scholarly journals High Genomic Variability in Equine Infectious Anemia Virus Obtained from Naturally Infected Horses in Pantanal, Brazil: An Endemic Region Case

Viruses ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 207 ◽  
Author(s):  
Camila Dantas Malossi ◽  
Eduardo Gorzoni Fioratti ◽  
Jedson Ferreira Cardoso ◽  
Angelo Jose Magro ◽  
Erna Geessien Kroon ◽  
...  
Keyword(s):  
Amino Acid ◽  
Equine Infectious Anemia Virus ◽  
Genomic Sequences ◽  
Endemic Region ◽  
Viral Genomes ◽  
Equine Infectious Anemia ◽  
Anemia Virus ◽  
Next Generation Sequencing Ngs ◽  
First Time ◽  
Generation Sequencing

Equine infectious anemia virus (EIAV) is a persistent lentivirus that causes equine infectious anemia (EIA). In Brazil, EIAV is endemic in the Pantanal region, and euthanasia is not mandatory in this area. All of the complete genomic sequences from field viruses are from North America, Asia, and Europe, and only proviral genomic sequences are available. Sequences from Brazilian EIAV are currently available only for gag and LTR regions. Thus, the present study aimed for the first time to sequence the entire EIAV genomic RNA in naturally infected horses from an endemic area in Brazil. RNA in plasma from naturally infected horses was used for next-generation sequencing (NGS), and gaps were filled using Sanger sequencing methodology. Complete viral genomes of EIAV from two horses were obtained and annotated (Access Number: MN560970 and MN560971). Putative genes were analyzed and compared with previously described genes, showing conservation in gag and pol genes and high variations in LTR and env sequences. Amino acid changes were identified in the p26 protein, one of the most common targets used for diagnosis, and p26 molecular modelling showed surface amino acid alterations in some epitopes. Brazilian genome sequences presented 88.6% nucleotide identity with one another and 75.8 to 77.3% with main field strains, such as EIAV Liaoning, Wyoming, Ireland, and Italy isolates. Furthermore, phylogenetic analysis suggested that this Brazilian strain comprises a separate monophyletic group. These results may help to better characterize EIAV and to overcome the challenges of diagnosing and controlling EIA in endemic regions.

scholarly journals Equine Infectious Anemia Virus Gag p9 Function in Early Steps of Virus Infection and Provirus Production

2005 ◽  
Vol 79 (14) ◽  
pp. 8793-8801 ◽  
Author(s):  
Sha Jin ◽  
Chaoping Chen ◽  
Ronald C. Montelaro
Keyword(s):  
Amino Acids ◽  
Equine Infectious Anemia Virus ◽  
Critical Role ◽  
Productive Infection ◽  
Viral Dna ◽  
Virus Particles ◽  
Viral Budding ◽  
Equine Infectious Anemia ◽  
Anemia Virus ◽  
First Time

ABSTRACT We have previously reported that serial truncation of the Gag p9 protein of equine infectious anemia virus (EIAV) revealed a progressive loss in replication phenotypes in transfected cells, such that a proviral mutant (E32) expressing the N-terminal 31 amino acids of p9 produced infectious virus particles similarly to parental provirus, while a proviral mutant (K30) with two fewer amino acids produced replication-defective virus particles, despite containing apparently normal levels of processed Gag and Pol proteins (C. Chen, F. Li, and R. C. Montelaro, J. Virol. 75:9762-9760, 2001). Based on these observations, we sought in the current study to identify the precise defect in K30 virion infection of permissive equine dermal (ED) cells. The results of these experiments clearly demonstrated that K30 virions entered target ED cells and produced early (minus-strand strong-stop) and late (Gag) viral DNA products as efficiently as did the replication-competent E32 mutant and parental EIAVUK viruses. However, in contrast to the replication-competent E32 mutant and parental viruses, infection with K30 mutant virus failed to produce detectable two-long-terminal-repeat DNA circles, stable integrated provirus, virus-specific Gag mRNA expression, or intracellular viral protein expression. Taken together, these data demonstrate that the K30 mutant is defective in the ability to produce sufficient nuclear viral DNA to establish a productive infection in ED cells. Thus, these observations indicate for the first time that the EIAV Gag p9 protein performs a critical role in viral DNA production and processing to provirus during EIAV infection, in addition to its previously defined role in viral budding mediated by the p9 L domain.

scholarly journals The S2 Gene of Equine Infectious Anemia Virus Is Dispensable for Viral Replication In Vitro

1998 ◽  
Vol 72 (10) ◽  
pp. 8344-8348 ◽  
Author(s):  
Feng Li ◽  
Bridget A. Puffer ◽  
Ronald C. Montelaro
Keyword(s):  
Equine Infectious Anemia Virus ◽  
Parental Virus ◽  
Target Cells ◽  
Monocyte Differentiation ◽  
Cell Culture Systems ◽  
Equine Infectious Anemia ◽  
Anemia Virus ◽  
First Time

