RHD*11 - RHD*weak partial 11
(ISBT table: RHD partial D v5.0)

This entry is an RHD allele.

RHD(M295I), RHD*885G>T, RHD*885T, RHD*885T (weak partial D type 11), partial weak D type 11, weak partial D type 11,
Download VCF file

Molecular data

Nucleotides: 885G>T;

Amino acids: M295I;

Hybrid allele encompassing at least one RHCE exon: no

Comments on the molecular basis:

  • see also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDRHD(M295I).htm
  • see also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype11.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

Splicing:

Unconventional prediction methods:

Phenotype

Main D phenotype: DEL (last update: Aug. 9, 2020)
Reports by D phenotype
  • Undetailed ambiguous D phenotype
    • Table S1
    • "weak D or questionnable D status"
    • "depressed D phenotype, discordant results between two anti-D reagents, or anti-D in individuals with a D+ phenotype"
  • See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDRHD(M295I).htm
  • See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype11.htm
  • Weak D phenotype with ce haplotype, DEL phenotype with Ce haplotype, which may be explained by suppressive effect of C in cis
  • 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/RHDRHD(M295I).htm
  • See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype11.htm
  • Weak D phenotype with ce haplotype, DEL phenotype with Ce haplotype, which may be explained by suppressive effect of C in cis
  • Weak D phenotype
    • study may overlap with 24679597
    • study may overlap with 24656493
    • ISBT classification with comments "Del phenotype when with Ce" and "weak partial or Del phenotype"
  • See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDRHD(M295I).htm
  • See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype11.htm
  • Weak D phenotype with ce haplotype, DEL phenotype with Ce haplotype, which may be explained by suppressive effect of C in cis
  • Very weak D phenotype
  • See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDRHD(M295I).htm
  • See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype11.htm
  • Weak D phenotype with ce haplotype, DEL phenotype with Ce haplotype, which may be explained by suppressive effect of C in cis
  • DEL
    • adsorption-elution was performed
    • study may overlap with 24679597
    • adsorption-elution was performed
    • initially typed as D negative, adsorption-elution was performed but results not clear
    • adsorption-elution was performed; authors evoke suppressive effect of C in trans
    • ISBT classification with comment "Del phenotype when with Ce"; "weak partial or Del phenotype"
    • adsorption-elution was performed; overlaps with 999999913
    • adsorption-elution was performed; overlaps with 999999988
    • adsorption-elution was performed on at least one sample
    • adsorption-elution was performed; 1 sample negative, 9 DEL
    • adsorption-elution was performed
  • See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDRHD(M295I).htm
  • See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype11.htm
  • Weak D phenotype with ce haplotype, DEL phenotype with Ce haplotype, which may be explained by suppressive effect of C in cis
  • D negative
    • adsorption-elution was not performed
    • study may overlap with 24679597; initially typed as D negative
    • study may overlap with 24656493; adsorption-elution was not performed
    • adsorption-elution was not performed
    • adsorption-elution was not performed
    • adsorption-elution was not performed
    • adsorption-elution not specified
    • adsorption-elution was performed; 1 sample negative, 9 DEL
    • adsorption-elution was not performed
    • adsorption-elution was not performed
    • adsorption-elution was performed, results not detailed
    • article states that adsorption-elution was performed, but for which samples it was done for is not clear
  • See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDRHD(M295I).htm
  • See also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDweakDtype11.htm
  • Weak D phenotype with ce haplotype, DEL phenotype with Ce haplotype, which may be explained by suppressive effect of C in cis
Other RH phenotypes: RH:-2, -3, -4,
  • RH:-2 inferred from the reported RHCE phenotypes of the carriers
  • RH:-3 inferred from the reported RHCE phenotypes of the carriers
  • RH:-4 inferred from the reported RHCE phenotypes of the carriers
Serology with monoclonal anti-D
  • epitope pattern by adsorption-elution, all anti-D tested could be eluted
  • tested with a panel of anti-D but results not detailed
  • 21 anti-D tested, results not detailed
  • tested with Diagast Dscreen kit
  • 7 monoclonal IgG anti-D non-reactive with variant, out of 60 monoclonal IgG anti 22 IgM anti-D tested
  • negative reactions, with a panel of 10 monoclonal anti-D
Antigen Density (Ag/RBC)
  • 38 Ag/RBC, 1 sample
  • 66 Ag/RBC, mean antigen density compared to a standard with 10,250 Ag/RBC
  • 183 Ag/RBC, derived from the results obtained with 59 of the 59 monoclonal IgG anti-D tested
  • 57 Ag/RBC, 1 R1r sample
  • 33 Ag/RBC, 1 sample
  • 29 Ag/RBC, 1 sample
  • 34 Ag/RBC, 1 sample
  • 36 Ag/RBC, 1 sample
  • <22 Ag/RBC, 1 sample
  • mean: 223 Ag/RBC, 4 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
Rhesus Similarity Index

  • 0.53 (derived from the results obtained with 59 of the 59 monoclonal IgG anti-D tested)

