “head”: the receptor-binding domain that mediates specific binding to host cell receptors. Such surface-changing mutations may lead to antigenically novel influenza A viruses hence in pandemics by host jump and in vaccine escape by antigenic drift. Changes in haemagglutinin surface electrostatics have been recently associated with antigenic drift and with clades evolution and spreading in H5N1 and H9N2 viruses. We performed a comparative analysis of haemagglutinin surface electrostatics to investigate clustering and eventual fingerprints among representative pandemic (H5 and H7) and nonpandemic (H4 and H6) avian influenza viral subtypes. We observed preferential sorting of viruses isolated from mammalian/human hosts among these electrostatic clusters of a subtype; however, sorting was not “100% specific” to the different clusters. Therefore, electrostatic fingerprints can help in understanding, but they cannot explain alone the host jumping mechanism.


Author(s):  
Sandra Martínez-Turiño ◽  
María Calvo ◽  
Leonor Cecilia Bedoya ◽  
Mingmin Zhao ◽  
Juan Antonio García

Understanding biological mechanisms that regulate emergence of viral diseases, in particular those events engaging cross-species pathogens spillover, are becoming increasingly important in Virology. Species barrier jumping has been extensively studied in animal viruses, and the critical role of a suitable intermediate host in animal viruses-generated human pandemics is highly topical. However, studies on host jumping involving plant viruses have been focused on shifting intra-species, leaving aside the putative role of “bridge hosts” in facilitating interspecies crossing. Here, we take advantage of several VPg mutants, derived from a chimeric construct of the potyvirus Plum pox virus (PPV), analysing its differential behaviour in three herbaceous species. Our results showed that two VPg mutations in a Nicotiana clevelandii-adapted virus, emerged during adaptation to the bridge-host Arabidopsis thaliana, drastically prompted partial adaptation to Chenopodium foetidum. Although, both changes are expected to facilitate productive interactions with eIF(iso)4E, polymorphims detected in PPV VPg and the three eIF(iso)4E studied, extrapolated to a recent VPg:eIF4E structural model, suggested that two adaptation ways can be operating. Remarkably, we found that VPg mutations driving host-range expansion in two non-related species, not only are not associated with cost trade-off constraints in the original host, but also improve fitness on it.


mBio ◽  
2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Ji Lian Li ◽  
R. Scott Cornman ◽  
Jay D. Evans ◽  
Jeffery S. Pettis ◽  
Yan Zhao ◽  
...  

ABSTRACT Emerging and reemerging diseases that result from pathogen host shifts are a threat to the health of humans and their domesticates. RNA viruses have extremely high mutation rates and thus represent a significant source of these infectious diseases. In the present study, we showed that a plant-pathogenic RNA virus, tobacco ringspot virus (TRSV), could replicate and produce virions in honeybees, Apis mellifera, resulting in infections that were found throughout the entire body. Additionally, we showed that TRSV-infected individuals were continually present in some monitored colonies. While intracellular life cycle, species-level genetic variation, and pathogenesis of the virus in honeybee hosts remain to be determined, the increasing prevalence of TRSV in conjunction with other bee viruses from spring toward winter in infected colonies was associated with gradual decline of host populations and winter colony collapse, suggesting the negative impact of the virus on colony survival. Furthermore, we showed that TRSV was also found in ectoparasitic Varroa mites that feed on bee hemolymph, but in those instances the virus was restricted to the gastric cecum of Varroa mites, suggesting that Varroa mites may facilitate the spread of TRSV in bees but do not experience systemic invasion. Finally, our phylogenetic analysis revealed that TRSV isolates from bees, bee pollen, and Varroa mites clustered together, forming a monophyletic clade. The tree topology indicated that the TRSVs from arthropod hosts shared a common ancestor with those from plant hosts and subsequently evolved as a distinct lineage after transkingdom host alteration. This study represents a unique example of viruses with host ranges spanning both the plant and animal kingdoms. IMPORTANCE Pathogen host shifts represent a major source of new infectious diseases. Here we provide evidence that a pollen-borne plant virus, tobacco ringspot virus (TRSV), also replicates in honeybees and that the virus systemically invades and replicates in different body parts. In addition, the virus was detected inside the body of parasitic Varroa mites, which consume bee hemolymph, suggesting that Varroa mites may play a role in facilitating the spread of the virus in bee colonies. This study represents the first evidence that honeybees exposed to virus-contaminated pollen could also be infected and raises awareness of potential risks of new viral disease emergence due to host shift events. About 5% of known plant viruses are pollen transmitted, and these are potential sources of future host-jumping viruses. The findings from this study showcase the need for increased surveillance for potential host-jumping events as an integrated part of insect pollinator management programs.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Carl Michael Deom ◽  
Marin Talbot Brewer ◽  
Paul M. Severns

