RHD*09.03.01 - RHD*DAR3.01
(ISBT table: RHD partial D v5.0)
This entry is an RHD allele.
DAR3.1, RHD(T201R,F223V), RHD(T201R,F223V,A273A), RHD*602C>G,667T>G,819G>A, RHD*602G,667G,819A, RHD*602G,667G,819A (weak D type 4.0, DAR3.01), weak D type 4.0,
Molecular data
Nucleotides:
602C>G; 667T>G; 819G>A;
Amino acids: T201R; F223V; A273A;
Hybrid allele encompassing at least one RHCE exon:
no
Comments on the molecular basis:
- additional intronic mutations detailed for one sample
- see also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype4.0.htm
- NGS
Extracellular position of one or more amino acid substitutions:
- none of the mutations are predicted to affect an extracellular amino acid
- membrane localization: TM and IC
Splicing:
Unconventional prediction methods:
Phenotype
Main D phenotype: weak D (last update: Dec. 28, 2020)Reports by D phenotype
- D positive (apparently normal D or undetailed positive D)
- See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype4.0.htm
- Undetailed ambiguous D phenotype
- See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype4.0.htm
- Discrepant D phenotype (negative or positive depending on anti-D reagents and techniques)
- See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype4.0.htm
- Weak D phenotype
- See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype4.0.htm
- D negative
- See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype4.0.htm
Other RH phenotypes: RH:-2, -3, -30,
Serology with monoclonal anti-D
- 0 monoclonal IgG anti-D non-reactive with variant, out of 60 monoclonal IgG anti 22 IgM anti-D tested
- 0 monoclonal IgG anti-D non-reactive with variant, tested with Diagast Dscreen kit
- tested with a panel of anti-D but results not detailed
- only a few anti-D tested
- 0 monoclonal IgG anti-D non-reactive with variant, out of 22 monoclonal IgG tested (Table 2)
- 0 monoclonal IgG anti-D non-reactive with variant, out of 23 monoclonal IgG anti-D tested; sample used as weak D control
- 1 monoclonal IgG anti-D non-reactive with variant, 12 monoclonal IgG anti-D tested, sample used as control (Table S2)
Antigen Density (Ag/RBC)
- 2288 Ag/RBC, derived from the results obtained with 59 of the 59 monoclonal IgG anti-D tested
- 1617 Ag/RBC, median for 1 sample with 11 IgG anti-D
- 1958 Ag/RBC, 1 sample used as control, with 12 anti-D (Table S1)
- 1689 Ag/RBC, with 6 monoclonal IgG anti-D; used as control
(data reproduced from
19309476 ) - 1624 Ag/RBC, 1 sample, 2 monoclonal anti-D
- 1862 Ag/RBC, 1 sample, 2 monoclonal anti-D
- 1970 Ag/RBC, 1 sample, 2 monoclonal anti-D
- 2554 Ag/RBC, 1 sample, 2 monoclonal anti-D
- range: 1687 - 2406, median: 1872 Ag/RBC, with 6 IgG anti-D; 7 RH:1,-2,-3,4,5 samples tested (table 3, listed as "weak D type 4", assumed RHef00313, considering the Ag density of RHef00315 clearly listed in Table 5)
- Ag/RBC, epitope density profile with 59 monoclonal IgG anti-D (Figure 1)
- mean: 3163 Ag/RBC, 5 samples; Ag density estimated from a measure with a single monoclonal IgG anti-D, compared to a RH:1,2,3,4,5 control sample with an antigen density assumed to be about 27.500 Ag/RBC
More phenotype data
Haplotype
Main CcEe phenotype association: ce (last update: Dec. 28, 2020)ce | Ce | cE | CE | |
---|---|---|---|---|
ce | 225 | 1 | 0 | 0 |
Ce | 0 | 1 | 0 | |
cE | 0 | 0 | ||
CE | 0 |
Reports by CcEe phenotype
- with ce 1 sample (1 sample used as control, may have been included in other studies) (sample heterozygous with RHef00301)
- with Ccee 1 sample (heterozygous with RHef00452) (not counted, but 3 samples could be RHef00442 associated with RHef00058 or, less likely, RHef00313 associated with RHef00056)
- with CcEe 1 sample (1 sample, heterozygous with RHef00059)
- with ccEe 0 samples (not counted, but 2 samples could be RHef00442 associated with RHef00058 or, less likely, RHef00313 associated with RHef00056)