Haplotype

Main CcEe phenotype association: Ce is the most frequent association, ce is less frequent (last update: Jan. 8, 2021)
Number of samples reported by haplotype
ce Ce cE CE
ce 1 82 2 0
Ce 15 1 0
cE 0 0
CE 0
Reports by CcEe phenotype
  • with Ce
    • 1 sample
    14 samples (haplotype given, not patient phenotypes)
    0 samples (haplotype listed, not complete phenotype; presented as a general association) (see also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDRHD(M295I).htm)
  • with Ccee
    • 1 sample (considering RHCE genotyping, RHD zygosity and RHD allele, R1 was considered the most likely haplotype)
    8 samples
    6 samples
    9 samples (study may overlap with 24679597)
    12 samples (study may overlap with 24656493)
    7 samples
    10 samples
    5 samples
    2 samples
    18 samples
    4 samples
  • with ccEe
    • 2 samples
  • with ce
    • 1 sample (1 heterozygous sample, probably with RHef00442)
    0 samples (haplotype listed, not complete phenotype; presented as a general association) (see also "Additional comments" section on the RhesusBase http://www.rhesusbase.info/RHDRHD(M295I).htm)
  • with CcEe
    • 1 sample
Main allele association: RHCE*02
Reports by allele association
  • RHCE*02 or RHCE*01
    • 1 sample

Alloimmunization

Antibodies in carriers
Antibody specificity: D (RH1)
Summary: probably allo-anti-D (last update: Aug. 9, 2020)
Detailed information
    Flegel WA et al. Curr Opin Hematol (2006) (some samples overlap with other reports)
    von Zabern I et al. Transfusion (2013)
    Wagner FF et al. Transfus Med Hemother (2014) (RIR n°64)
  • Ab specificity: D (RH1)
  • Number (auto- or allo-):
  • Number listed as allo-: 1
  • Number listed as auto-:
  • Number of carriers of the allele assessed: 1
  • DAT: ND
  • Autologuous control: ND
  • Elution: ND
  • Autoadsorption: ND
  • Titer: ND
  • Was anti-LW excluded?: yes
  • 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"
    Pham BN et al. Immunohematology (2013)
  • Ab specificity: D (RH1)
  • Number (auto- or allo-): 0
  • Number listed as allo-:
  • Number listed as auto-: 1
  • Number of carriers of the allele assessed: 18
  • DAT: negative
  • Autologuous control: negative
  • Elution: negative
  • Autoadsorption: anti-D was auto-adsorbed
  • Titer: ND
  • 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
  • Context: ND
  • Hemolytic consequences: ND
  • Comment:
    Daniels G et al. Br J Haematol (2013) (review; Table I)
  • Ab specificity: D (RH1)
  • Number (auto- or allo-):
  • Number listed as allo-: no new case detailed (listed as allo-anti-D)
  • Number listed as auto-: NA
  • Number of carriers of the allele assessed: NA
  • DAT: NA
  • Autologuous control: NA
  • Elution: NA
  • Autoadsorption: NA
  • Titer: NA
  • Was anti-LW excluded?: NA
  • Other antibodies detected: NA
  • Cross matches (with Ab and RBCs from different partial types): NA
  • Transfusion history: NA
  • Pregnancy history:
  • Anti-D Ig history: NA
  • Context: NA
  • Hemolytic consequences: NA
  • Comment: list of D variants associated with alloanti-D formation
Antibodies in D negative recipients

Alloimmunization in recipients: expected to be possible, see detailed reports and phenotype data

    Gassner C et al. Transfusion (2005)
  • Ab specificity: D (RH1)
  • Number of cases:
  • Exposures: transfusion, allele carried by the donor
  • Imputability:
  • Comment: contains data regarding the transfusion of units from such donors to D negative recipients

