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Children with Plasmodium vivax infection previously observed in Namibia, were Duffy negative and carried a c.136G > A mutation

Haiyambo, Daniel Hosea ; Aleksenko, Larysa LU ; Mumbengegwi, Davies ; Bock, Ronnie ; Uusiku, Petrina ; Malleret, Benoit ; Rénia, Laurent and Quaye, Isaac Kweku (2021) In BMC Infectious Diseases 21(1).
Abstract

Background: In a previous study, using a molecular approach, we reported the presence of P. vivax in Namibia. Here, we have extended our investigation to the Duffy antigen genetic profile of individuals of the same cohort with and without Plasmodium infections. Methods: Participants with P. vivax (n = 3), P. falciparum (n = 23) mono-infections and co-infections of P. vivax/P. falciparum (n = 4), and P. falciparum/P. ovale (n = 3) were selected from seven regions. Participants with similar age but without any Plasmodium infections (n = 47) were also selected from all the regions. Duffy allelic profile was examined using standard PCR followed by sequencing of amplified products. Sequenced samples were also examined for the presence or... (More)

Background: In a previous study, using a molecular approach, we reported the presence of P. vivax in Namibia. Here, we have extended our investigation to the Duffy antigen genetic profile of individuals of the same cohort with and without Plasmodium infections. Methods: Participants with P. vivax (n = 3), P. falciparum (n = 23) mono-infections and co-infections of P. vivax/P. falciparum (n = 4), and P. falciparum/P. ovale (n = 3) were selected from seven regions. Participants with similar age but without any Plasmodium infections (n = 47) were also selected from all the regions. Duffy allelic profile was examined using standard PCR followed by sequencing of amplified products. Sequenced samples were also examined for the presence or absence of G125A mutation in codon 42, exon 2. Results: All individuals tested carried the − 67 T > C mutation. However, while all P. vivax infected participants carried the c.G125A mutation, 7/28 P. falciparum infected participants and 9/41 of uninfected participants did not have the c.G125A mutation. The exon 2 region surrounding codon 42, had a c.136G > A mutation that was present in all P. vivax infections. The odds ratio for lack of this mutation with P. vivax infections was (OR 0.015, 95% CI 0.001–0.176; p = 0.001). Conclusion: We conclude that P. vivax infections previously reported in Namibia, occurred in Duffy negative participants, carrying the G125A mutation in codon 42. The role of the additional mutation c.136 G > A in exon 2 in P. vivax infections, will require further investigations.

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author
; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Duffy gene mutations, Namibia, Plasmodium vivax
in
BMC Infectious Diseases
volume
21
issue
1
article number
856
publisher
BioMed Central (BMC)
external identifiers
  • scopus:85113201762
  • pmid:34418990
ISSN
1471-2334
DOI
10.1186/s12879-021-06573-y
language
English
LU publication?
yes
id
e83be6f5-9baa-4c76-a6a3-ec22b69b8b94
date added to LUP
2021-09-07 11:45:22
date last changed
2024-04-06 08:25:16
@article{e83be6f5-9baa-4c76-a6a3-ec22b69b8b94,
  abstract     = {{<p>Background: In a previous study, using a molecular approach, we reported the presence of P. vivax in Namibia. Here, we have extended our investigation to the Duffy antigen genetic profile of individuals of the same cohort with and without Plasmodium infections. Methods: Participants with P. vivax (n = 3), P. falciparum (n = 23) mono-infections and co-infections of P. vivax/P. falciparum (n = 4), and P. falciparum/P. ovale (n = 3) were selected from seven regions. Participants with similar age but without any Plasmodium infections (n = 47) were also selected from all the regions. Duffy allelic profile was examined using standard PCR followed by sequencing of amplified products. Sequenced samples were also examined for the presence or absence of G125A mutation in codon 42, exon 2. Results: All individuals tested carried the − 67 T &gt; C mutation. However, while all P. vivax infected participants carried the c.G125A mutation, 7/28 P. falciparum infected participants and 9/41 of uninfected participants did not have the c.G125A mutation. The exon 2 region surrounding codon 42, had a c.136G &gt; A mutation that was present in all P. vivax infections. The odds ratio for lack of this mutation with P. vivax infections was (OR 0.015, 95% CI 0.001–0.176; p = 0.001). Conclusion: We conclude that P. vivax infections previously reported in Namibia, occurred in Duffy negative participants, carrying the G125A mutation in codon 42. The role of the additional mutation c.136 G &gt; A in exon 2 in P. vivax infections, will require further investigations.</p>}},
  author       = {{Haiyambo, Daniel Hosea and Aleksenko, Larysa and Mumbengegwi, Davies and Bock, Ronnie and Uusiku, Petrina and Malleret, Benoit and Rénia, Laurent and Quaye, Isaac Kweku}},
  issn         = {{1471-2334}},
  keywords     = {{Duffy gene mutations; Namibia; Plasmodium vivax}},
  language     = {{eng}},
  number       = {{1}},
  publisher    = {{BioMed Central (BMC)}},
  series       = {{BMC Infectious Diseases}},
  title        = {{Children with Plasmodium vivax infection previously observed in Namibia, were Duffy negative and carried a c.136G > A mutation}},
  url          = {{http://dx.doi.org/10.1186/s12879-021-06573-y}},
  doi          = {{10.1186/s12879-021-06573-y}},
  volume       = {{21}},
  year         = {{2021}},
}