AbstractViruses within the Geminiviridae family cause extensive agricultural losses. Members of four genera of geminiviruses contain a C4 gene (AC4 in geminiviruses with bipartite genomes). C4(AC4) genes are entirely overprinted on the C1(AC1) genes, which encode the replication-associated proteins. The C4(AC4) proteins exhibit diverse functions that may be important for geminivirus diversification. In this study, the influence of natural selection on the evolutionary diversity of 211 C4(AC4) genes relative to the C1(AC1) sequences they overlap was determined from isolates of the Begomovirus and Curtovirus genera. The ratio of nonsynonymous (dN) to synonymous (dS) nucleotide substitutions indicated that C4(AC4) genes are under positive selection, while the overlapped C1(AC1) sequences are under purifying selection. Ninety-one of 200 Begomovirus C4(AC4) genes encode elongated proteins with the extended regions being under neutral selection. C4(AC4) genes from begomoviruses isolated from tomato from native versus exotic regions were under similar levels of positive selection. Analysis of protein structure suggests that C4(AC4) proteins are entirely intrinsically disordered. Our data suggest that non-synonymous mutations and mutations that increase the length of C4(AC4) drive protein diversity that is intrinsically disordered, which could explain C4/AC4 functional variation and contribute to both geminivirus diversification and host jumping.


2016 ◽  
Vol 397 ◽  
pp. 33-42 ◽  
Author(s):  
Thomas Caraco ◽  
Carrie A. Cizauskas ◽  
Ing-Nang Wang

2021 ◽  
Author(s):  
Perumal Arumugam Desingu ◽  
K. Nagarajan
Keyword(s):  
New Host ◽  

AbstractThe emergence of the novel SARS-CoV-2 in 2019 sparked a dispute concerning its origin. Here, we report that the SARS-CoV-2 originated through pangolin-coronavirus (Pan-CoVs) from the SARS-CoV-related-bat-coronaviruses (SARS-CoV-1-rB-CoVs) rather than from SARS-CoV-2-related-bat-coronaviruses (SARS-CoV-2-rB-CoVs), in contrast to the previous thought. Further, our analyses strongly suggest that the Pan-CoVs evolved from the SARS-CoV-1-rB-CoVs without recombination. Further, our results suggest that the SARS-CoV-1-rB-CoVs’ perhaps jumped into the pangolin, which forced the viruses to mutate and adapt to the new host, and resulted in the origin of Pan-CoVs. Surprisingly, the Pan-CoVs formed an evolutionary intermediate between SARS-CoV-2 and SARS-CoV-2-rB-CoVs at the spike gene. Our findings also suggest that the Pan-CoV/GX and Pan-CoV/Guangdong lineages recombined to form the SARS-CoV-2 spike gene. We also found evidence that the SARS-CoV-2-rB-CoVs spike gene evolved via recombination between Pan-CoV/Guangdong and SARS-CoV-1-rB-CoVs. Overall, our findings suggest that the SARS-CoV-2 emerged from SARS-CoV-1-rB-CoVs through host jumping.


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