10 samples
5 samples (haplotype given, not complete phenotype)
12 samples
11 samples
2 samples
0 samples (16 samples could be RHef00442 associated with RHef00058 or, less likely, RHef00313 associated with RHef00056) (no sample count possible) (haplotype given, not complete phenotype; presented as a general association) (Figure 2; presented as a general association, no sample count)
51 samples (haplotype given, not complete phenotype)
4 samples
47 samples
82 samples (haplotype listed, not complete phenotype)
Reports by allele association
- RHCE*ce105T,733G,744C,1025T
- RHCE*ceCF or RHCE*02
- RHCE*02 or RHCE*ce105T,733G,744C,1025T
- RHCE*01.20.01 (RHCE*733G)
- RHCE*01
- RHCE*ceTI
- RHCE*ce733G or RHCE*ce48C
- RHCE*ce48C,733G
- RHCE*ceAG
- RHCE*02 or RHCE*ce48,733,1006
- RHCE*ce733G or RHCE*ce48,733,1006
- RHCE*ceVS.02 or RHCE*ce.01
- RHCE*ceVS.02(900T) or RHCE*ce
- RHCE*ceVS.04 or RHCE*ce
- RHCE*ceVS.04 or RHCE*ceAG
- RHCE*DAR3.1(31T) or RHCE*ceCF
- RHCE*ceCF or RHCE*ce.16
- RHCE*ce.16
Alloimmunization
Antibodies in carriers
Antibody specificity: D (RH1)
Summary: maybe allo-anti-D? (last update: Dec. 28, 2020)Detailed information
-
Pham BN et al. Immunohematology (2013)
- Ab specificity: D (RH1)
- Number (auto- or allo-): 6
- Number listed as allo-: 1
- Number listed as auto-: 2
- Number of carriers of the allele assessed: 47
- DAT: 4 negative, 1 positive
- Autologuous control: 4 negative, 1 positive
- Elution: 3 negative, 1 positive (anti-D), 1 not tested
- Autoadsorption: 1 not autoadsorbable, 2 auto-adsorbable, 2 not tested
- Titer: ND
- Was anti-LW excluded?: ND
- Other antibodies detected: ND
- Cross matches (with Ab and RBCs from different partial types): ND
- Transfusion history: 2/9 potentially exposed through transfusion, including the patient with allo-anti-D
- Pregnancy history:
- Anti-D Ig history: ND
- Context: ND
- Hemolytic consequences: ND
- Comment: 9 anti-D in 47 individuals with this allele, 1 was allo-anti-D, 2 were auto-anti-D, 2 cases could not be concluded from the incomplete serologic data, 4 were not tested due to recent transfusion
-
Sandler SG et al. Transfusion (2015)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-: 1
- Number listed as auto-:
- Number of carriers of the allele assessed: 16
- DAT:
- Autologuous control:
- Elution:
- Autoadsorption:
- Titer:
- Was anti-LW excluded?:
- Other antibodies detected:
- Cross matches (with Ab and RBCs from different partial types):
- Transfusion history:
- Pregnancy history:
- Anti-D Ig history:
- Context:
- Hemolytic consequences:
- Comment:
-
Yu X et al. Transfusion (2006)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-:
- Number listed as auto-:
- Number of carriers of the allele assessed:
- DAT:
- Autologuous control:
- Elution:
- Autoadsorption:
- Titer:
- Was anti-LW excluded?:
- Other antibodies detected:
- Cross matches (with Ab and RBCs from different partial types):
- Transfusion history:
- Pregnancy history:
- Anti-D Ig history:
- Context:
- Hemolytic consequences:
- Comment: "D+ transfusion of RHef00313 and RHef00315 recipients must occur frequently, and anti-D immunizations in these phenotypes must be rare"
-
Dezan MR et al. Blood Cells Mol Dis (2017)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-: 1 sample, heterozygous with RHef00442 in trans
- Number listed as auto-:
- Number of carriers of the allele assessed:
- DAT: 46.2% of D+ patients with anti-D in this study had positive DAT (which patients are not specified)
- Autologuous control: ND
- Elution: ND
- Autoadsorption: ND
- Titer: ND
- Was anti-LW excluded?: ND
- Other antibodies detected: none
- Cross matches (with Ab and RBCs from different partial types): ND
- Transfusion history: yes, number and phenotypes ND
- Pregnancy history:
- Anti-D Ig history: ND, probably none
- Context: SCD patient
- Hemolytic consequences:
- Comment: 1 sample heterozygous with RHef00442, listed as probable allo-anti-D; authors underline that "self-directed anti-D may have been missed"
-
Ouchari M et al. Blood Transfus (2015)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-:
- Number listed as auto-:
- Number of carriers of the allele assessed:
- DAT:
- Autologuous control:
- Elution:
- Autoadsorption:
- Titer:
- Was anti-LW excluded?:
- Other antibodies detected:
- Cross matches (with Ab and RBCs from different partial types):
- Transfusion history:
- Pregnancy history:
- Anti-D Ig history:
- Context:
- Hemolytic consequences:
- Comment:
El Housse H et al. Blood Transfus (2019)
Westhoff CM et al. Blood Transfus (2019)
Flegel WA et al. Blood Transfus (2019)
Ouchari M et al. Transfusion (2018)
Ouchari M et al. Transfus Clin Biol (2014)
-
Sippert E et al. Blood Transfus (2015)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-: 4
- Number listed as auto-:
- Number of carriers of the allele assessed:
- DAT: ND
- Autologuous control: ND
- Elution: ND
- Autoadsorption: ND
- Titer: ND
- Was anti-LW excluded?: ND
- Other antibodies detected: ND
- Cross matches (with Ab and RBCs from different partial types): ND
- Transfusion history: yes, number and phenotypes ND
- Pregnancy history:
- Anti-D Ig history: ND, probably none
- Context: among 48 SCD patients with RH antibodies despite antigen-matched transfusion protocols
- Hemolytic consequences: none of the 13 patients with delayed hemolytic transfusion reactions or decreased survival of transfused RBCs had this allele
- Comment: study does not detail serology for each sample, but mentions performing DAT, autologuous control, eluate studies and adsorption on autologuous RBCs to aid the differenciation of autoantibodies and alloantibodies
-
Flegel WA et al. Curr Opin Hematol (2006)
(some samples overlap with other reports)
- Ab specificity: D (RH1)
- Number (auto- or allo-): 3
- Number listed as allo-:
- Number listed as auto-:
- Number of carriers of the allele assessed: 3
- DAT: ND
- Autologuous control: ND
- Elution: ND
- Autoadsorption: ND
- Titer: low-titer anti-D prevented the distinction between auto- and allo-anti-D
- Was anti-LW excluded?: ND
- Other antibodies detected: ND
- Cross matches (with Ab and RBCs from different partial types): ND
- Transfusion history: ND
- Pregnancy history:
- Anti-D Ig history: ND, probably none
- Context: ND
- Hemolytic consequences: ND
- Comment: "reports of the Rhesus Immunization Registery as of June 2006"
Wagner FF et al. Transfus Med Hemother (2014)
-
Chou ST et al. Blood (2013)
(Patient ID 214)
- Ab specificity: D (RH1)
- Number (auto- or allo-): 1 (patient heterozygous with RHef00008)
- Number listed as allo-:
- Number listed as auto-:
- Number of carriers of the allele assessed:
- DAT: ND
- Autologuous control: ND
- Elution: ND
- Autoadsorption: ND
- Titer: ND
- Was anti-LW excluded?: ND
- Other antibodies detected: anti-C
- Cross matches (with Ab and RBCs from different partial types): ND
- Transfusion history: 4 RBC exposures
- Pregnancy history:
- Anti-D Ig history: ND, probably none
- Context: SCD child
- Hemolytic consequences: unknown
- Comment:
-
Chou ST et al. Blood (2013)
(Patient ID 117)
- Ab specificity: D (RH1)
- Number (auto- or allo-): 1
- Number listed as allo-:
- Number listed as auto-:
- Number of carriers of the allele assessed:
- DAT: ND
- Autologuous control: ND
- Elution: ND
- Autoadsorption: ND
- Titer: ND
- Was anti-LW excluded?: ND
- Other antibodies detected: none
- Cross matches (with Ab and RBCs from different partial types): ND
- Transfusion history: 32 RBC exposures
- Pregnancy history:
- Anti-D Ig history: ND, probably none
- Context: SCD child
- Hemolytic consequences: none
- Comment: Anti-D not detectable after 2 months
Antibodies in D negative recipients
Alloimmunization in recipients: expected to be possible, see phenotype data
