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High frequency of SEN virus infection in thalassemic patients and healthy blood donors in Iran.

Karimi-Rastehkenari A, Bouzari M - Virol. J. (2010)

Bottom Line: Frequency of SENV-H viremia was significantly higher than SENV-D among healthy individuals.In comparison to SENV-D negative patients, the mean of mean corpuscular hemoglobin was significantly higher in SENV-D positive and co-infection cases (P < 0.05).In conclusion, SENV-D isolate in Guilan Province may be having a pathogenic agent for thalassemic patients.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biology, Faculty of Science, University of Isfahan, Isfahan, Iran.

ABSTRACT

Background: SEN virus is a blood-borne, circular ssDNA virus and possessing nine genotypes (A to I). Among nine genotypes, SENV-D and SENV-H genotypes have the strong link with patients with unknown (none-A to E) hepatitis infections. Infection with blood-borne viruses is the second important cause of death in thalassemic patients. The aim of this study was to determine the frequency of SENV-D and SENV-H genotypes viremia by performing nested-PCR in 120 and 100 sera from healthy blood donors and thalassemic patients in Guilan Province, North of Iran respectively. Also, to explicate a possible role of SEN virus in liver disease and established changes in blood factors, the serum aminotransferases (ALT and AST) and some of the blood factors were measured.

Results: Frequency of SENV-D, SENV (SENV-H or SENV-D) and co-infection (both SENV-D and SENV-H) viremia was significantly higher among thalassemic patients than healthy individuals. Frequency of SENV-H viremia was significantly higher than SENV-D among healthy individuals. In comparison to SENV-D negative patients, the mean of mean corpuscular hemoglobin was significantly higher in SENV-D positive and co-infection cases (P < 0.05). The means of AST and ALT were significantly higher in thalassemic patients than healthy blood donors, but there were not any significant differences in the means of the liver levels between SENV-positive and -negative individuals in healthy blood donors and thalassemic patients. High nucleotide homology observed among PCR amplicon's sequences in healthy blood donors and thalassemic patients.

Conclusions: The high rate of co-infection shows that different genotypes of SENV have no negative effects on each other. The high frequency of SENV infection among thalassemic patients suggests blood transfusion as main route of transmission. High frequency of SENV infection in healthy individuals indicates that other routes rather than blood transfusion also are important. Frequency of 90.8% of SENV infection among healthy blood donors as well as high nucleotide homology of sequenced amplicons between two groups can probably suggest that healthy blood donors infected by SENV act partly as a source of SENV transmission to the thalassemic patients. In conclusion, SENV-D isolate in Guilan Province may be having a pathogenic agent for thalassemic patients.

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Phylogenetic tree constructed by neighbor-joining method within partial ORF1 with 100 Bootstrap replicates. Our sequences with accession numbers of GQ179968 and GQ179969 for SENV-D, and accession numbers of GQ179972 and GQ452051 for SENV-H, for healthy individuals and thalassemic patients, respectively. These 16 isolates comprise eight SEN virus isolates (SENV-A(AX025667), SENV-B(AX025677), SENV-C(AX025718), SENV-D(AX025730), SENV-E(AX025761), SENV-F(AX025822), SENV-G(AX025830), SENV-H(AX025838), and Five TT virus isolates (TA278(AB017610), TJN01(AB028668), ZC-2002-1(FM881988), 2467NG3(AY093401), ZC-2001-1(FM882007), and tree TTV variants PMV(AF261761), SANBAN(AB025946), TLMV(AB038631) obtained GenBank databases on NCBI website. The evolutionary distances were computed using the Maximum Composite Likelihood model based on the units of the number of base substitutions per site.
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Figure 3: Phylogenetic tree constructed by neighbor-joining method within partial ORF1 with 100 Bootstrap replicates. Our sequences with accession numbers of GQ179968 and GQ179969 for SENV-D, and accession numbers of GQ179972 and GQ452051 for SENV-H, for healthy individuals and thalassemic patients, respectively. These 16 isolates comprise eight SEN virus isolates (SENV-A(AX025667), SENV-B(AX025677), SENV-C(AX025718), SENV-D(AX025730), SENV-E(AX025761), SENV-F(AX025822), SENV-G(AX025830), SENV-H(AX025838), and Five TT virus isolates (TA278(AB017610), TJN01(AB028668), ZC-2002-1(FM881988), 2467NG3(AY093401), ZC-2001-1(FM882007), and tree TTV variants PMV(AF261761), SANBAN(AB025946), TLMV(AB038631) obtained GenBank databases on NCBI website. The evolutionary distances were computed using the Maximum Composite Likelihood model based on the units of the number of base substitutions per site.

Mentions: As shown in figure 3, high genomic homology observed between our sequences and some of the TTV isolates.


