RHD*06.01 - RHD*DVI.1
(ISBT table: RHD partial D v5.0)

This entry is an hybrid RHD allele.

DVI (DEL), DVI deletion type (obsolete), DVI type 1, DVI-1, RHD*D-cE(4-5)-D, RHD*D-cE(4-5)-D (DVI type 1), RHD-RHcE(4-5)-RHD,
Download VCF file

Molecular data

Nucleotides: 505A>C; 509T>G; 514A>T; 544T>A; 577G>A; 594A>T; 602C>G; 667T>G; 676G>C; 697G>C; 712G>A; 733G>C; 744C>T; 787G>A; 800A>T;

Amino acids: M169L; M170R; I172F; S182T; E193K; K198N; T201R; F223V; A226P; E233Q; V238M; V245L; S248S; G263R; K267M;

Hybrid allele encompassing at least one RHCE exon: RHD-RHcE(4-5)-RHD

Comments on the molecular basis:

  • molecular analysis initially erroneously interpreted as deletion of exons 4 to 6
  • same samples initially interpreted as "deletion type" are demonstrated to be hybrid alleles
  • demonstrates Proline 226 on RHD hybrid allele
  • demonstrates Proline 226 on hybrid allele
  • molecular basis deduced by authors from the results of cDNA analysis
  • PCR pattern, exons 3, 4, 5, 6, 7 and 9

Extracellular position of one or more amino acid substitutions:

  • hybrid RHD-RHCE, several residues are predicted to be extracellular

Splicing:

Unconventional prediction methods:

Phenotype

Main D phenotype: variable/discrepant (last update: Aug. 9, 2020)
Reports by D phenotype
Other RH phenotypes: RH:-2, -5, -23, -52,
  • RH:-2 inferred from the reported RHCE phenotypes of the carriers
  • RH:-5 inferred from the reported RHCE phenotypes of the carriers
  • RH:-23
  • RH:-52 no new sample
Serology with monoclonal anti-D
  • 14 anti-D non-reactive with variant, out of 22 monoclonal IgG tested; adsorption-elution was performed (Table 2)
  • only a few anti-D tested
  • epitope pattern (reproduced from 9490704)
  • variable reactions: ++ to +++ or negative, with a panel of 10 monoclonal anti-D
Antigen Density (Ag/RBC)
  • 1050 Ag/RBC, derived from the results obtained with 14 of the 59 monoclonal IgG anti-D tested
  • range: 276 - 378, median: 318 Ag/RBC, 3 samples, median (range) with 11 IgG anti-D
  • range: 204 - 1169, median: 489 Ag/RBC, for 5 samples tested
  • 300 Ag/RBC (Table 2)
More phenotype data
Rhesus Similarity Index

  • 0.0 (derived from the results obtained with 14 of the 59 monoclonal IgG anti-D tested)

Haplotype

Main CcEe phenotype association: cE (last update: Jan. 8, 2021)
Number of samples reported by haplotype
ce Ce cE CE
ce 0 0 10 0
Ce 0 3 0
cE 24 0
CE 0
Reports by CcEe phenotype
  • with ccEe
    • 2 samples
    1 sample (some samples overlap with 8111052, not counted twice)
    3 samples (3 samples used as controls, may have been included in other studies)
    4 samples
  • with cE
    • 10 samples (haplotype given, not complete phenotype)
    14 samples (haplotype given, not complete phenotype)
    0 samples (Table 2; no sample count, presented as a general association) (Figure 2; presented as a general association, no sample count)
  • with CcEe
    • 2 samples
    1 sample
Main allele association: RHCE*03
Reports by allele association
  • RHCE*03
    • 0 samples
  • RHCE*03 or RHCE*01
    • 1 sample

