Multiple APOBEC3 Restriction Factors for HIV-1 and One Vif to Rule Them All

Desimmie, Belete Ayele; Delviks-Frankenberrry, Krista A.; Burdick, Ryan C.; Qi, Dawei; Izumi, Tatsuro; Pathak, Vinay K.

doi:10.1016/j.jmb.2013.10.033

Cited by 182 publications

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References 276 publications

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“…Several human APOBEC3 (apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3) proteins, notably APOBEC3D, APOBEC3F, APOBEC3G and APOBEC3H, have the capacity to restrict human immunodeficiency virus type 1 (HIV-1) replication (Albin & Harris, 2010;Desimmie et al, 2014;Feng et al, 2014;Kitamura et al, 2011;Refsland & Harris, 2013). These restriction factors are incorporated into the progeny virions and enzymically convert viral cDNA cytosines to uracils during reverse transcription, which can debilitate viral function (Albin & Harris, 2010;Desimmie et al, 2014;Feng et al, 2014;Kitamura et al, 2011;Refsland & Harris, 2013).…”

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confidence: 99%

“…These restriction factors are incorporated into the progeny virions and enzymically convert viral cDNA cytosines to uracils during reverse transcription, which can debilitate viral function (Albin & Harris, 2010;Desimmie et al, 2014;Feng et al, 2014;Kitamura et al, 2011;Refsland & Harris, 2013). Although original studies focused on human APOBEC3G (Harris et al, 2003;Mariani et al, 2003;Sheehy et al, 2002;Zhang et al, 2003), subsequent work revealed that all placental mammals have APOBEC3 enzymes (Münk et al, 2012), albeit different numbers, and that these enzymes have the potential to attenuate the infectivity of a broad spectrum of viruses, including simian immunodeficiency virus (SIV) (Mariani et al, 2003), feline immunodeficiency virus (FIV) (Münk et al, 2008;Zielonka et al, 2010), bovine immunodeficiency virus (BIV) (LaRue et al, 2010) and small ruminant lentiviruses (SRLVs; e.g.…”

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“…However, to counteract APOBEC3-mediated restriction, these lentiviruses encode a protein called Vif (viral infectivity factor). Vif recruits a cellular E3 ubiquitin ligase complex including cullin 5 (CUL5) and elongin B/C (ELOB/C), and degrades host APOBEC3 proteins through a ubiquitin/proteasomedependent pathway (Albin & Harris, 2010;Desimmie et al, 2014;Feng et al, 2014;Kitamura et al, 2011;Refsland & Harris, 2013).…”

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Vif determines the requirement for CBF-β in APOBEC3 degradation

Yoshikawa

Takeuchi

Yamada

et al. 2015

Journal of General Virology

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APOBEC3 (apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3) proteins are cellular DNA deaminases that restrict a broad spectrum of lentiviruses. This process is counteracted by Vif (viral infectivity factor) of lentiviruses, which binds APOBEC3s and promotes their degradation. CBF-b (core binding factor subunit b) is an essential co-factor for the function of human immunodeficiency virus type 1 Vif to degrade human APOBEC3s. However, the requirement for CBF-b in Vif-mediated degradation of other mammalian APOBEC3 proteins is less clear. Here, we determined the sequence of feline CBFB and performed phylogenetic analyses. These analyses revealed that mammalian CBFB is under purifying selection. Moreover, we demonstrated that CBF-b is dispensable for feline immunodeficiency virus Vif-mediated degradation of APOBEC3s of its host. These findings suggested that primate lentiviruses have adapted to use CBF-b, an evolutionary stable protein, to counteract APOBEC3 proteins of their hosts after diverging from other lentiviruses.

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Vif determines the requirement for CBF-β in APOBEC3 degradation

Yoshikawa

Takeuchi

Yamada

et al. 2015

Journal of General Virology

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“…Together they play an important role in preventing the replication and spread of a wide range of viruses, retroviruses and retroelements (reviewed by Desimmie et al, 2014;Harris & Dudley, 2015;Koito & Ikeda, 2013). A3F and A3G are potent and well-characterized members of the A3 family that are mostly recognized for their roles in mutating and restricting the infection of human immunodeficiency virus type 1 (HIV-1).…”

