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J Acquir Immune Defic Syndr. 2019 Aug 15;81(5):508-515. doi: 10.1097/QAI.0000000000002077.

HIV Transmission Chains Exhibit Greater HLA-B Homogeneity Than Randomly Expected.

Author information

Division of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, University of Zurich, Zurich, Switzerland.
Institute of Medical Virology, Swiss National Center for Retroviruses, University of Zurich, Zurich, Switzerland.
School of Life Sciences, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Swiss Institute of Bioinformatics, Lausanne, Switzerland.
Laboratory of Virology, Geneva University Hospital, University of Geneva, Geneva, Switzerland.
Division of Immunology and Allergy, University Hospital Lausanne, University of Lausanne, Lausanne, Switzerland.
Department of Biomedicine, University of Basel, Basel, Switzerland.
Division of Infectious Diseases and Hospital Epidemiology, Children's Research Center, University Children's Hospital Zurich, Zurich, Switzerland.
University Clinic of Infectious Diseases, University Hospital of Bern, University of Bern, Bern, Switzerland.
Infectious Diseases and Infection Control Clinic, Department of Medicine, University Hospital Basel, University of Basel, Basel, Switzerland.
Department of Infectious Diseases, Centre Hospitalier Universitaire Vaudois, University of Lausanne, Lausanne, Switzerland.
Division of Infectious Diseases and Hospital Epidemiology, Kantonsspital St. Gallen, St. Gallen, Switzerland.
Division of Infectious Diseases, Regional Hospital, Lugano, Switzerland.



HIV's capacity to escape immune recognition by human leukocyte antigen (HLA) is a core component of HIV pathogenesis. A better understanding of the distribution of HLA class I in HIV-infected patients would improve our knowledge of pathogenesis in relation to the host HLA type and could better improve therapeutic strategies against HIV.


Three hundred one to 325 transmission pairs and 469-496 clusters were identified for analysis among Swiss HIV Cohort Study (SHCS) participants using HIV pol sequences from the drug resistance database. HLA class I data were compiled at 3 specificity levels: 4-digit, 2-digit alleles, and HLA-B supertype. The analysis tabulated HLA-I homogeneity as 2 measures: the proportion of transmission pairs, which are HLA concordant, and the average percentage of allele matches within all clusters. These measures were compared with the mean value across randomizations with randomly assorted individuals.


We repeated the analysis for different HLA classification levels and separately for HLA-A, -B, and -C. Subanalyses by the risk group were performed for HLA-B. HLA-B showed significantly greater homogeneity in the transmission chains (2-digit clusters: 0.291 vs. 0.251, P value = 0.009; supertype clusters: 0.659 vs. 0.611, P value = 0.002; supertype pairs: 0.655 vs. 0.608, P value = 0.014). Risk group restriction caused the effect to disappear for men-who-have-sex-with-men but not for other risk groups. We also examined if protective HLA alleles B27 and B57 were under- or overrepresented in the transmission chains, although this yielded no significant pattern.


The HLA-B alleles of patients within HIV-1 transmission chains segregate in homogenous clusters/pairs, potentially indicating preferential transmission among HLA-B concordant individuals.

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