Reports

Summary: common allele, mainly described in predominantly Caucasian populations or compatible with such descent (last update: Dec. 14, 2020)
Detailed reports
  • 1/161 random donors with weak D phenotype; DVI samples were excluded by serologic testing in the German population (Southwestern Germany), White (Table 6)
  • 0/146 donors with weak D phenotype White, in the Austrian (Tyrol) population
  • 0/270 donors with weak D phenotype White, in the German (Northern Germany) population
  • 7/8442 8442 donors with D negative phenotype, screened for presence of the RHD gene in two surveys; 754 donors were C and/or E positive, the rest were ccee phenotype; 5 donors were revealed to be weakly D positive in the German population (Baden-Wurttemberg)
  • 1/168 among 168 samples referred for weak D phenotype and/or allo anti-D in D positive individuals, 137 were characterized in the study (70 by serology, 67 by molecular analysis, 31 could not be typed because serologic typing was inconclusive and molecular typing could not be performed) in the French population (Caucasian)
  • 5/738 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the Austrian (state of Tyrol) population
  • 0/104 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the Swiss (Bern and the canton of Bern) population
  • 1/400 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the German (states of Lower Saxony, Saxony- Anhalt, Thuringia, Oldenburg, and Bremen) population
  • 0/71 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the Russian (Kirov Oblast) population
  • 1/333 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the Slovenian population
  • 1/54 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the German (city of Braunschweig and eastern parts of Lower Saxony) population
  • 1/500 500 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)
  • 0/250 250 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)
  • 6 samples Austrian Caucasian
  • 2/45 45 samples referred for D typing discrepancies in the USA population (Table 2)
  • 7/289 289 samples with ambiguous D phenotype (333 consecutive samples with ambiguous D phenotype studied but 44 were hybrid alleles, excluded from the study) in the French (Western France) population
  • 1/1113 pregnant D negative women tested for fetal non invasive genotyping, RHD exons 5 and 7 in the German population
  • 2/23330 donor samples with D negative phenotype tested for RHD exons 4, 7 and 10 (94 were PCR positive, 74 weak D or DEL in subsequent serologic analysis) in the Austrian population, Upper Austria
  • 14/96 among almost 3 million blood donations, 621685 had D negative phenotype; 46133 donors were first time donors with D negative phenotype and, when tested, 96 had RHD intron 4 in the German population
  • 0/279 DEL (or /400253 all phenotypes) among 400253 random donors, 1585 with apparent D negative phenotype, but among those, 279 were DEL in the Chinese (Shanghai) population
  • 10/141 donors and patients with ambiguous D phenotype (and 1 heterozyguous RHef00288 / RHef00197 sample) in French population
  • 2/11 pregnant women with ambiguous fetal genotyping in French population
  • 1/25 donors with "weak D or questionnable D status" explored by NGS to compare with Sanger sequencing in the Austrian population, Upper Austria
  • 5/167 discrepant D testing results (donors?) Croatian
  • 2/448 448 donors with D negative phenotype, tested for the presence of RHD exon 10 in the Tunisian population
  • 5/163 selected variants included for the development of a genotyping assay mainly in the Dutch population (samples may have been included in other studies)
  • 6/430 (1 heterozygous) among samples with ambigous D phenotype in the French population (Table S1)
  • 7/31200 consecutive donors with D negative phenotype, tested for presence of RHD intron 4, exon 7 and/or exon 10 in the Polish population
  • 18/748 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 RHef00317, 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
  • 1/520 among 520 donors with apparent D negative phenotype, C and/or E positive in the Brazilian population (Sao Paulo)
  • 9/26243 donors with D negative phenotype in three studies with different inclusion criteria in the Swiss population (Zurich and Berne) (study may overlap with 24679597)
  • 12/25370 donors with D negative phenotype, screened for RHD exons 3 or 7, plus 5 and 10 in the Swiss population (study may overlap with 24656493)
  • 10/2027 2027 donors with D positive, C and/or E positive phenotype, screened for RHD exons 4, 5 and 10 and for DEL phenotype in the Australian population
  • 1/2000 (heterozygous) random donors (1777 with D positive phenotype), all donors genotyped for RHD c.885T in the Tunisian population (study may overlap with 24014941)
  • 1/627 weak D typing (95% from patients, 5% from donors; 21,2% were identified as RHef00442 or RHef00446 by authors, "mostly (…) inconclusive serology consequent to recent transfusion") in the Belgian (Flanders) population
  • 9/37782 270 women with variant alleles among 37782 women with D negative phenotype, tested by quantitative fetal RHD genotyping designed to detect RHD exons 5 and 7 in the Dutch population
  • 1/100 donors with weak D phenotype Australia
  • 2/1174 donors with D negative phenotype United States population (Los Angeles)
  • 4/92 donors with apparent D negative phenotype, C and/or E positive Bosnia Herzegovina
  • 2/61 donors with apparent D negative phenotype, C and/or E positive Serbia
  • 5/64 among 175000 donors, 64 had weak D phenotype and underwent molecular identification in the Greek population
  • 7/273 donors with weak D phenotype in the Brazilian population
  • 12/18537 18537 donors with D negative phenotype were tested for the presence of RHD DNA sequences, 154 samples were positive for one or several RHD exons in the Swiss population
  • 1/75 RH:–1,–4 or RH:–1,–5 donors reported by a French lab
  • 2/310 donors with D negative phenotype, C and/or E positive in the Italian population
  • 3/274 donor with D negative phenotype Spanish
  • 1/4000 repeat donors with D negative phenotype genotyped for RHD, of which 13 had an RHD allele in Canadian (Quebec) population
  • 47/136000 among about 136.000 donors with D negative phenotype, systematically tested for the presence of the RHD gene; the RHD gene was detected in 300 donors in the German population (some samples may overlap with other studies)
  • 26 / 46,756 first time donors with D negative phenotype, tested for RHD exon 7 and adsorption-elution with a polyclonal anti-D in the German population (Northern) (overlaps with 999999913; some samples may overlap with full publications) (overlaps with 999999988; some samples may overlap with full publications)
  • 1/16,253 samples of pregnant women with D negative of weak D (2+ or less), screened for fetal RHD in the Finnish population
  • 4/6523 D negative donors underwent molecular screening for RHD exons 7 and 10 (RHD sequences were detected in 23/6523) in the Croatian population
  • 1 hemizygote 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
  • 1/90909 estimated allele frequency in the German population (Southwestern Germany), White
  • 1/6493 (CI: 1/3302 - 1/13827) estimated allele frequency by testing 8442 donors with D negative phenotype, screened for presence of the RHD gene in two surveys; 754 donors were C and/or E positive, the rest were ccee phenotype; 5 donors were revealed to be weakly D positive in the German population (Baden-Wurttemberg)
  • 1/14449 (CI: 1/2715 - 1/283297) estimated allele frequency in samples with D negative phenotype but C and/or E positive, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the German (states of Lower Saxony, Saxony- Anhalt, Thuringia, Oldenburg, and Bremen) population
  • 1/3710 (CI: 1/1660 - 1/9415) estimated allele frequency in samples with D negative phenotype but C and/or E positive, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the Austrian (state of Tyrol) population
  • 1/7641 (CI: 1/1436 - 1/149823) estimated allele frequency in samples with D negative phenotype but C and/or E positive, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the Slovenian population
  • 1/30120 (CI: 1/5658 - 1/590597) 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)
  • > 0.0009% estimated prevalence with the R1 (DCe) haplotype in the German population
  • 9e-06 estimated prevalence with the R0 (Dce) haplotype in the German population
  • 1/11665 (CI: 1/3704 - 1/66667) estimated allele frequency in individuals with D negative phenotype in the Austrian population, Upper Austria
  • 1/4457 (CI: 1/2373 - 1/9497) estimated allele frequency in individuals with D negative phenotype in the Polish population
  • 0.038 allele frequency in 106 donors with weakened D phenotype Brazilian (mixed origin, mainly between African and European descent)
  • 1/587 (CI: 1/4632 - 1/155) estimated allele frequency in donors with D negative phenotype United States population (Los Angeles)
  • 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
  • 1/160 calculated allele frequency among donors with D negative and C and/or E positive phenotype in the Croatian population
  • 1/1630 calculated allele frequency among donors with D negative phenotype in the Croatian population

