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GWAS Study

Africa-specific human genetic variation near CHD1L associates with HIV-1 load.

McLaren PJ, Porreca I, Iaconis G et al.

37532928 PubMed ID
GWAS Study Type
3879 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

MP
McLaren PJ
PI
Porreca I
IG
Iaconis G
MH
Mok HP
MS
Mukhopadhyay S
KE
Karakoc E
CS
Cristinelli S
PC
Pomilla C
BI
Bartha I
TC
Thorball CW
TR
Tough RH
AP
Angelino P
KC
Kiar CS
CT
Carstensen T
FS
Fatumo S
PT
Porter T
JI
Jarvis I
SW
Skarnes WC
BA
Bassett A
DM
DeGorter MK
SM
Sathya Moorthy MP
TJ
Tuff JF
KE
Kim EY
WM
Walter M
SL
Simons LM
BA
Bashirova A
BS
Buchbinder S
CM
Carrington M
CA
Cossarizza A
DL
De Luca A
GJ
Goedert JJ
GD
Goldstein DB
HD
Haas DW
HJ
Herbeck JT
JE
Johnson EO
KP
Kaleebu P
KW
Kilembe W
KG
Kirk GD
KN
Kootstra NA
KA
Kral AH
LO
Lambotte O
LM
Luo M
MS
Mallal S
MJ
Martinez-Picado J
ML
Meyer L
MJ
Miro JM
MP
Moodley P
MA
Motala AA
MJ
Mullins JI
NK
Nam K
ON
Obel N
PF
Pirie F
PF
Plummer FA
PG
Poli G
PM
Price MA
RA
Rauch A
TI
Theodorou I
TA
Trkola A
WB
Walker BD
WC
Winkler CA
ZJ
Zagury JF
MS
Montgomery SB
CA
Ciuffi A
HJ
Hultquist JF
WS
Wolinsky SM
DG
Dougan G
LA
Lever AML
GD
Gurdasani D
GH
Groom H
SM
Sandhu MS
FJ
Fellay J
Chapter II

Abstract

Summary of the research findings

HIV-1 remains a global health crisis1, highlighting the need to identify new targets for therapies. Here, given the disproportionate HIV-1 burden and marked human genome diversity in Africa2, we assessed the genetic determinants of control of set-point viral load in 3,879 people of African ancestries living with HIV-1 participating in the international collaboration for the genomics of HIV3. We identify a previously undescribed association signal on chromosome 1 where the peak variant associates with an approximately 0.3 log10-transformed copies per ml lower set-point viral load per minor allele copy and is specific to populations of African descent. The top associated variant is intergenic and lies between a long intergenic non-coding RNA (LINC00624) and the coding gene CHD1L, which encodes a helicase that is involved in DNA repair4. Infection assays in iPS cell-derived macrophages and other immortalized cell lines showed increased HIV-1 replication in CHD1L-knockdown and CHD1L-knockout cells. We provide evidence from population genetic studies that Africa-specific genetic variation near CHD1L associates with HIV replication in vivo. Although experimental studies suggest that CHD1L is able to limit HIV infection in some cell types in vitro, further investigation is required to understand the mechanisms underlying our observations, including any potential indirect effects of CHD1L on HIV spread in vivo that our cell-based assays cannot recapitulate.

3,879 African American or Afro-Caribbean, African ancestry individuals

Chapter III

Study Statistics

Key metrics and study information

3879
Total Participants
GWAS
Study Type
No
Replicated
African American or Afro-Caribbean, African unspecified
Ancestry
U.S., United Republic of Tanzania, Uganda, South Africa, Kenya, Switzerland
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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Analysis In Progress

Our analysis of this publication is currently being prepared. Please check back soon for comprehensive insights into the health and genetic findings discussed in this research.