ABSTRACT Equine infectious anemia virus (EIAV) contains the simplest genome among lentiviruses in that it encodes only three putative regulatory genes (S1, S2, S3) in addition to the canonical gag, pol, and envgenes, presumably reflecting its limited tropism to cells of monocyte/macrophage lineage. Tat and Rev functions have been assigned to S1 and S3, respectively, but the specific function for the S2 gene has yet to be determined. Thus, the function of S2 in virus replication in vitro was investigated by using an infectious molecular viral clone, EIAVUK. Various EIAVUK mutants lackingS2 were constructed, and their replication kinetics were examined in several equine cell culture systems, including the natural in vivo target equine macrophage cells. The EIAV S2 mutants showed replication kinetics similar to those of the parental virus in all of the tested primary and transformed equine cell cultures, without any detectable reversion of mutant genomes. The EIAVUKmutants also showed replication kinetics similar to those of the parental virus in an equine blood monocyte differentiation-maturation system. These results demonstrate for the first time that the EIAVS2 gene is not essential and does not appear to affect virus infection and replication properties in target cells in vitro.

scholarly journals Genetic characterization by composite sequence analysis of a new pathogenic field strain of equine infectious anemia virus from the 2006 outbreak in Ireland

2013 ◽  
Vol 94 (3) ◽  
pp. 612-622 ◽  
Author(s):  
Michelle Quinlivan ◽  
Frank Cook ◽  
Rachel Kenna ◽  
John J. Callinan ◽  
Ann Cullinane
Keyword(s):  
Sequence Analysis ◽  
North American ◽  
Molecular Mechanisms ◽  
Equine Infectious Anemia Virus ◽  
Genomic Organization ◽  
Genomic Sequences ◽  
The North ◽  
Equine Infectious Anemia ◽  
Iatrogenic Transmission ◽  
Anemia Virus

Equine infectious anemia virus (EIAV), the causative agent of equine infectious anaemia (EIA), possesses the least-complex genomic organization of any known extant lentivirus. Despite this relative genetic simplicity, all of the complete genomic sequences published to date are derived from just two viruses, namely the North American EIAVWYOMING (EIAVWY) and Chinese EIAVLIAONING (EIAVLIA) strains. In 2006, an outbreak of EIA occurred in Ireland, apparently as a result of the importation of contaminated horse plasma from Italy and subsequent iatrogenic transmission to foals. This EIA outbreak was characterized by cases of severe, sometimes fatal, disease. To begin to understand the molecular mechanisms underlying this pathogenic phenotype, complete proviral genomic sequences in the form of 12 overlapping PCR-generated fragments were obtained from four of the EIAV-infected animals, including two of the index cases. Sequence analysis of multiple molecular clones produced from each fragment demonstrated the extent of diversity within individual viral genes and permitted construction of consensus whole-genome sequences for each of the four viral isolates. In addition, complete env gene sequences were obtained from 11 animals with differing clinical profiles, despite exposure to a common EIAV source. Although the overall genomic organization of the Irish EIAV isolates was typical of that seen in all other strains, the European viruses possessed ≤80 % nucleotide sequence identity with either EIAVWY or EIAVLIA. Furthermore, phylogenetic analysis suggested that the Irish EIAV isolates developed independently of the North American and Chinese viruses and that they constitute a separate monophyletic group.

scholarly journals Replication of Equine Infectious Anemia Virus in Engineered Mouse NIH 3T3 Cells

2008 ◽  
Vol 83 (4) ◽  
pp. 2034-2037 ◽  
Author(s):  
Baoshan Zhang ◽  
Ronald C. Montelaro
Keyword(s):  
Equine Infectious Anemia Virus ◽  
3T3 Cells ◽  
Cyclin T1 ◽  
Immunodeficiency Virus ◽  
Equine Infectious Anemia ◽  
Anemia Virus ◽  
Nih 3T3 ◽  
First Time ◽  
Hiv 1 ◽  
Nih 3T3 Cells

ABSTRACT We employed the equine lentivirus equine infectious anemia virus (EIAV) to investigate the cellular restrictions for lentivirus replication in murine NIH 3T3 cells. The results of these studies demonstrate that NIH 3T3 cells expressing the EIAV receptor ELR1 and equine cyclin T1 supported productive replication of EIAV and produced infectious virions at levels similar to those found in a reference permissive equine cell line. The studies presented here demonstrate, for the first time, differential levels of restriction for EIAV and human immunodeficiency virus type 1 (HIV-1) replication in murine cells and suggest that these differences can be exploited to reveal critical virus-cell interactions required for HIV-1 assembly and budding of lentivirus particles.

