Citations

ABSTRACT HLA‐DRB1*03:234 differs from HLA‐DRB1*03:01:01:01 by two adjacent nucleotide substitutions in exon 2.

ABSTRACT HLA‐C*07:1268 differs from HLA‐C*07:02:01:01 by one nucleotide substitution in exon 3.

ABSTRACT HLA‐B*08:345Q differs from HLA‐B*08:238 by one nucleotide substitution, introducing a premature stop codon in exon 5.

ABSTRACT HLA‐A*32:202 differs from HLA‐A*32:01:01:01 by two nucleotide substitutions in exons 1 and 2.

ABSTRACT HLA‐DQB1*06:144N differs from HLA‐DQB1*06:03:01:01 by one nucleotide substitution, introducing a premature stop codon in exon 2.

ABSTRACT HLA‐B*57:205 differs from HLA‐B*57:01:01:01 by one nucleotide substitution in Exon 1.

ABSTRACT HLA‐A*24:675 differs from HLA‐A*24:02:01:01 by one nucleotide substitution in exon 3.

ABSTRACT HLA‐DQB1*06:549 differs from HLA‐DQB1*06:02:01:01 by one nucleotide substitution in exon 2.

ABSTRACT HLA‐C*03:737 differs from HLA‐C*03:05:01:01 by one nucleotide substitution in exon 3.

Abstract Background Lymphocytic choriomeningitis virus (LCMV) infection in immunocompromised hosts can result in disseminated disease, meningoencephalitis, and death. Published cases in transplant recipients have been traced to transmission from infected donors. We report 2 cases of serious, non–donor-derived LCMV infection in solid organ transplant recipients. Methods Initial identification of LCMV infection was done by using metagenomic next-generation sequencing (mNGS). Subsequent evaluations and confirmatory testing involved molecular diagnostics, serology, and phylogenetic analysis. A detailed epidemiologic investigation was conducted. Results LCMV was detected by mNGS in 2 solid organ transplant recipients from distinct donors. A heart transplant recipient (from donor 1) died of progressive, disseminated LCMV infection, while a kidney transplant recipient (from donor 2) with LCMV meningoencephalitis survived. A multistate laboratory and epidemiologic investigation of both donors and all their organ recipients was initiated. Postmortem samples were obtained from both donors, and pretransplant and/or posttransplant samples were obtained from 5 of the 6 organ recipients. mNGS, serologic, and real-time reverse-transcription polymerase chain reaction testing confirmed LCMV infection in both solid organ transplant recipients. Epidemiologic investigation revealed significant pretransplant rodent exposures for both LCMV-infected recipients. Laboratory studies for the other organ recipients from both donors were negative for LCMV infection. Conclusions Our investigations suggest that LCMV infection in 2 solid organ transplant recipients originated from rodent exposure preceding transplantation and were not donor derived. Although uncommon, healthcare providers should be aware of LCMV-associated serious and life-threatening illness in immunocompromised hosts. Diagnostic modalities are limited to reference laboratories.