2D diagram

generated using Protter extraintra Met1 Met1 Ser2 Ser2 Ser3 Ser3 Lys4 Lys4 Tyr5 Tyr5 Pro6 Pro6 Arg7 Arg7 Ser8 Ser8 Val9 Val9 Arg10 Arg10 10Arg11 Arg11 Cys12 Cys12 Leu13 Leu13 Pro14 Pro14 Leu15 Leu15 Trp16 Trp16 Ala17 Ala17 Leu18 Leu18 Thr19 Thr19 Leu20 Leu20 20Glu21 Glu21 Ala22 Ala22 Ala23 Ala23 Leu24 Leu24 Ile25 Ile25 Leu26 Leu26 Leu27 Leu27 Phe28 Phe28 Tyr29 Tyr29 Phe30 Phe30 30Phe31 Phe31 Thr32 Thr32 His33 His33 Tyr34 Tyr34 Asp35 Asp35 Ala36 Ala36 Ser37 Ser37 Leu38 Leu38 Glu39 Glu39 Asp40 Asp40 40Gln41 Gln41 Lys42 Lys42 Gly43 Gly43 Leu44 Leu44 Val45 Val45 Ala46 Ala46 Ser47 Ser47 Tyr48 Tyr48 Gln49 Gln49 Val50 Val50 50Gly51 Gly51 Gln52 Gln52 Asp53 Asp53 Leu54 Leu54 Thr55 Thr55 Val56 Val56 Met57 Met57 Ala58 Ala58 Ala59 Ala59 Ile60 Ile60 60Gly61 Gly61 Leu62 Leu62 Gly63 Gly63 Phe64 Phe64 Leu65 Leu65 Thr66 Thr66 Ser67 Ser67 Ser68 Ser68 Phe69 Phe69 Arg70 Arg70 70Arg71 Arg71 His72 His72 Ser73 Ser73 Trp74 Trp74 Ser75 Ser75 Ser76 Ser76 Val77 Val77 Ala78 Ala78 Phe79 Phe79 Asn80 Asn80 80Leu81 Leu81 Phe82 Phe82 Met83 Met83 Leu84 Leu84 Ala85 Ala85 Leu86 Leu86 Gly87 Gly87 Val88 Val88 Gln89 Gln89 Trp90 Trp90 90Ala91 Ala91 Ile92 Ile92 Leu93 Leu93 Leu94 Leu94 Asp95 Asp95 Gly96 Gly96 Phe97 Phe97 Leu98 Leu98 Ser99 Ser99 Gln100 Gln100 100Phe101 Phe101 Pro102 Pro102 Ser103 Ser103 Gly104 Gly104 Lys105 Lys105 Val106 Val106 Val107 Val107 Ile108 Ile108 Thr109 Thr109 Leu110 Leu110 110Phe111 Phe111 Ser112 Ser112 Ile113 Ile113 Arg114 Arg114 Leu115 Leu115 Ala116 Ala116 Thr117 Thr117 Met118 Met118 Ser119 Ser119 Ala120 Ala120 120Leu121 Leu121 Ser122 Ser122 Val123 Val123 Leu124 Leu124 Ile125 Ile125 Ser126 Ser126 Val127 Val127 Asp128 Asp128 Ala129 Ala129 Val130 Val130 130Leu131 Leu131 Gly132 Gly132 Lys133 Lys133 Val134 Val134 Asn135 Asn135 Leu136 Leu136 Ala137 Ala137 Gln138 Gln138 Leu139 Leu139 Val140 Val140 140Val141 Val141 Met142 Met142 Val143 Val143 Leu144 Leu144 Val145 Val145 Glu146 Glu146 Val147 Val147 Thr148 Thr148 Ala149 Ala149 Leu150 Leu150 150Gly151 Gly151 Asn152 Asn152 Leu153 Leu153 Arg154 Arg154 Met155 Met155 Val156 Val156 Ile157 Ile157 Ser158 Ser158 Asn159 Asn159 Ile160 Ile160 160Phe161 Phe161 Asn162 Asn162 Thr163 Thr163 Asp164 Asp164 Tyr165 Tyr165 His166 His166 Met167 Met167 Asn168 Asn168 Met169 Met169 Met170 Met170 170His171 His171 Ile172 Ile172 Tyr173 Tyr173 Val174 Val174 Phe175 Phe175 Ala176 Ala176 Ala177 Ala177 Tyr178 Tyr178 Phe179 Phe179 Gly180 Gly180 180Leu181 Leu181 Ser182 Ser182 Val183 Val183 Ala184 Ala184 Trp185 Trp185 Cys186 Cys186 Leu187 