Reports
Summary: common allele, mainly in individuals of North African or African descent or compatible with such descent (last update: Dec. 28, 2020)Detailed reports
- 5/161 random donors with weak D phenotype; DVI samples were excluded by serologic testing in the German population (Southwestern Germany), White (Table 6)
- 1 sample "Caucasoid", reported by a German lab
- 5/500 500 donors with RH:1,–2,–3,4,5 phenotype among 1000 donors screened for RHD molecular variants by several PCR-SSP and exon 5 sequencing of all samples (500 R0r, 250 R1R, 250 R2r) in the German population (southwestern Germany)
- 1/700 among 1702 samples tested for the combined presence of RHD c.602G and c.667G (700 Dutch White, 310 South African Black, 319 South African Asians, 197 Curacao Black, 176 Ethiopian Black) Dutch (White)
- 2/167 (2 heterozygous with RHef00442; 1 more sample could be RHef00442 associated with RHef00058 or, less likely, RHef00313 associated with RHef00056) among 1702 samples tested for the combined presence of RHD c.602G and c.667G (700 Dutch White, 310 South African Black, 319 South African Asians, 197 Curacao Black, 176 Ethiopian Black) Ethiopian (Black)
- 1/197 (heterozygous with Rhef00442) among 1702 samples tested for the combined presence of RHD c.602G and c.667G (700 Dutch White, 310 South African Black, 319 South African Asians, 197 Curacao Black, 176 Ethiopian Black) Curacao (Black)
- 1/319 (heterozygous with Rhef00442) among 1702 samples tested for the combined presence of RHD c.602G and c.667G (700 Dutch White, 310 South African Black, 319 South African Asians, 197 Curacao Black, 176 Ethiopian Black) South African (Asian)
- 3/310 (1 heterozygous with RHef00452, 1 with RHef00020, 1 with RHef00442; 20 more samples could be RHef00442 associated with RHef00058 or, less likely, RHef00313 associated with RHef00056) among 1702 samples tested for the combined presence of RHD c.602G and c.667G (700 Dutch White, 310 South African Black, 319 South African Asians, 197 Curacao Black, 176 Ethiopian Black) South African (Black)
- 4/16 514 RH:1,-2,-3,4,5 random donor samples were tested for D antigen density, 16 were in the lower range of antigen density and were genotyped German
- 1/10 (heterozygous with RHef00442) individuals with D positive phenotype Bantu, subgroup Teke, Kukuya from villages around Djambala city
- 0 or 1/10 (1 sample could be RHef00008 heterozygous with RHef00317 or RHef00313 with RHef00056) individuals with D positive phenotype Bantu, subgroup Teke, Boma from villages in the north of Léfini river
- 1/141 donors and patients with ambiguous D phenotype in French population
- 1/11 pregnant women with ambiguous fetal genotyping in French population
- 2/26 (heterozygous: one with RHef00447, the other with RHef00059) donors with "weak D or questionnable D status" explored by NGS to compare with Sanger sequencing in the Austrian population, Upper Austria
- 2/26 (heterozygous, one with RHef00059, the other with RHef00301) donors with "weak D or questionnable D status" explored by NGS in the Austrian population, Upper Austria
- 9/43 (prevalence among weak D) or 9/5707 (phenotypic prevalence in population) 43 patients with weak D phenotype were genotyped in a cohort of 5707 patients from a private laboratory Argentinean
- 2/45 (prevalence among weak D phenotype) or 2/12672 (phenotypic prevalence in population) 45 patients with weak D phenotype were genotyped in a cohort of 12672 patients from a public hospital Argentinean
- 1/448 448 donors with D negative phenotype, tested for the presence of RHD exon 10 in the Tunisian population
- 11/50 (5 blood donors and 5 patients) 50 samples (33 donors and 17 patients) with discrepant or weak D phenotyping in the Egyptian population
- 22 alleles in 226 patients SCD children systematically genotyped in an alloimmunization study in the USA population (Philadelphia)
