EQUINE INFECTIOUS ANEMIA VIRUS (EIAV): EVIDENCE OF CIRCULATION IN DONKEYS FROM THE BRAZILIAN NORTHEAST REGION

Author(s):  
Viviane Maria Dias Costa ◽  
Andreia Elisa Cursino ◽  
Ana Paula Moreira Franco Luiz ◽  
Gissandra Farias Braz ◽  
Paulo Henrique Cavalcante ◽  
...  
2021 ◽  
Vol 49 ◽  
Author(s):  
Camila De Souza Bezerra ◽  
Denize Monteiro dos Anjos ◽  
Brunna Muniz Rodrigues Falcão ◽  
Cícero Wanderlô Casimiro Bezerra ◽  
Davidianne De Andrade Moraes ◽  
...  

Background: Equine infectious anemia (EIA) is a viral infection, caused by a lentivirus of the Retroviridae family, Orthoretrovirinael subfamily and its occurrence generates significant economic losses due to culling of positive animals as a measure of infection control. The objective of this work was to determine the prevalence of horses positive for equine infectious anemia virus (EIAV) and to identify the occurrence of areas with higher densities of cases in the states of Paraíba (PB), Pernambuco (PE), Rio Grande do Norte (RN) and Ceará (CE), Northeast region of Brazil, during the rainy (May and June) and dry (October and November) periods of 2017 and 2018.Materials, Methods & Results: Serum samples from 6,566 horses from the states of PB, PE, RN and CE, Brazil, provided by the Laboratório Veterinária Diagnóstico - Ltda., were used. Serological diagnosis of EIA was performed using indirect enzyme-linked immunosorbent assay (ELISA) as a screening test and agar gel immunodiffusion test (AGID) as a confirmatory test. The apparent prevalence was obtained by dividing the number of seroreactive animals by the total number of animals, while the true prevalence was estimated by adjusting the apparent prevalence, considering the sensitivity (100%) and specificity (98.6%) of the diagnostic protocol used. For the construction of Kernel estimates, the Quartic function was used. In the dry season, of the 1,564 animals sampled, 28 were serologically positive, of which 19 belonged to the state of Ceará, 7 to Paraíba and 2 to Rio Grande do Norte. In 2018, it was observed that, during the rainy season, 26 of the 1,635 horses were seroreactive, with 19 cases resulting from Ceará, 4 from Paraíba and 3 from Pernambuco. In the dry season, 32 of the 1,526 animals were seroreactive to EIAV, of which 26 were from Ceará, 3 from Paraíba, 1 from Rio Grande do Norte and 2 from Pernambuco. In the dry period of 2017, the CE had a real prevalence of 1.22% (95% CI = 0.05 - 2.99%). In 2018, during the rainy season, prevalences of 0.03% (95% CI = 0 - 1.18%) were identified in CE and 1.69% (95% CI = 0 - 8.38%) in PE. Regarding the 2018 dry period, a prevalence of 1.32% (95% CI = 0.26 - 2.84%) was found in the state of CE. In both dry and rainy periods of 2017, the presence of spatial clusters of animals positive for EIA was observed, mainly in the border areas among the states of CE, PE, PB and RN. In 2018, there was a variation in the distribution of areas with higher densities of cases between the rainy and dry periods.Discussion: The state of CE had the highest prevalence of positive animals and the presence of areas with higher densities of EIA cases in both climatic periods, in the years 2017 and 2018. In some municipalities of the CE, important sporting events of agglomeration of animals take place, which can favor the transmission of EIAV by facilitating the contact of infected and susceptible animals. Population density may be a factor associated with the higher prevalence observed in this region, as it has the second largest herd among the states studied. Higher densities indirectly contribute to the occurrence of infectious diseases, as they favor the contact of infected and susceptible animals. The occurrence of higher densities of cases in the border areas of the states of PE, RN, CE, and PB may be related to the greater movement of animals in these regions, favoring the indirect contact of infected horses with susceptible ones. The observed results demonstrate the circulation of the EIAV in four states in the Northeast region of Brazil.Keywords: Equine infectious anemia virus, prevalence, spatial clusters, epidemiology.


Author(s):  
Maria Carla Rodríguez Domínguez ◽  
Roberto Montes-de-Oca-Jiménez ◽  
Juan Carlos Vázquez Chagoyan ◽  
Alberto Barbabosa Pliego ◽  
Jorge Antonio Varela Guerrero ◽  
...  

2007 ◽  
Vol 82 (3) ◽  
pp. 1204-1213 ◽  
Author(s):  
Baoshan Zhang ◽  
Chengqun Sun ◽  
Sha Jin ◽  
Michael Cascio ◽  
Ronald C. Montelaro

ABSTRACT The equine lentivirus receptor 1 (ELR1), a member of the tumor necrosis factor receptor (TNFR) protein family, has been identified as a functional receptor for equine infectious anemia virus (EIAV). Toward defining the functional interactions between the EIAV SU protein (gp90) and its ELR1 receptor, we mapped the gp90 binding domain of ELR1 by a combination of binding and functional assays using the EIAV SU gp90 protein and various chimeric receptor proteins derived from exchanges between the functional ELR1 and the nonbinding homolog, mouse herpesvirus entry mediator (murine HveA). Complementary exchanges of the respective cysteine-rich domains (CRD) between the ELR1 and murine HveA proteins revealed CRD1 as the predominant determinant of functional gp90 binding to ELR1 and also to a chimeric murine HveA protein expressed on the surface of transfected Cf2Th cells. Mutations of individual amino acids in the CRD1 segment of ELR1 and murine HveA indicated the Leu70 in CRD1 as essential for functional binding of EIAV gp90 and for virus infection of transduced Cf2Th cells. The specificity of the EIAV SU binding domain identified for the ELR1 receptor is fundamentally identical to that reported previously for functional binding of feline immunodeficiency virus SU to its coreceptor CD134, another TNFR protein. These results indicate unexpected common features of the specific mechanisms by which diverse lentiviruses can employ TNFR proteins as functional receptors.