Leu187 Pro188 Pro188 Lys189 Lys189 Pro190 Pro190 190Leu191 Leu191 Pro192 Pro192 Glu193 Glu193 Gly194 Gly194 Thr195 Thr195 Glu196 Glu196 Asp197 Asp197 Lys198 Lys198 Asp199 Asp199 Gln200 Gln200 200Thr201 Thr201 Ala202 Ala202 Thr203 Thr203 Ile204 Ile204 Pro205 Pro205 Ser206 Ser206 Leu207 Leu207 Ser208 Ser208 Ala209 Ala209 Met210 Met210 210Leu211 Leu211 Gly212 Gly212 Ala213 Ala213 Leu214 Leu214 Phe215 Phe215 Leu216 Leu216 Trp217 Trp217 Met218 Met218 Phe219 Phe219 Trp220 Trp220 220Pro221 Pro221 Ser222 Ser222 Phe223 Phe223 Asn224 Asn224 Ser225 Ser225 Ala226 Ala226 Leu227 Leu227 Leu228 Leu228 Arg229 Arg229 Ser230 Ser230 230Pro231 Pro231 Ile232 Ile232 Glu233 Glu233 Arg234 Arg234 Lys235 Lys235 Asn236 Asn236 Ala237 Ala237 Val238 Val238 Phe239 Phe239 Asn240 Asn240 240Thr241 Thr241 Tyr242 Tyr242 Tyr243 Tyr243 Ala244 Ala244 Val245 Val245 Ala246 Ala246 Val247 Val247 Ser248 Ser248 Val249 Val249 Val250 Val250 250Thr251 Thr251 Ala252 Ala252 Ile253 Ile253 Ser254 Ser254 Gly255 Gly255 Ser256 Ser256 Ser257 Ser257 Leu258 Leu258 Ala259 Ala259 His260 His260 260Pro261 Pro261 Gln262 Gln262 Gly263 Gly263 Lys264 Lys264 Ile265 Ile265 Ser266 Ser266 Lys267 Lys267 Thr268 Thr268 Tyr269 Tyr269 Val270 Val270 270His271 His271 Ser272 Ser272 Ala273 Ala273 Val274 Val274 Leu275 Leu275 Ala276 Ala276 Gly277 Gly277 Gly278 Gly278 Val279 Val279 Ala280 Ala280 280Val281 Val281 Gly282 Gly282 Thr283 Thr283 Ser284 Ser284 Cys285 Cys285 His286 His286 Leu287 Leu287 Ile288 Ile288 Pro289 Pro289 Ser290 Ser290 290Pro291 Pro291 Trp292 Trp292 Leu293 Leu293 Ala294 Ala294 Met295 Met295 Val296 Val296 Leu297 Leu297 Gly298 Gly298 Leu299 Leu299 Val300 Val300 300Ala301 Ala301 Gly302 Gly302 Leu303 Leu303 Ile304 Ile304 Ser305 Ser305 Val306 Val306 Gly307 Gly307 Gly308 Gly308 Ala309 Ala309 Lys310 Lys310 310Tyr311 Tyr311 Leu312 Leu312 Pro313 Pro313 Gly314 Gly314 Cys315 Cys315 Cys316 Cys316 Asn317 Asn317 Arg318 Arg318 Val319 Val319 Leu320 Leu320 320Gly321 Gly321 Ile322 Ile322 Pro323 Pro323 His324 His324 Ser325 Ser325 Ser326 Ser326 Ile327 Ile327 Met328 Met328 Gly329 Gly329 Tyr330 Tyr330 330Asn331 Asn331 Phe332 Phe332 Ser333 Ser333 Leu334 Leu334 Leu335 Leu335 Gly336 Gly336 Leu337 Leu337 Leu338 Leu338 Gly339 Gly339 Glu340 Glu340 340Ile341 Ile341 Ile342 Ile342 Tyr343 Tyr343 Ile344 Ile344 Val345 Val345 Leu346 Leu346 Leu347 Leu347 Val348 Val348 Leu349 Leu349 Asp350 Asp350 350Thr351 Thr351 Val352 Val352 Gly353 Gly353 Ala354 Ala354 Gly355 Gly355 Asn356 Asn356 Gly357 Gly357 Met358 Met358 Ile359 Ile359 Gly360 Gly360 360Phe361 