Faculty Opinions recommendation of Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein.

By M. Carrington. 2002

891 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/10d8e5bd98d46779ddc3c214cad54038a544e7d4

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Citations in the corpus

The antiretroviral enzyme APOBEC3G is degraded by the proteasome in response to HIV-1 Vif (2003, unknown): “The packaging of APOBEC3G into retroviral particle”
Quasispecies Theory and the Behavior of RNA Viruses (2010, background): “The cytidine deaminase APOBEC3G was initially identified as a protein targeted by the HIV Vif protein during replication [50].”
HIV-1 Vif protein binds the editing enzyme APOBEC3G and induces its degradation (2003, background): “jpg" NDATA ITEM> ]> HIV-1 Vif is a small ( M r 23,000) basic protein that is necessary for HIV-1 replication in vivo and in nonpermissive cells, including T lymphocytes and macrophages and several leukemic T-cell lines, but is irrelevant in many other permissive cell”
DNA deamination mediates innate immunity to retroviral infection. (2003, background): “major targets for HIV infection in vivo) and has been shown to be a potent inhibitor of Vif-deficient HIV (Sheehy et al., 2002).”
Retroviral restriction by APOBEC proteins (2004, background): “It is now appreciated that these cells are non-permissive owing to APOBEC protein expressio”
The Evolution and Emergence of RNA Viruses (2009, background): “As a case in point, despite the potent affect of APOBEC3G, HIV-1 has evolved an anti-APOBEC3G response controlled by the vif gene (Sheehy et al. 2002).”
Avoiding the void: cell-to-cell spread of human viruses (2008, background): “These are exemplified by the family of cytidine deaminases of which the prototype, APOBEC3G, interferes with retroviruse”
HIV-1 accessory proteins--ensuring viral survival in a hostile environment. (2008, background): “By comparing mRNA expression profiles in cells where Vif is, or is not, required for HIV-1 replication, the human gene APOBEC3G (A3G) was identified as being fully sufficient to prevent productive infection in the absence of Vif (Sheehy et al., 2002).”
Origins of HIV and the AIDS pandemic. (2011, background): “These include (1) APOBEC3G (apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G), which interferes with reverse transcription (Sheehy et al. 2002); (2) TRIM5a (tripartite motif 5a protein), which interferes with viral uncoating (Stremlau et al.”
Evidence of HIV-1 Adaptation to HLA-Restricted Immune Responses at a Population Level (2002, background): “Vif is necessary for regulating the production of virions from peripheral blood lymphocytes, macrophages and certain other cells(223) and may act by blocking an antiviral factor within CD4+ T-cells.(224) It also appears to aid in the synthesis of proviral DNA.”
The cytidine deaminase CEM15 induces hypermutation in newly synthesized HIV-1 DNA (2003, methodology): “In the bottom panel, the rows are: (7) wild-type viruses, without CEM15; (8) wild-type viruses, with CEM15.”
Broad antiretroviral defence by human APOBEC3G through lethal editing of nascent reverse transcripts (2003, background): “The virion infectivity factor (Vif) protein of human immunodeficiency virus (HIV) is required during the late stages of viral production to counter the antiviral activity of APOBEC3G (apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G; also known as CEM15), a protein expressed notab”