2021 ◽  
pp. 104063872110061
Author(s):  
César I. Romo-Sáenz ◽  
Patricia Tamez-Guerra ◽  
Aymee Olivas-Holguin ◽  
Yareellys Ramos-Zayas ◽  
Nelson Obregón-Macías ◽  
...  

Equine infectious anemia (EIA) is a highly infectious disease in members of the Equidae family, caused by equine infectious anemia virus (EIAV). The disease severity ranges from subclinical to acute or chronic, and causes significant economic losses in the equine industry worldwide. Serologic tests for detection of EIAV infection have some concerns given the prolonged seroconversion time. Therefore, molecular methods are needed to improve surveillance programs for this disease. We attempted detection of EIAV in 6 clinical and 42 non-clinical horses in Nuevo Leon State, Mexico, using the agar gel immunodiffusion (AGID) test for antibody detection, and nested and hemi-nested PCR for detection of proviral DNA. We found that 6 of 6, 5 of 6, and 6 of 6 clinical horses were positive by AGID, nested PCR, and hemi-nested PCR, respectively, whereas 0 of 42, 1 of 42, and 9 of 42 non-clinical horses were positive by these tests, respectively. BLAST analysis of the 203-bp 5′-LTR/ tat segment of PCR product revealed 83–93% identity with EIAV isolates in GenBank and reference strains from other countries. By phylogenetic analysis, our Mexican samples were grouped in a different clade than other sequences reported worldwide, indicating that the LRT/ tat region represents an important target for the detection of non-clinical horses.


2002 ◽  
Vol 76 (4) ◽  
pp. 1569-1577 ◽  
Author(s):  
Feng Li ◽  
Chaoping Chen ◽  
Bridget A. Puffer ◽  
Ronald C. Montelaro

ABSTRACT We have previously demonstrated by Gag polyprotein budding assays that the Gag p9 protein of equine infectious anemia virus (EIAV) utilizes a unique YPDL motif as a late assembly domain (L domain) to facilitate release of the budding virus particle from the host cell plasma membrane (B. A. Puffer, L. J. Parent, J. W. Wills, and R. C. Montelaro, J. Virol. 71:6541-6546, 1997). To characterize in more detail the role of the YPDL L domain in the EIAV life cycle, we have examined the replication properties of a series of EIAV proviral mutants in which the parental YPDL L domain was replaced by a human immunodeficiency virus type 1 (HIV-1) PTAP or Rous sarcoma virus (RSV) PPPY L domain in the p9 protein or by proviruses in which the parental YPDL or HIV-1 PTAP L domain was inserted in the viral matrix protein. The replication properties of these L-domain variants were examined with respect to Gag protein expression and processing, virus particle production, and virus infectivity. The data from these experiments indicate that (i) the YPDL L domain of p9 is required for replication competence (assembly and infectivity) in equine cell cultures, including the natural target equine macrophages; (ii) all of the functions of the YPDL L domain in the EIAV life cycle can be replaced by replacement of the parental YPDL sequence in p9 with the PTAP L-domain segment of HIV-1 p6 or the PPPY L domain of RSV p2b; and (iii) the assembly, but not infectivity, functions of the EIAV proviral YPDL substitution mutants can be partially rescued by inclusions of YPDL and PTAP L-domain sequences in the C-terminal region of the EIAV MA protein. Taken together, these data demonstrate that the EIAV YPDL L domain mediates distinct functions in viral budding and infectivity and that the HIV-1 PTAP and RSV PPPY L domains can effectively facilitate these dual replication functions in the context of the p9 protein. In light of the fact that YPDL, PTAP, and PPPY domains evidently have distinct characteristic binding specificities, these observations may indicate different portals into common cellular processes that mediate EIAV budding and infectivity, respectively.


2005 ◽  
Vol 86 (1) ◽  
pp. 139-149 ◽  
Author(s):  
Laryssa Howe ◽  
Jodi K. Craigo ◽  
Charles J. Issel ◽  
Ronald C. Montelaro

It has been previously reported that transient corticosteroid immune suppression of ponies experimentally infected with a highly neutralization resistant envelope variant of equine infectious anemia virus (EIAV), designated EIAVΔPND, resulted in the appearance of type-specific serum antibodies to the infecting EIAVΔPND virus. The current study was designed to determine if this induction of serum neutralizing antibodies was associated with changes in the specificity of envelope determinants targeted by serum antibodies or caused by changes in the nature of the antibodies targeted to previously defined surface envelope gp90 V3 and V4 neutralization determinants. To address this question, the envelope determinants of neutralization by post-immune suppression serum were mapped. The results demonstrated that the neutralization sensitivity to post-immune suppression serum antibodies mapped specifically to the surface envelope gp90 V3 and V4 domains, individually or in combination. Thus, these data indicate that the development of serum neutralizing antibodies to the resistant EIAVΔPND was due to an enhancement of host antibody responses caused by transient immune suppression and the associated increase in virus replication.


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