Alloimmunization

Antibodies in carriers
Antibody specificity: D (RH1)
Summary: allo-anti-D (last update: Aug. 9, 2020)
Detailed information
    von Zabern I et al. Transfusion (2013)
    Wagner FF et al. Transfus Med Hemother (2014) (RIR n°66, 69, 72)
  • Ab specificity: D (RH1)
  • Number (auto- or allo-):
  • Number listed as allo-: 3
  • 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?: 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:
    Mouro I et al. Blood (1994)
  • Ab specificity: D (RH1)
  • Number (auto- or allo-): "some"
  • 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: "some individuals included in this study have developped anti-D"
Antibodies in D negative recipients

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

Reports

Summary: frequent descriptions, mainly in individuals of Central European (Caucasian) descent or compatible with such descent (last update: Aug. 9, 2020)
Detailed reports
  • 2 samples in French population
  • 1 sample sample tested during a workshop referred by a UK lab
  • 3 samples in the Czech (Prague) population
  • 1 sample in the Finnish population
  • 9/9 distribution of DVI samples from Tyrol (Austria) Austrian
  • 5/15 distribution of DVI samples from Southwestern Germany German
  • 0/270 donors with weak D phenotype White, in the German (Northern Germany) population
  • 15/146 donors with weak D phenotype White, in the Austrian (Tyrol) population
  • 2/8442 (2 of the 5 donors who were really weakly D positive) 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)
  • 1/738 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
  • 0/333 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
  • 0/54 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
  • 0/400 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
  • 4/17 distribution of DVI samples in donors Spanish
  • 8/191 (5 donors and 3 patients) among 191 samples with weak D expression or unclear D phenotype within 44,743 donors and 8,604 patients tested in the Austrian population, Upper Austria
  • 2/163 selected variants included for the development of a genotyping assay mainly in the Dutch population (samples may have been included in other studies)
  • 1 sample (heterozygous with RHef00085) reported by a French lab from Brest, Brittany
  • 10/627 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
  • 6/37782 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
  • 10/104 (prevalence among weak D) or 10/21353 (phenotypic prevalence in population) 104 with weak D phenotype were genotyped in a cohort of 21353 pregnant women admixed Brazilian
  • 1/223 donors with D negative phenotype initially, found to have D antigen expression (67 of the 223 samples of the cohort) or samples referred with discrepant or weak D typing, or discrepancies with previous typings, or anti-D in D positive individuals (156 of the 223 samples of the cohort) in the Indian population
  • 1/185 RH:–1,–4 or RH:–1,–5 recipients reported by a French lab
  • 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
  • 0.0047 allele frequency in 106 donors with weak D phenotype Brazilian (mixed origin, mainly between African and European descent)

