Format

Send to

Choose Destination
Genes Immun. 2019 May 20. doi: 10.1038/s41435-019-0077-9. [Epub ahead of print]

Relationship between human leukocyte antigen alleles and risk of Kaposi's sarcoma in Cameroon.

Author information

1
Viral Oncology Section, AIDS and Cancer Virus Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc, Frederick, MD, USA.
2
CCR Collaborative Bioinformatics Resource (CCBR), Center for Cancer Research, NCI, Bethesda, MD, USA.
3
Advanced Biomedical Computational Science, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.
4
SOCHIMO, Yaoundé, Cameroon.
5
RTI International, Research Triangle Park, Triangle Park, NC, USA.
6
Basic Science Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.
7
University of California San Diego, San Diego, CA, USA.
8
Ragon Institute of MGH, MIT and Harvard, Cambridge, MA, USA.
9
Viral Oncology Section, AIDS and Cancer Virus Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc, Frederick, MD, USA. whitbyd@mail.nih.gov.

Abstract

Several studies published to date report associations between human leukocyte antigen (HLA) alleles and different types of Kaposi's Sarcoma (KS). However, there is little concordance between the HLA alleles identified and the populations studied. To test whether HLA alleles associate with KS in a Cameroonian case-control study, we performed high-resolution HLA typing in KSHV seropositive individuals. Among HIV-positive individuals, carriers of HLA-B*14:01 were at a significantly higher risk of AIDS-KS (p = 0.033). For HIV-negative patients, a gene-wise comparison of allele frequencies identified the HLA-B (p = 0.008) and -DQA1 (p = 0.002) loci as possible risk factors for endemic KS. Our study provides additional understanding of genetic determinants of KS and their implications in disease pathogenesis. Further validation of these findings is needed to define the functional relevance of these associations.

PMID:
31105266
DOI:
10.1038/s41435-019-0077-9

Grant support

Grant support

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center