Phe361 Gln362 Gln362 Val363 Val363 Leu364 Leu364 Leu365 Leu365 Ser366 Ser366 Ile367 Ile367 Gly368 Gly368 Glu369 Glu369 Leu370 Leu370 370Ser371 Ser371 Leu372 Leu372 Ala373 Ala373 Ile374 Ile374 Val375 Val375 Ile376 Ile376 Ala377 Ala377 Leu378 Leu378 Met379 Met379 Ser380 Ser380 380Gly381 Gly381 Leu382 Leu382 Leu383 Leu383 Thr384 Thr384 Gly385 Gly385 Leu386 Leu386 Leu387 Leu387 Leu388 Leu388 Asn389 Asn389 Leu390 Leu390 390Lys391 Lys391 Ile392 Ile392 Trp393 Trp393 Lys394 Lys394 Ala395 Ala395 Pro396 Pro396 His397 His397 Glu398 Glu398 Ala399 Ala399 Lys400 Lys400 400Tyr401 Tyr401 Phe402 Phe402 Asp403 Asp403 Asp404 Asp404 Gln405 Gln405 Val406 Val406 Phe407 Phe407 Trp408 Trp408 Lys409 Lys409 Phe410 Phe410 410Pro411 Pro411 His412 His412 Leu413 Leu413 Ala414 Ala414 Val415 Val415 Gly416 Gly416 Phe417 Phe417 417 MSSKYPRSVRRCLPLWALTLEAALILLFYFFTHYDASLEDQKGLVASYQVGQDLTVMAAIGLGFLTSSFRRHSWSSVAFNLFMLALGVQWAILLDGFLSQFPSGKVVITLFSIRLATMSALSVLISVDAVLGKVNLAQLVVMVLVEVTALGNLRMVISNIFNTDYHMNMMHIYVFAAYFGLSVAWCLPKPLPEGTEDKDQTATIPSLSAMLGALFLWMFWPSFNSALLRSPIERKNAVFNTYYAVAVSVVTAISGSSLAHPQGKISKTYVHSAVLAGGVAVGTSCHLIPSPWLAMVLGLVAGLISVGGAKYLPGCCNRVLGIPHSSIMGYNFSLLGLLGEIIYIVLLVLDTVGAGNGMIGFQVLLSIGELSLAIVIALMSGLLTGLLLNLKIWKAPHEAKYFDDQVFWKFPHLAVGF MSSKYPRSVRRCLPLWALTLEAALILLFYFFTHYDASLEDQKGLVASYQVGQDLTVMAAIGLGFLTSSFRRHSWSSVAFNLFMLALGVQWAILLDGFLSQFPSGKVVITLFSIRLATMSALSVLISVDAVLGKVNLAQLVVMVLVEVTALGNLRMVISNIFNTDYHMNMMHIYVFAAYFGLSVAWCLPKPLPEGTEDKDQTATIPSLSAMLGALFLWMFWPSFNSALLRSPIERKNAVFNTYYAVAVSVVTAISGSSLAHPQGKISKTYVHSAVLAGGVAVGTSCHLIPSPWLAMVLGLVAGLISVGGAKYLPGCCNRVLGIPHSSIMGYNFSLLGLLGEIIYIVLLVLDTVGAGNGMIGFQVLLSIGELSLAIVIALMSGLLTGLLLNLKIWKAPHEAKYFDDQVFWKFPHLAVGF MSSKYPRSVRRCLPLWALTLEAALILLFYFFTHYDASLEDQKGLVASYQVGQDLTVMAAIGLGFLTSSFRRHSWSSVAFNLFMLALGVQWAILLDGFLSQFPSGKVVITLFSIRLATMSALSVLISVDAVLGKVNLAQLVVMVLVEVTALGNLRMVISNIFNTDYHMNMMHIYVFAAYFGLSVAWCLPKPLPEGTEDKDQTATIPSLSAMLGALFLWMFWPSFNSALLRSPIERKNAVFNTYYAVAVSVVTAISGSSLAHPQGKISKTYVHSAVLAGGVAVGTSCHLIPSPWLAMVLGLVAGLISVGGAKYLPGCCNRVLGIPHSSIMGYNFSLLGLLGEIIYIVLLVLDTVGAGNGMIGFQVLLSIGELSLAIVIALMSGLLTGLLLNLKIWKAPHEAKYFDDQVFWKFPHLAVGF MSSKYPRSVRRCLPLWALTLEAALILLFYFFTHYDASLEDQKGLVASYQVGQDLTVMAAIGLGFLTSSFRRHSWSSVAFNLFMLALGVQWAILLDGFLSQFPSGKVVITLFSIRLATMSALSVLISVDAVLGKVNLAQLVVMVLVEVTALGNLRMVISNIFNTDYHMNMMHIYVFAAYFGLSVAWCLPKPLPEGTEDKDQTATIPSLSAMLGALFLWMFWPSFNSALLRSPIERKNAVFNTYYAVAVSVVTAISGSSLAHPQGKISKTYVHSAVLAGGVAVGTSCHLIPSPWLAMVLGLVAGLISVGGAKYLPGCCNRVLGIPHSSIMGYNFSLLGLLGEIIYIVLLVLDTVGAGNGMIGFQVLLSIGELSLAIVIALMSGLLTGLLLNLKIWKAPHEAKYFDDQVFWKFPHLAVGF