- 12/316 (2 homo- or hemizygous, 2 heterozygous with RHef00447, 1 with RHef00020, 1 with RHef00009, 6 with RHef00442) 316 (280 D positive and 36 D negative) donors were genotyped African descent (FY:-1,-2) in the French population
- 8/220 the cohort was composed of 164 Teke-Congolese (ethnic groups: 60 Akwa, 52 Mbochi, 52 Kuyu) from Congo, 19 Mandenka from Senegal, 25 Yoruba from Nigeria, 12 Bantu from Kenya Nonpygmoid Central African
- 8/127 the cohort was composed of 77 Tswa from Congo, 36 Biaka from Central African Republic, 14 Mbuti from Democratic Republic of the Congo Pygmoid Central African
- 47/748 among 748 individuals with D anomaly (weak or discrepant D phenotype or anti-D in individuals with D positive phenotype), 459 had D variants "that could be named weak D" (including alleles RHef00313, RHef00317 and RHef00318, as well as RHef00197 and RHef00283), 138 had partial D, 65 had no variant, 86 were not persued further (two variant alleles or incomplete or pending analysis) in the French population
- 81/360 (+1 heterozygous) donors with atypical D phenotype (discrepancies or reactivity weaker than 3+) Brazilian
- 4/48 (1 sample heterozygous with RHef00452) among 48 SCD patients with RH antibodies despite antigen-matched transfusion protocols African Brazilian
- 1/35 donors with D negative phenotype who underwent molecular analysis in the Tunisian population
- 2/67 (heterozygous with RHef00442) among 405 random donor samples used to evaluate RHD zygosity tests (35 typed D negative, 303 typed D positive, 67 of the latter had discordant results with different methods and were sequenced) in the Tunisian population
- 9/351 (+7 heterozygous: 6 for RHef00313 and RHef00319, 1 for RHef00288 and RHef00313) out of 351 prenatal patients with discrepant D phenotyping results (population tested 608486 patients) Canada
- 2/100 donors with weak D phenotype Australia
- 51/104 (prevalence among weak D) or 51/21353 (phenotypic prevalence in population) 104 with weak D phenotype were genotyped in a cohort of 21353 pregnant women admixed Brazilian
- 2/35 (heterozygous with RHef00442) SCD patients with unexplained RH antibodies, explored by NGS sequencing in the Brazilian population (Sao Paolo)
- 11/23 donors with weak D phenotype (among 4458 random donors, 4028 types D positive including 19 weak D phenotype, 420 typed D negative including 4 showed to be weak D by further serological testing; in total 23 donors had weak D phenotype) in the Maroccan population
- 12/231 231 donors with weak D phenotype in the Argentinean population (Northwestern Argentina)
- 34/273 (7 htz with RHef00605) donors with weak D phenotype in the Brazilian population
- 4/163 (including 3 heterozygous with RHef00452) selected variants included for the development of a genotyping assay mainly in the Dutch population (samples may have been included in other studies)
-
19/2000 4 homozygous and 15 heterozygous samples; among 2000 random donors (1777 typed D positive), all samples were genotyped for 602G and 667G, but only these 19 were fully sequenced to separate weak D type 4 subtypes in the Tunisian population
(study may overlap with
24014941 ) - 63/353 (including 1 heterozygous with RHef00022) samples referred for discrepant or weak D typing in the USA population
- 1/16,253 samples of pregnant women with D negative of weak D (2+ or less), screened for fetal RHD in the Finnish population
- 2 heterozygotes, 5 hemizygotes among 278 samples selected for the development of nonspecific quantitative next-generation sequencing. (non-random samples, may have been reported in other studies)
Allele or phenotype frequency
- 1/6024 (CI: 1/2695 - 1/15291) estimated population frequency among 1000 donors screened for RHD molecular variants by several PCR-SSP and exon 5 sequencing of all samples (500 R0r, 250 R1R, 250 R2r) in the German population (southwestern Germany)