High frequency of SEN virus infection in thalassemic patients and healthy blood donors in Iran.

Karimi-Rastehkenari A, Bouzari M - Virol. J. (2010)

Phylogenetic tree constructed by neighbor-joining method within partial ORF1 with 100 Bootstrap replicates. Our sequences with accession numbers of GQ179968 and GQ179969 for SENV-D, and accession numbers of GQ179972 and GQ452051 for SENV-H, for healthy individuals and thalassemic patients, respectively. These 16 isolates comprise eight SEN virus isolates (SENV-A(AX025667), SENV-B(AX025677), SENV-C(AX025718), SENV-D(AX025730), SENV-E(AX025761), SENV-F(AX025822), SENV-G(AX025830), SENV-H(AX025838), and Five TT virus isolates (TA278(AB017610), TJN01(AB028668), ZC-2002-1(FM881988), 2467NG3(AY093401), ZC-2001-1(FM882007), and tree TTV variants PMV(AF261761), SANBAN(AB025946), TLMV(AB038631) obtained GenBank databases on NCBI website. The evolutionary distances were computed using the Maximum Composite Likelihood model based on the units of the number of base substitutions per site.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2819036&req=5

Figure 3: Phylogenetic tree constructed by neighbor-joining method within partial ORF1 with 100 Bootstrap replicates. Our sequences with accession numbers of GQ179968 and GQ179969 for SENV-D, and accession numbers of GQ179972 and GQ452051 for SENV-H, for healthy individuals and thalassemic patients, respectively. These 16 isolates comprise eight SEN virus isolates (SENV-A(AX025667), SENV-B(AX025677), SENV-C(AX025718), SENV-D(AX025730), SENV-E(AX025761), SENV-F(AX025822), SENV-G(AX025830), SENV-H(AX025838), and Five TT virus isolates (TA278(AB017610), TJN01(AB028668), ZC-2002-1(FM881988), 2467NG3(AY093401), ZC-2001-1(FM882007), and tree TTV variants PMV(AF261761), SANBAN(AB025946), TLMV(AB038631) obtained GenBank databases on NCBI website. The evolutionary distances were computed using the Maximum Composite Likelihood model based on the units of the number of base substitutions per site.
Mentions: As shown in figure 3, high genomic homology observed between our sequences and some of the TTV isolates.

Bottom Line: Frequency of SENV-H viremia was significantly higher than SENV-D among healthy individuals.In comparison to SENV-D negative patients, the mean of mean corpuscular hemoglobin was significantly higher in SENV-D positive and co-infection cases (P < 0.05).In conclusion, SENV-D isolate in Guilan Province may be having a pathogenic agent for thalassemic patients.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biology, Faculty of Science, University of Isfahan, Isfahan, Iran.

ABSTRACT

Background: SEN virus is a blood-borne, circular ssDNA virus and possessing nine genotypes (A to I). Among nine genotypes, SENV-D and SENV-H genotypes have the strong link with patients with unknown (none-A to E) hepatitis infections. Infection with blood-borne viruses is the second important cause of death in thalassemic patients. The aim of this study was to determine the frequency of SENV-D and SENV-H genotypes viremia by performing nested-PCR in 120 and 100 sera from healthy blood donors and thalassemic patients in Guilan Province, North of Iran respectively. Also, to explicate a possible role of SEN virus in liver disease and established changes in blood factors, the serum aminotransferases (ALT and AST) and some of the blood factors were measured.

Results: Frequency of SENV-D, SENV (SENV-H or SENV-D) and co-infection (both SENV-D and SENV-H) viremia was significantly higher among thalassemic patients than healthy individuals. Frequency of SENV-H viremia was significantly higher than SENV-D among healthy individuals. In comparison to SENV-D negative patients, the mean of mean corpuscular hemoglobin was significantly higher in SENV-D positive and co-infection cases (P < 0.05). The means of AST and ALT were significantly higher in thalassemic patients than healthy blood donors, but there were not any significant differences in the means of the liver levels between SENV-positive and -negative individuals in healthy blood donors and thalassemic patients. High nucleotide homology observed among PCR amplicon's sequences in healthy blood donors and thalassemic patients.

Conclusions: The high rate of co-infection shows that different genotypes of SENV have no negative effects on each other. The high frequency of SENV infection among thalassemic patients suggests blood transfusion as main route of transmission. High frequency of SENV infection in healthy individuals indicates that other routes rather than blood transfusion also are important. Frequency of 90.8% of SENV infection among healthy blood donors as well as high nucleotide homology of sequenced amplicons between two groups can probably suggest that healthy blood donors infected by SENV act partly as a source of SENV transmission to the thalassemic patients. In conclusion, SENV-D isolate in Guilan Province may be having a pathogenic agent for thalassemic patients.

Show MeSH
Related in: MedlinePlus