Structure mapping

Movement    Mouse Input    Touch Input
RotationPrimary Mouse ButtonSingle touch
TranslationMiddle Mouse Button or Ctrl+PrimaryTriple touch
ZoomScroll Wheel or Second Mouse Button or Shift+PrimaryPinch (double touch)
SlabCtrl+SecondNot Available

Links

The Human RhesusBase The Human RhesusBase
Genbank:
Erythrogene

References

  1. International Society of Blood Transfusion et al. International Society of Blood Transfusion (ISBT) allele table Online ressource, 1935. — Online ressource — [RHeference]
  2. Wagner FF et al. Molecular basis of weak D phenotypes. Blood, 1999. [Citation] [RHeference]
  3. Wagner FF et al. Weak D alleles express distinct phenotypes. Blood, 2000. [Citation] [RHeference]
  4. Wagner FF et al. RHD positive haplotypes in D negative Europeans. BMC Genet, 2001. [Citation] [RHeference]
  5. Müller TH et al. PCR screening for common weak D types shows different distributions in three Central European populations. Transfusion, 2001. [Citation] [RHeference]
  6. Ansart-Pirenne H et al. RhD variants in Caucasians: consequences for checking clinically relevant alleles. Transfusion, 2004. [Citation] [RHeference]
  7. Gassner C et al. Presence of RHD in serologically D-, C/E+ individuals: a European multicenter study. Transfusion, 2005. [Citation] [RHeference]
  8. Chen Q et al. Random survey for RHD alleles among D+ European persons. Transfusion, 2005. [Citation] [RHeference]
  9. Körmöczi GF et al. A comprehensive analysis of DEL types: partial DEL individuals are prone to anti-D alloimmunization. Transfusion, 2005. [Citation] [RHeference]
  10. Flegel WA et al. How I manage donors and patients with a weak D phenotype. Curr Opin Hematol, 2006. [Citation] [RHeference]
  11. Westhoff CM et al. Rh complexities: serology and DNA genotyping. Transfusion, 2007. [Citation] [RHeference]
  12. Le Maréchal C et al. Identification of 12 novel RHD alleles in western France by denaturing high-performance liquid chromatography analysis. Transfusion, 2007. [Citation] [RHeference]
  13. Nogues N et al. RHD null alleles in the Spanish population Vox Sanguinis, 2007. — Abstract — [RHeference]
  14. Müller SP et al. The determination of the fetal D status from maternal plasma for decision making on Rh prophylaxis is feasible. Transfusion, 2008. [Citation] [RHeference]
  15. Polin H et al. Identification of RHD alleles with the potential of anti-D immunization among seemingly D- blood donors in Upper Austria. Transfusion, 2009. [Citation] [RHeference]
  16. Flegel WA et al. Six years' experience performing RHD genotyping to confirm D- red blood cell units in Germany for preventing anti-D immunizations. Transfusion, 2009. [Citation] [RHeference]
  17. Li Q et al. Molecular basis of the RHD gene in blood donors with DEL phenotypes in Shanghai. Vox Sang, 2009. [Citation] [RHeference]
  18. Stabentheiner S et al. Overcoming methodical limits of standard RHD genotyping by next-generation sequencing. Vox Sang, 2011. [Citation] [RHeference]
  19. Wagner FF and Flegel WA et al. The Human RhesusBase Online ressource, 2011. — Online ressource — [RHeference]
  20. Silvy M et al. Weak D and DEL alleles detected by routine SNaPshot genotyping: identification of four novel RHD alleles. Transfusion, 2011. [Citation] [RHeference]
  21. Dogic V et al. Distribution of weak D types in the Croatian population. Transfus Med, 2011. [Citation] [RHeference]
  22. Wagner FF et al. RHD PCR of blood donors in Northern Germany: use of adsorption/elution to determine D antigen status Vox Sanguinis, 2012. — Abstract — [RHeference]
  23. F F Wagner et al. Single Adsorption / Elution with Anti-D May Be Insufficient to Determine the D Antigen Status of Very Weak DEL Alleles Transfusion, 2012. — Abstract — [RHeference]
  24. St-Louis R et al. DEL Blood donors alloimmunised patients: the Canadian experience Vox Sanguinis, 2012. — Abstract — [RHeference]
  25. Moussa H et al. Molecular background of D-negative phenotype in the Tunisian population. Transfus Med, 2012. [Citation] [RHeference]
  26. Rizzo C et al. Weak D and partial D: our experience in daily activity. Blood Transfus, 2012. [Citation] [RHeference]
  27. Haer-Wigman L et al. RHD and RHCE variant and zygosity genotyping via multiplex ligation-dependent probe amplification. Transfusion, 2013. [Citation] [RHeference]
