Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Lack of association between intact/deletion polymorphisms of the APOBEC3B gene and HIV-1 risk.

PloS one - 1 Jan 2014

Imahashi Mayumi, Izumi Taisuke, Watanabe Dai, Imamura Junji, Matsuoka Kazuhiro, Ode Hirotaka, Masaoka Takashi, Sato Kei, Kaneko Noriyo, Ichikawa Seiichi, Koyanagi Yoshio, Takaori-Kondo Akifumi, Utsumi Makoto, Yokomaku Yoshiyuki, Shirasaka Takuma, Sugiura Wataru, Iwatani Yasumasa, Naoe Tomoki

Abstract excerpt

OBJECTIVE: The human APOBEC3 family of proteins potently restricts HIV-1 replication APOBEC3B, one of the family genes, is frequently deleted in human populations. Two previous studies reached inconsistent conclusions regarding the effects of APOBEC3B loss on HIV-1 acquisition and pathogenesis. Therefore, it was necessary to verify the effects of APOBEC3B on HIV-1 infection in vivo. METHODS: Intact (I) and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Asian People
Share to Cohort Studies

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cytidine Deaminase

Share to HIV Infections

Share to Minor Histocompatibility Antigens

Share to Polymorphism, Genetic

Source

Open in PubMed Open full text

Identifiers

PMID: 24667791
DOI: 10.1371/journal.pone.0092861
PMCID: PMC3965477

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Lack of association between intact/deletion polymorphisms of the APOBEC3B gene and HIV-1 risk.PMID 24667791Read ↗

APOBEC3B deletion and risk of HIV-1 acquisition.Semantic proximity Read ↗

Human APOBEC3B is a potent inhibitor of HIV-1 infectivity and is resistant to HIV-1 VifSemantic proximity Read ↗

Moderate Influence of Human APOBEC3F on HIV-1 Replication in Primary LymphocytesSemantic proximity Read ↗

APOBEC3B deletion impacts on susceptibility to acquire HIV-1 and its advancement among individuals in western India.Semantic proximity Read ↗

APOBEC3F can inhibit the accumulation of HIV-1 reverse transcription products in the absence of hypermutation. Comparisons with APOBEC3G.Semantic proximity Read ↗

The APOBEC3B deletion polymorphism is associated with prevalence of hepatitis B virus, hepatitis C virus, Torque Teno virus, and Toxoplasma gondii co-infection among HIV-infected individuals.Semantic proximity Read ↗

Association of single nucleotide polymorphisms of APOBEC3G with susceptibility to HIV-1 infection and disease progression among men engaging in homosexual activity in northern China.Semantic proximity Read ↗

APOBEC3G expression is dysregulated in primary HIV-1 infection and polymorphic variants influence CD4+ T-cell counts and plasma viral load.Semantic proximity Read ↗

Human Apolipoprotein B mRNA-editing Enzyme-catalytic Polypeptide-like 3G (APOBEC3G) Is Incorporated into HIV-1 Virions through Interactions with Viral and Nonviral RNAsSemantic proximity Read ↗

Suppression of HIV-1 Infection by APOBEC3 Proteins in Primary Human CD4 <sup>+</sup> T Cells Is Associated with Inhibition of Processive Reverse Transcription as Well as Excessive Cytidine DeaminationSemantic proximity Read ↗

Apolipoprotein B mRNA–Editing Enzyme, Catalytic Polypeptide–Like 3G: A Possible Role in the Resistance to HIV of HIV‐Exposed Seronegative IndividualsSemantic proximity Read ↗

APOBEC3G and APOBEC3F Require an Endogenous Cofactor to Block HIV-1 ReplicationSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.