APOBEC3BDeletion and Risk of HIV‐1 Acquisition | Zendy

Ping An | Zendy; Randall C. Johnson | Zendy; John Phair | Zendy; Gregory D. Kirk | Zendy; Xiaofang Yu | Zendy; Sharyne Donfield | Zendy; Susan Buchbinder | Zendy; James J. Goedert | Zendy; Cheryl A. Winkler | Zendy

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APOBEC3BDeletion and Risk of HIV‐1 Acquisition

Author(s) -

Ping An,

Randall C. Johnson,

John Phair,

Gregory D. Kirk,

Xiaofang Yu,

Sharyne Donfield,

Susan Buchbinder,

James J. Goedert,

Cheryl A. Winkler

Publication year - 2009

Publication title -

the journal of infectious diseases

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.69

H-Index - 252

eISSN - 1537-6613

pISSN - 0022-1899

DOI - 10.1086/605644

Subject(s) - cytidine deaminase , biology , genotype , immunology , virology , lentivirus , odds ratio , gene , viral disease , virus , genetics , medicine

The human APOBEC3 family of cytidine deaminases provides intrinsic immunity to retroviral infection. A naturally occurring 29.5-kb deletion removes the entire APOBEC3B gene. We examined the impact of the APOBEC3B gene deletion in >4000 individuals from 5 human immunodeficiency virus type 1 (HIV-1) natural history cohorts. The hemizygous genotype had no effect on either acquisition of HIV-1 infection or progression to AIDS. However, the homozygous deletion was significantly associated with unfavorable outcomes for HIV-1 acquisition (odds ratio, 7.37; P= .024), progression to AIDS (relative hazard, 4.01; P=. 03), and viral set point (P= .04). These findings suggest that the loss of APOBEC3B may increase host susceptibility to HIV-1 acquisition and progression to AIDS and warrant further study.

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