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confidence: 99%

“…A3F and A3G are potent and well-characterized members of the A3 family that are mostly recognized for their roles in mutating and restricting the infection of human immunodeficiency virus type 1 (HIV-1). However, this virus has evolved effective strategies to dodge the effects of these host intrinsic proteins; one of them is through the expression of the viral infectivity factor (Vif) (Desimmie et al, 2014). The main role of Vif is to protect HIV-1 from the deleterious actions of A3G and A3F (and some other members of the A3 family) by linking these proteins to the E3 ubiquitin ligase complex, which then targets them for degradation in the proteasome (Kobayashi et al, 2005;Liu et al, 2004;Mehle et al, 2004;Yu et al, 2003).…”

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Comparative analysis of the gene-inactivating potential of retroviral restriction factors APOBEC3F and APOBEC3G

Bélanger

Langlois

2015

Journal of General Virology

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APOBEC3 (A3) proteins are host-encoded restriction factors that inhibit retrovirus infection by mutagenic deamination of cytosines in minus-strand DNA replication intermediates. APOBEC3F (A3F) and APOBEC3G (A3G) are two of the most potent A3 enzymes in humans with each having a different target DNA specificity. A3G prefers to deaminate cytosines preceded by a cytosine (59-CC), whereas A3F preferentially targets cytosines preceded by a thymine (59-TC).Here we performed a detailed comparative analysis of retrovirus-encoded gene sequences edited by A3F and A3G, with the aim of correlating the context and intensity of the mutations with their effects on gene function. Our results revealed that, when there are few (TGG) tryptophan codons in the sequence, both enzymes alter gene function with a similar efficiency when given equal opportunities to deaminate in their preferred target DNA context. In contrast, tryptophan-rich genes are efficiently inactivated in the presence of a low mutational burden, through termination codon generation by A3G but not A3F. Overall, our results clearly demonstrated that the target DNA specificity of an A3 enzyme along with the intensity of the mutational burden and the tryptophan content of the gene being targeted are the factors that have the most forceful influence on whether A3-induced mutations will favour either terminal inactivation or genetic diversification of a retrovirus.

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HIV Life Cycle and Inherited Co‐Receptors

Bukrinsky

2014

Encyclopedia of Life Sciences

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Human immunodeficiency virus (HIV) is a Lentivirus of the family Retroviridae , members of which cause a number of neurological and immunological diseases in humans and animals. HIV is the causative agent of the acquired immune deficiency syndrome. The disease is caused by virus‐mediated depletion of CD4+ T lymphocytes, preferentially CCR5‐positive memory T cells. Most of these cells localise to mucosal tissue, in particular gut mucosa, and disruption of the gut mucosal barrier is an early feature of HIV infection that determines the pathogenesis of the disease. More than 20 years of intensive studies identified the molecular mechanisms underlying viral replication and disease pathogenesis and provided the foundation for development of antiviral therapeutics and vaccine. This article provides a brief overview of the HIV life cycle and focuses on receptors that determine viral binding and entry into the target cells. Key Concepts: Virus entry into target cell is initiated by interaction between gp120 and cell receptors. HIV preferentially targets memory CD4+ T cells that localise to mucosal lymphoid tissue, in particular the gut mucosa. HIV replication includes a number of distinct steps: virus–cell fusion and entry, uncoating, reverse transcription and formation of the pre‐integration complex (PIC), PIC nuclear entry and integration, transcription and translation of proviral DNA, viral assembly and release of nascent virions and maturation and formation of infectious virions. To infect a target cell, virus needs to counteract the activity of multiple cellular antiviral factors (APOBEC3, SAMHD1, tetherin), most of which activated by interferon. HIV accessory proteins have evolved to perform this function. Receptors determine not only the first step of HIV interaction with the target cell, but also regulate post‐entry events in viral replication. Characterisation of the molecular mechanisms underlying HIV replication and interaction with the target cells provides an opportunity to develop anti‐HIV therapeutics and vaccine.

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Multiple APOBEC3 Restriction Factors for HIV-1 and One Vif to Rule Them All

Cited by 182 publications

References 276 publications

Vif determines the requirement for CBF-β in APOBEC3 degradation

Vif determines the requirement for CBF-β in APOBEC3 degradation

Comparative analysis of the gene-inactivating potential of retroviral restriction factors APOBEC3F and APOBEC3G

HIV Life Cycle and Inherited Co‐Receptors

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