This case was reported in a literature article and described the occurrence of vaccination failure in a infant subject who received Rotavirus vaccine for prophylaxis. On an unknown date, less than a year after receiving Rotavirus vaccine and 126 days after receiving Rotavirus vaccine, the subject developed vaccination failure. Serious criteria included GSK medically significant. Additional event(s) included severe - grade 3 diarrhea rotavirus with serious criteria of GSK medically significant. The outcome of vaccination failure was unknown. The outcome(s) of the additional event(s) included diarrhea rotavirus (unknown). The investigator considered that there was a reasonable possibility that the vaccination failure and diarrhea rotavirus may have been caused by Rotavirus vaccine and Rotavirus vaccine. Relevant Tests: Lab tests were performed on an unspecified dates. The patient's stool specimen was collected and rotavirus diarrhoea (RVD) was determined by RV antigen detection in diarrheal specimens using the enzyme immunoassay. RVD stool specimens underwent total nucleic acid extraction. Reverse-transcription polymerase chain reaction (RT-PCR) was performed on total nucleic acid extracts. The amplicons underwent Sanger sequencing. Sequences were analysed, followed by Basic Local Alignment Search Tool (BLAST) analysis to determine the P genotype of each infecting strain. Subsequently the patient was diagnosed with severe rotavirus diarrhoea with P[6] genotype. [In this study, Lea and Leb antigen phenotyping was performed on stored saliva specimens. Infants were defined as Lewis-positive (Le+) if either Le a or Le b antigen was detected. Secretor status was inferred from Lewis phenotyping: Lea+b- infants were defined as non-secretors; Lea-b+ and Lea+b+ (partial-secretor) infants were defined as (Secretors) Se (results not provided for this patient]. The patient was diagnosed with severe RVD. [In this study, severe RVD was defined as Vesikari score equal to or more than 11].  Diagnostic results (unless otherwise stated, normal values were not provided): On an unknown date, Gene sequencing result was see text unknown. On an unknown date, Polymerase chain reaction result was see text unknown. On an unknown date, Rotavirus test positive result was P[6] genotype unknown. On an unknown date, Stool analysis result was see text unknown. Additional information was provided. This case was reported in a literature and described the vaccination failure in an infant of unspecified age and gender who was vaccinated with unspecified ROTARIX (GlaxoSmithKline) for prophylaxis. The patient was part of study with the objective to determine the effects of secretor status and Lewis phenotype on susceptibility to natural rotavirus (RV) infection and oral RV vaccine underperformance, A sub-study among infants participating in an RV1 vaccine effectiveness (VE) trial Oral Polio Vaccines in Developing Countries (PROVIDE) in a specific country was conducted from 2010 to 2014. Infants were enrolled within 7 days of life randomized 1:1 to receive RV1 or no RV1 at 10 and 17 weeks, followed with active community-based diarrheal surveillance. No information on patient's medical or family history or concurrent condition or concomitant medication was provided. On unspecified dates, at 10 and 17 weeks of age, the patient received 2 doses of ROTARIX (batch number not provided). On an unspecified date, between 18 and 52 weeks after vaccination, the patient developed first episode of rotavirus diarrhoea. The patient's stool specimen was collected and rotavirus diarrhoea (RVD) was determined by RV antigen detection in diarrheal specimens using the enzyme immunoassay. RVD stool specimens underwent total nucleic acid extraction. Reverse-transcription polymerase chain reaction (RT-PCR) was performed on total nucleic acid extracts. The amplicons underwent Sanger sequencing. Sequences were analysed, followed by Basic Local Alignment Search Tool (BLAST) analysis to determine the P genotype of each infecting strain. Subsequently the patient was diagnosed with severe rotavirus diarrhoea with P[6] genotype. [In this study, Lea and Leb antigen phenotyping was performed on stored saliva specimens. Infants were defined as Lewis-positive (Le+) if either Le a or Le b antigen was detected. Secretor status was inferred from Lewis phenotyping: Lea+b- infants were defined as non-secretors; Lea-b+ and Lea+b+ (partial-secretor) infants were defined as (Secretors) Se (results not provided for this patient]. The patient was diagnosed with severe RVD. [In this study, severe RVD was defined as Vesikari score equal to or more than 11]. The case has been considered as vaccination failure being time to onset was unknown. This case has been considered as serious due to vaccination failure. The treatment was unknown. The outcome of the event was not provided. The author considered the event severe RVD casually related to ROTARIX. The author concluded "we demonstrated in a cohort of infants that non secretors were at decreased risk of RVD due to complete protection from P[4] RVs. This effect could significantly impact estimates of VE, particularly in regions with high frequencies of non-secretors and P[4] RV. We found no evidence of resistance to P[8] RVs as a mechanism for decreased vaccine effectiveness. Le -infants appeared to be protected from P[8] RVD, but this effect was offset by a markedly increased risk for RVD and vaccine failure due to P[6] infection. Secretor status, Lewis phenotype, and RV genotype should be accounted for in future oral RV vaccine trials." This is 1 of 2 valid cases reported in this literature article. Lab Comments: Lab tests were performed on an unspecified dates. The patient's stool specimen was collected and rotavirus diarrhoea (RVD) was determined by RV antigen detection in diarrheal specimens using the enzyme immunoassay. RVD stool specimens underwent total nucleic acid extraction. Reverse-transcription polymerase chain reaction (RT-PCR) was performed on total nucleic acid extracts. The amplicons underwent Sanger sequencing. Sequences were analysed, followed by Basic Local Alignment Search Tool (BLAST) analysis to determine the P genotype of each infecting strain. Subsequently the patient was diagnosed with severe rotavirus diarrhoea with P[6] genotype. [In this study, Lea and Leb antigen phenotyping was performed on stored saliva specimens. Infants were defined as Lewis-positive (Le+) if either Le a or Le b antigen was detected. Secretor status was inferred from Lewis phenotyping: Lea+b- infants were defined as non-secretors; Lea-b+ and Lea+b+ (partial-secretor) infants were defined as (Secretors) Se (results not provided for this patient]. The patient was diagnosed with severe RVD. [In this study, severe RVD was defined as Vesikari score equal to or more than 11].