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

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Links

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. Mouro I et al. Rearrangements of the blood group RhD gene associated with the DVI category phenotype. Blood, 1994. [Citation] [RHeference]
  3. Armstrong-Fisher SS et al. Molecular analysis of DVI variant ISBT 35 (R2VIr). Transfus Clin Biol, 1996. [Citation] [RHeference]
  4. Huang CH et al. Human DVI category erythrocytes: correlation of the phenotype with a novel hybrid RhD-CE-D gene but not an internally deleted RhD gene. Blood, 1997. [Citation] [RHeference]
  5. Avent ND et al. Molecular analysis of Rh transcripts and polypeptides from individuals expressing the DVI variant phenotype: an RHD gene deletion event does not generate All DVIccEe phenotypes. Blood, 1997. [Citation] [RHeference]
  6. Maaskant-van Wijk PA et al. Evidence That the RHDVI Deletion Genotype Does Not Exist Blood, 1997. [Citation] [RHeference]
  7. Maaskant-van Wijk PA et al. Genotyping of RHD by multiplex polymerase chain reaction analysis of six RHD-specific exons. Transfusion, 1998. [Citation] [RHeference]
  8. Legler TJ et al. RHD genotyping in weak D phenotypes by multiple polymerase chain reactions. Transfusion, 1998. [Citation] [RHeference]
  9. Wagner FF et al. Three molecular structures cause rhesus D category VI phenotypes with distinct immunohematologic features. Blood, 1998. [Citation] [RHeference]
  10. Avent ND et al. The rhesus blood group system: insights from recent advances in molecular biology. Transfus Med Rev, 1999. [Citation] [RHeference]
  11. Wagner FF et al. Weak D alleles express distinct phenotypes. Blood, 2000. [Citation] [RHeference]
  12. Wagner FF et al. RHD positive haplotypes in D negative Europeans. BMC Genet, 2001. [Citation] [RHeference]
  13. Müller TH et al. PCR screening for common weak D types shows different distributions in three Central European populations. Transfusion, 2001. [Citation] [RHeference]
  14. Wagner FF et al. A D(V)-like phenotype is obliterated by A226P in the partial D DBS. Transfusion, 2001. [Citation] [RHeference]
  15. Omi T et al. Isolation, characterization, and family study of DTI, a novel partial D phenotype affecting the fourth external loop of D polypeptides. Transfusion, 2002. [Citation] [RHeference]
  16. Wagner FF et al. The DAU allele cluster of the RHD gene. Blood, 2002. [Citation] [RHeference]
  17. Gassner C et al. Presence of RHD in serologically D-, C/E+ individuals: a European multicenter study. Transfusion, 2005. [Citation] [RHeference]
  18. 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]
  19. Esteban R et al. The D category VI type 4 allele is prevalent in the Spanish population. Transfusion, 2006. [Citation] [RHeference]
  20. Polin H et al. Effective molecular RHD typing strategy for blood donations. Transfusion, 2007. [Citation] [RHeference]
  21. Silvy M et al. Weak D and DEL alleles detected by routine SNaPshot genotyping: identification of four novel RHD alleles. Transfusion, 2011. [Citation] [RHeference]
  22. Daniels G et al. Variants of RhD--current testing and clinical consequences. Br J Haematol, 2013. [Citation] [RHeference]
  23. Fichou Y et al. A convenient qualitative and quantitative method to investigate RHD-RHCE hybrid genes. Transfusion, 2013. [Citation] [RHeference]
  24. Haer-Wigman L et al. RHD and RHCE variant and zygosity genotyping via multiplex ligation-dependent probe amplification. Transfusion, 2013. [Citation] [RHeference]
  25. von Zabern I et al. D category IV: a group of clinically relevant and phylogenetically diverse partial D. Transfusion, 2013. [Citation] [RHeference]
  26. Wagner FF et al. The Rhesus Site. Transfus Med Hemother, 2014. [Citation] [RHeference]
  27. Van Sandt VS et al. RHD variants in Flanders, Belgium. Transfusion, 2015. [Citation] [RHeference]
  28. 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]
  29. Srivastava K et al. The DAU cluster: a comparative analysis of 18 RHD alleles, some forming partial D antigens. Transfusion, 2016. [Citation] [RHeference]
  30. Zacarias JM et al. Frequency of RHD variants in Brazilian blood donors from Parana State, Southern Brazil. Transfus Apher Sci, 2016. [Citation] [RHeference]
  31. Bub CB et al. RHD alleles among pregnant women with serologic discrepant weak D phenotypes from a multiethnic population and risk of alloimmunization. J Clin Lab Anal, 2018. [Citation] [RHeference]
  32. 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]
  33. Fichou Y et al. Molecular basis of weak D expression in the Indian population and report of a novel, predominant variant RHD allele. Transfusion, 2018. [Citation] [RHeference]
  34. Jérôme Babinet et al. Erratum à l’article : « Résumés des Posters » [Transfus. Clin. Biol. 24 (2017) 3S] Transfusion Clinique et Biologique, 2018. — Abstract — [RHeference]
  35. Floch A et al. Comment from Rheference Online ressource, 2020. — Online ressource — [RHeference]
  36. Stef M et al. RH genotyping by nonspecific quantitative next-generation sequencing. Transfusion, 2020. [Citation] [RHeference]

Last update: Jan. 8, 2021