scholarly journals Equine Infectious Anemia Virus Genomic Evolution in Progressor and Nonprogressor Ponies

2001 ◽  
Vol 75 (10) ◽  
pp. 4570-4583 ◽  
Author(s):  
Caroline Leroux ◽  
Jodi K. Craigo ◽  
Charles J. Issel ◽  
Ronald C. Montelaro
Keyword(s):  
Steady State ◽  
Viral Replication ◽  
Virus Replication ◽  
Equine Infectious Anemia Virus ◽  
Genomic Rna ◽  
Equine Infectious Anemia ◽  
Steady State Levels ◽  
Anemia Virus ◽  
First Time

ABSTRACT A primary mechanism of lentivirus persistence is the ability of these viruses to evolve in response to biological and immunological selective pressures with a remarkable array of genetic and antigenic variations that constitute a perpetual natural experiment in genetic engineering. A widely accepted paradigm of lentivirus evolution is that the rate of genetic variation is correlated directly with the levels of virus replication: the greater the viral replication, the more opportunities that exist for genetic modifications and selection of viral variants. To test this hypothesis directly, we examined the patterns of equine infectious anemia virus (EIAV) envelope variation during a 2.5-year period in experimentally infected ponies that differed markedly in clinical progression and in steady-state levels of viral replication as indicated by plasma virus genomic RNA assays. The results of these comprehensive studies revealed for the first time similar extents of envelope gp90 variation in persistently infected ponies regardless of the number of disease cycles (one to six) and viremia during chronic disease. The extent of envelope variation was also independent of the apparent steady-state levels of virus replication during long-term asymptomatic infection, varying from undetectable to 105 genomic RNA copies per ml of plasma. In addition, the data confirmed the evolution of distinct virus populations (genomic quasispecies) associated with sequential febrile episodes during acute and chronic EIA and demonstrated for the first time ongoing envelope variation during long-term asymptomatic infections. Finally, comparison of the rates of evolution of the previously defined EIAV gp90 variable domains demonstrated distinct differences in the rates of nucleotide and amino acid sequence variation, presumably reflecting differences in the ability of different envelope domains to respond to immune or other biological selection pressures. Thus, these data suggest that EIAV variation can be associated predominantly with ongoing low levels of virus replication and selection in target tissues, even in the absence of substantial levels of plasma viremia, and that envelope variation continues during all stages of persistent infection as the virus successfully avoids clearance by host defense mechanisms.

scholarly journals Adaptive Immunity Is the Primary Force Driving Selection of Equine Infectious Anemia Virus Envelope SU Variants during Acute Infection

2004 ◽  
Vol 78 (17) ◽  
pp. 9295-9305 ◽  
Author(s):  
Robert H. Mealey ◽  
Steven R. Leib ◽  
Sarah L. Pownder ◽  
Travis C. McGuire
Keyword(s):  
Amino Acid ◽  
Adaptive Immunity ◽  
Equine Infectious Anemia Virus ◽  
Acute Infection ◽  
Adaptive Immune ◽  
Ctl Epitope ◽  
Glycosylation Sites ◽  
Equine Infectious Anemia ◽  
Anemia Virus ◽  
Selection Of

ABSTRACT Equine infectious anemia virus (EIAV) is a lentivirus that causes persistent infection in horses. The appearance of antigenically distinct viral variants during recurrent viremic episodes is thought to be due to adaptive immune selection pressure. To test this hypothesis, we evaluated envelope SU cloned sequences from five severe combined immunodeficient (SCID) foals infected with EIAV. Within the SU hypervariable V3 region, 8.5% of the clones had amino acid changes, and 6.4% had amino acid changes within the known cytotoxic T lymphocyte (CTL) epitope Env-RW12. Of all the SU clones, only 3.1% had amino acid changes affecting potential N-linked glycosylation sites. In contrast, a much higher degree of variation was evident in SU sequences obtained from four EIAV-infected immunocompetent foals. Within V3, 68.8% of the clones contained amino acid changes, and 50% of the clones had amino acid changes within the Env-RW12 CTL epitope. Notably, 31.9% of the clones had amino acid changes affecting one or more glycosylation sites. Marked amino acid variation occurred in cloned SU sequences from an immune-reconstituted EIAV-infected SCID foal. Of these clones, 100% had amino acid changes within V3, 100% had amino acid changes within Env-RW12, and 97.5% had amino acid changes affecting glycosylation sites. Analysis of synonymous and nonsynonymous nucleotide substitutions revealed statistically significant differences between SCID and immunocompetent foals and between SCID foals and the reconstituted SCID foal. Interestingly, amino acid selection at one site occurred independently of adaptive immune status. Not only do these data indicate that adaptive immunity primarily drives the selection of EIAV SU variants, but also they demonstrate that other selective forces exist during acute infection.

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