- 0.006 estimated allele frequency from a study of 1702 samples tested for the combined presence of RHD c.602G and c.667G (700 Dutch White, 310 South African Black, 319 South African Asians, 197 Curacao Black, 176 Ethiopian Black) Ethiopian (Black)
- 0.005 estimated allele frequency from a study of 1702 samples tested for the combined presence of RHD c.602G and c.667G (700 Dutch White, 310 South African Black, 319 South African Asians, 197 Curacao Black, 176 Ethiopian Black) South African (Black)
- 0.0016 estimated allele frequency from a study of 1702 samples tested for the combined presence of RHD c.602G and c.667G (700 Dutch White, 310 South African Black, 319 South African Asians, 197 Curacao Black, 176 Ethiopian Black) Curacao (Black)
- 1/6060 (CI: 1/2525 - 1/17745) estimated allele frequency by testing random donor samples for D antigen density, those in the lower range of antigen density were genotyped German
- 0.00014 estimated prevalence in the German population
- 0.017 allele frequency among 480 African American donors African American (in the USA population)
- 0.025 allele frequency among 140 SCD patients African American (in the USA population)
- 0.024 allele frequency from molecular typing of 101 random samples Dogon Malian
- 0.0094 allele frequency in 106 donors with weak D phenotype Brazilian (mixed origin, mainly between African and European descent)
- 0.006 calculated in 16,253 samples of pregnant women with D negative of weak D (2+ or less), screened for fetal RHD in the Finnish population
Structure mapping
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References
- International Society of Blood Transfusion et al. International Society of Blood Transfusion (ISBT) allele table Online ressource, 1935. — Online ressource — [RHeference]
- Wagner FF et al. Molecular basis of weak D phenotypes. Blood, 1999. [Citation] [RHeference]
- Hemker MB et al. DAR, a new RhD variant involving exons 4, 5, and 7, often in linkage with ceAR, a new Rhce variant frequently found in African blacks. Blood, 1999. [Citation] [RHeference]
- Wagner FF et al. Weak D alleles express distinct phenotypes. Blood, 2000. [Citation] [RHeference]
- Singleton BK et al. The presence of an RHD pseudogene containing a 37 base pair duplication and a nonsense mutation in africans with the Rh D-negative blood group phenotype. Blood, 2000. [Citation] [RHeference]
- Müller TH et al. PCR screening for common weak D types shows different distributions in three Central European populations. Transfusion, 2001. [Citation] [RHeference]
- Wagner FF et al. The DAU allele cluster of the RHD gene. Blood, 2002. [Citation] [RHeference]
- Perco P et al. Testing for the D zygosity with three different methods revealed altered Rhesus boxes and a new weak D type. Transfusion, 2003. [Citation] [RHeference]
- Körmöczi GF et al. Novel weak D types 31 and 32: adsorption-elution-supported D antigen analysis and comparison to prevalent weak D types. Transfusion, 2005. [Citation] [RHeference]
- Chen Q et al. Random survey for RHD alleles among D+ European persons. Transfusion, 2005. [Citation] [RHeference]
- Yu X et al. Outliers in RhD membrane integration are explained by variant RH haplotypes. Transfusion, 2006. [Citation] [RHeference]
- Grootkerk-Tax MG et al. RHD(T201R, F223V) cluster analysis in five different ethnic groups and serologic characterization of a new Ethiopian variant DARE, the DIII type 6, and the RHD(F223V). Transfusion, 2006. [Citation] [RHeference]
- Flegel WA et al. How I manage donors and patients with a weak D phenotype. Curr Opin Hematol, 2006. [Citation] [RHeference]
- Flegel WA et al. D variants at the RhD vestibule in the weak D type 4 and Eurasian D clusters. Transfusion, 2009. [Citation] [RHeference]