  28. von Zabern I et al. D category IV: a group of clinically relevant and phylogenetically diverse partial D. Transfusion, 2013. [Citation] [RHeference]
  29. 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]
  30. Orzińska A et al. RHD variants in Polish blood donors routinely typed as D-. Transfusion, 2013. [Citation] [RHeference]
  31. Daniels G et al. Variants of RhD--current testing and clinical consequences. Br J Haematol, 2013. [Citation] [RHeference]
  32. Fichou Y et al. Establishment of a medium-throughput approach for the genotyping of RHD variants and report of nine novel rare alleles. Transfusion, 2013. [Citation] [RHeference]
  33. Gowland P et al. Molecular RHD screening of RhD negative donors can replace standard serological testing for RhD negative donors. Transfus Apher Sci, 2014. [Citation] [RHeference]
  34. Crottet SL et al. Implementation of a mandatory donor RHD screening in Switzerland. Transfus Apher Sci, 2014. [Citation] [RHeference]
  35. Costa S et al. RHD alleles and D antigen density among serologically D- C+ Brazilian blood donors. Transfus Med, 2014. [Citation] [RHeference]
  36. Wagner FF et al. The Rhesus Site. Transfus Med Hemother, 2014. [Citation] [RHeference]
  37. Scott SA et al. The RHD(1227G>A) DEL-associated allele is the most prevalent DEL allele in Australian D- blood donors with C+ and/or E+ phenotypes. Transfusion, 2014. [Citation] [RHeference]
  38. Trucco Boggione C et al. Molecular structures identified in serologically D- samples of an admixed population. Transfusion, 2014. [Citation] [RHeference]
  39. Van Sandt VS et al. RHD variants in Flanders, Belgium. Transfusion, 2015. [Citation] [RHeference]
  40. Ouchari M et al. Weak D in the Tunisian population. Blood Transfus, 2015. [Citation] [RHeference]
  41. Stegmann TC et al. Frequency and characterization of known and novel RHD variant alleles in 37 782 Dutch D-negative pregnant women. Br J Haematol, 2016. [Citation] [RHeference]
  42. C Henny et al. Impact of the mandatory donor RHD screening in Switzerland Vox Sanguinis, 2016. — Abstract — [RHeference]
  43. McGowan EC et al. Diverse and novel RHD variants in Australian blood donors with a weak D phenotype: implication for transfusion management. Vox Sang, 2017. [Citation] [RHeference]
  44. Dezan MR et al. High frequency of variant RHD genotypes among donors and patients of mixed origin with serologic weak-D phenotype. J Clin Lab Anal, 2018. [Citation] [RHeference]
  45. Jérôme Babinet et al. Erratum à l’article : « Résumés des Posters » [Transfus. Clin. Biol. 24 (2017) 3S] Transfusion Clinique et Biologique, 2018. — Abstract — [RHeference]
  46. Izaskun Apraiz et al. Performance Evaluation Study of ID RHD XT as a Molecular Tool for RHD Gene Screening in Pooled Blood Samples of Serologically D− C/E+ Donors Transfusion, 2019. — Abstract — [RHeference]
  47. Wagner F. et al. Results of more than ten years testing of RhD negative first time donors by RHD PCR Transfus Med Hemother, 2019. — Abstract — [RHeference]
  48. Arnoni CP et al. Correlation among automated scores of agglutination, antigen density by flow cytometry and genetics of D variants. Transfus Apher Sci, 2019. [Citation] [RHeference]
  49. Perez-Alvarez I et al. RHD genotyping of serologic RhD-negative blood donors in a hospital-based blood donor center. Transfusion, 2019. [Citation] [RHeference]
  50. Guzijan G et al. Implementation of Molecular RHD Typing at Two Blood Transfusion Institutes from Southeastern Europe. Transfus Med Hemother, 2019. [Citation] [RHeference]
  51. Koutsouri T et al. Frequency distribution of RHD alleles among Greek donors with weak D phenotypes demonstrates a distinct pattern in central European countries. Transfus Med, 2019. [Citation] [RHeference]
  52. Stef M et al. RH genotyping by nonspecific quantitative next-generation sequencing. Transfusion, 2020. [Citation] [RHeference]
  53. Tammi SM et al. Next-generation sequencing of 35 RHD variants in 16 253 serologically D- pregnant women in the Finnish population. Blood Adv, 2020. [Citation] [RHeference]
  54. Floch A et al. Comment from Rheference Online ressource, 2020. — Online ressource — [RHeference]
  55. Safic Stanic H et al. D variants in the population of D-negative blood donors in the north-eastern region of Croatia. Transfus Med, 2021. [Citation] [RHeference]

Last update: Jan. 8, 2021