ArticleJournal of immunology (Baltimore, Md. : 1950)2013
IFN-α treatment inhibits acute Friend retrovirus replication primarily through the antiviral effector molecule Apobec3.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 21 citations in OpenAlex.
- Interferon Receptor Chain Deficiency in Murine Friend Erythroleukemia Cell Clone Resistant to Type I or Type I and II Interferons.International journal of molecular sciences · 2026Article
- Stenotrophomonas promotes gastrointestinal tumor progression via STING degradation in tumour cells and mitigated immune response.Nature communications · 2026Article
- Systemic Expression of a Viral RdRP Protects against Retrovirus Infection and Disease.Journal of virology · 2020Article
- Friend retrovirus studies reveal complex interactions between intrinsic, innate and adaptive immunity.FEMS microbiology reviews · 2019Review
- A compartmentalized type I interferon response in the gut during chronic HIV-1 infection is associated with immunopathogenesis.AIDS (London, England) · 2018Article
- Type I interferon signaling is required for the APOBEC3/Rfv3-dependent neutralizing antibody response but not innate retrovirus restriction.Retrovirology · 2017Article
- Interferon Alpha Subtype-Specific Suppression of HIV-1 Infection In Vivo.Journal of virology · 2016Article
- SAMHD1 transcript upregulation during SIV infection of the central nervous system does not associate with reduced viral load.Scientific reports · 2016Article
- Tetherin/BST-2 promotes dendritic cell activation and function during acute retrovirus infection.Scientific reports · 2016Article
- Tetherin/BST-2: Restriction Factor or Immunomodulator?Current HIV research · 2016Review
- Modulating APOBEC expression enhances DNA vaccine immunogenicity.Immunology and cell biology · 2015Article
- Immunoglobulin VH gene diversity and somatic hypermutation during SIV infection of rhesus macaques.Immunogenetics · 2015Article
- Requirement for Fc effector mechanisms in the APOBEC3/Rfv3-dependent neutralizing antibody response.Journal of virology · 2015Article
- Interferon-α Subtypes in an Ex Vivo Model of Acute HIV-1 Infection: Expression, Potency and Effector Mechanisms.PLoS pathogens · 2015Article
- Article
- Mouse knockout models for HIV-1 restriction factors.Cellular and molecular life sciences : CMLS · 2014Review
- Tetherin promotes the innate and adaptive cell-mediated immune response against retrovirus infection in vivo.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Interferon-stimulated genes: roles in viral pathogenesis.Current opinion in virology · 2014Review
- Immunoglobulin somatic hypermutation by APOBEC3/Rfv3 during retroviral infection.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Ribonuclease L is not critical for innate restriction and adaptive immunity against Friend retrovirus infection.Virology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Therapeutic administration of IFN-α in clinical trials significantly reduced HIV-1 plasma viral load and human T-lymphotropic virus type I proviral load in infected patients. The mechanism may involve the concerted action of multiple antiretroviral effectors collectively known as "restriction factors," which could vary in relative importance according to the magnitude of transcriptional induction. However, direct genetic approaches to identify the relevant IFN-α restriction factors will not be feasible in humans in vivo. Meanwhile, mice encode an analogous set of restriction factor genes and could be used to obtain insights on how IFN-α could inhibit retroviruses in vivo. As expected, IFN-α treatment of mice significantly upregulated the transcription of multiple restriction factors including Tetherin/BST2, SAMHD1, Viperin, ISG15, OAS1, and IFITM3. However, a dominant antiretroviral factor, Apobec3, was only minimally induced. To determine whether Apobec3 was necessary for direct IFN-α antiretroviral action in vivo, wild-type and Apobec3-deficient mice were infected with Friend retrovirus, then treated with IFN-α. Treatment of infected wild-type mice with IFN-α significantly reduced acute plasma viral load 28-fold, splenic proviral load 5-fold, bone marrow proviral load 14-fold, and infected bone marrow cells 7-fold, but no inhibition was observed in Apobec3-deficient mice. These findings reveal that IFN-α inhibits acute Friend retrovirus infection primarily through the antiviral effector Apobec3 in vivo, demonstrate that transcriptional induction levels did not predict the mechanism of IFN-α-mediated control, and highlight the potential of the human APOBEC3 proteins as therapeutic targets against pathogenic retrovirus infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.