- Touinssi M et al. Molecular analysis of inactive and active RHD alleles in native Congolese cohorts. Transfusion, 2009. [Citation] [RHeference]
- Wagner FF and Flegel WA et al. The Human RhesusBase Online ressource, 2011. — Online ressource — [RHeference]
- Silvy M et al. Weak D and DEL alleles detected by routine SNaPshot genotyping: identification of four novel RHD alleles. Transfusion, 2011. [Citation] [RHeference]
- Stabentheiner S et al. Overcoming methodical limits of standard RHD genotyping by next-generation sequencing. Vox Sang, 2011. [Citation] [RHeference]
- Brajovich ME et al. Comprehensive analysis of RHD alleles in Argentineans with variant D phenotypes. Transfusion, 2012. [Citation] [RHeference]
- Moussa H et al. Molecular background of D-negative phenotype in the Tunisian population. Transfus Med, 2012. [Citation] [RHeference]
- Granier T et al. A comprehensive survey of both RHD and RHCE allele frequencies in sub-Saharan Africa. Transfusion, 2013. [Citation] [RHeference]
- Pham BN et al. Molecular analysis of patients with weak D and serologic analysis of those with anti-D (excluding type 1 and type 2). Immunohematology, 2013. [Citation] [RHeference]
- Chou ST et al. High prevalence of red blood cell alloimmunization in sickle cell disease despite transfusion from Rh-matched minority donors. Blood, 2013. [Citation] [RHeference]
- Reid ME et al. The low-prevalence Rh antigen STEM (RH49) is encoded by two different RHCE*ce818T alleles that are often in cis to RHD*DOL. Transfusion, 2013. [Citation] [RHeference]
- O'Suoji C et al. Alloimmunization in sickle cell anemia in the era of extended red cell typing. Pediatr Blood Cancer, 2013. [Citation] [RHeference]
- von Zabern I et al. D category IV: a group of clinically relevant and phylogenetically diverse partial D. Transfusion, 2013. [Citation] [RHeference]
- Abdelrazik AM et al. Combining serology and molecular typing of weak D role in improving D typing strategy in Egypt. Transfusion, 2013. [Citation] [RHeference]
- Haer-Wigman L et al. RHD and RHCE variant and zygosity genotyping via multiplex ligation-dependent probe amplification. Transfusion, 2013. [Citation] [RHeference]
- Reid ME et al. Genomic analyses of RH alleles to improve transfusion therapy in patients with sickle cell disease. Blood Cells Mol Dis, 2014. [Citation] [RHeference]
- Wagner FF et al. The Rhesus Site. Transfus Med Hemother, 2014. [Citation] [RHeference]
- Arnoni CP et al. How do we identify RHD variants using a practical molecular approach? Transfusion, 2014. [Citation] [RHeference]
- Ouchari M et al. Anti-D auto-immunization in a patient with weak D type 4.0. Transfus Clin Biol, 2014. [Citation] [RHeference]
- Kappler-Gratias S et al. Systematic RH genotyping and variant identification in French donors of African origin. Blood Transfus, 2014. [Citation] [RHeference]
- Sippert E et al. Variant RH alleles and Rh immunisation in patients with sickle cell disease. Blood Transfus, 2015. [Citation] [RHeference]
- Kacem N et al. Paternal RHD zygosity determination in Tunisians: evaluation of three molecular tests. Blood Transfus, 2015. [Citation] [RHeference]
- Sandler SG et al. It's time to phase in RHD genotyping for patients with a serologic weak D phenotype. College of American Pathologists Transfusion Medicine Resource Committee Work Group. Transfusion, 2015. [Citation] [RHeference]
- Ouchari M et al. Weak D in the Tunisian population. Blood Transfus, 2015. [Citation] [RHeference]
- Ba A et al. RH diversity in Mali: characterization of a new haplotype RHD*DIVa/RHCE*ceTI(D2). Transfusion, 2015. [Citation] [RHeference]
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- Srivastava K et al. The DAU cluster: a comparative analysis of 18 RHD alleles, some forming partial D antigens. Transfusion, 2016. [Citation] [RHeference]
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Last update: Jan. 8, 2021