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https://www.readbyqxmd.com/read/28443724/genetic-diversity-of-hiv-1-gene-vif-among-treatment-na%C3%A3-ve-brazilians
#1
Fabiola Villanova, Marta Barreiros, Luiz Mario Janini, Ricardo Sobhie Diaz, Elcio Leal
HIV-1 has the Vif protein, which binds to human antiviral proteins APOBEC3 to form complexes to be degraded by cellular proteolysis. To further explore HIV-1 diversity at the population level, we analyzed blood samples from 317 treatment-naïve patients in Brazil. Here, we explored the correlations of Vif polymorphisms with clinical parameters of the patients and found that mutation K22H is associated with low CD4+ cell counts and higher viral loads. Phylogenetic analysis of the vif gene indicated that subtype B was predominant in ∼77% (243/317) of the patients, followed by HIV-1 F ∼18% (56/317) and subtype C ∼4% (12/317); five samples were BF recombinants (∼1% of patients), and one was an AG recombinant...
April 26, 2017: AIDS Research and Human Retroviruses
https://www.readbyqxmd.com/read/28439266/a-novel-regulator-of-activation-induced-cytidine-deaminase-apobecs-in-immunity-and-cancer-schr%C3%A3-dinger-s-catalytic-pocket
#2
REVIEW
Justin J King, Mani Larijani
Activation-induced cytidine deaminase (AID) and its relative APOBEC3 cytidine deaminases boost immune response by mutating immune or viral genes. Because of their genome-mutating activities, AID/APOBECs are also drivers of tumorigenesis. Due to highly charged surfaces, extensive non-specific protein-protein/nucleic acid interactions, formation of polydisperse oligomers, and general insolubility, structure elucidation of these proteins by X-ray crystallography and NMR has been challenging. Hence, almost all available AID/APOBEC structures are of mutated and/or truncated versions...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28429755/opossum-apobec1-is-a-dna-mutator-with-retrovirus-and-retroelement-restriction-activity
#3
Terumasa Ikeda, Mayuko Shimoda, Diako Ebrahimi, John L VandeBerg, Reuben S Harris, Atsushi Koito, Kazuhiko Maeda
APOBEC3s (A3s) are single-stranded DNA cytosine deaminases that provide innate immune defences against retroviruses and mobile elements. A3s are specific to eutherian mammals because no direct homologs exist at the syntenic genomic locus in metatherian (marsupial) or prototherian (monotreme) mammals. However, the A3s in these species have the likely evolutionary precursors, the antibody gene deaminase AID and the RNA/DNA editing enzyme APOBEC1 (A1). Here, we used cell culture-based assays to determine whether opossum A1 restricts the infectivity of retroviruses including human immunodeficiency virus type 1 (HIV-1) and the mobility of LTR/non-LTR retrotransposons...
April 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28415995/type-i-interferon-signaling-is-required-for-the-apobec3-rfv3-dependent-neutralizing-antibody-response-but-not-innate-retrovirus-restriction
#4
Bradley S Barrett, Michael S Harper, Sean T Jones, Kejun Guo, Karl J Heilman, Ross M Kedl, Kim J Hasenkrug, Mario L Santiago
BACKGROUND: APOBEC3/Rfv3 restricts acute Friend retrovirus (FV) infection and promotes virus-specific neutralizing antibody (NAb) responses. Classical Rfv3 studies utilized FV stocks containing lactate-dehydrogenase elevating virus (LDV), a potent type I interferon inducer. Previously, we showed that APOBEC3 is required for the anti-FV activity of exogenous IFN-alpha treatment. Thus, type I interferon receptor (IFNAR) signaling may be required for the APOBEC3/Rfv3 response. RESULTS: To test if the APOBEC3/Rfv3 response is dependent on type I IFN signaling, we infected IFNAR knockout versus IFNAR/APOBEC3 double-knockout mice with FV/LDV or LDV-free FV, and evaluated acute FV infection and subsequent NAb titers...
April 17, 2017: Retrovirology
https://www.readbyqxmd.com/read/28405512/high-expression-of-pd-1-ligands-is-associated-with-kataegis-mutational-signature-and-apobec3-alterations
#5
Amélie Boichard, Igor F Tsigelny, Razelle Kurzrock
Immunotherapy with checkpoint inhibitors, such as antibodies blocking the programmed cell-death receptor-1 (PD-1), has resulted in remarkable responses in patients having traditionally refractory cancers. Although response to PD-1 inhibitors correlates with PD-1 ligand (PD-L1 or PD-L2) expression, PD-1 ligand positivity represents only a part of the predictive model necessary for selecting patients predisposed to respond to immunotherapy. We used all genomic, transcriptomic, proteomic and phenotypic data related to 8,475 pan-cancer samples available in The Cancer Genome Atlas (TCGA) and conducted a logistic regression analysis based on a large set of variables, such as microsatellite instability (MSI-H), mismatch repair (MMR) alterations, polymerase δ (POLD1) and polymerase ε (POLE) mutations, activation-induced/apolipoprotein-B editing cytidine deaminases (AID/APOBEC) alterations, lymphocyte markers and mutation burden estimates to determine independent factors that associate with PD-1 ligand overexpression...
2017: Oncoimmunology
https://www.readbyqxmd.com/read/28369637/nmr-based-method-of-small-changes-reveals-how-dna-mutator-apobec3a-interacts-with-its-single-stranded-dna-substrate
#6
Stefan Harjes, Geoffrey B Jameson, Vyacheslav V Filichev, Patrick J B Edwards, Elena Harjes
APOBEC3 proteins are double-edged swords. They deaminate cytosine to uracil in single-stranded DNA and provide protection, as part of our innate immune system, against viruses and retrotransposons, but they are also involved in cancer evolution and development of drug resistance. We report a solution-state model of APOBEC3A interaction with its single-stranded DNA substrate obtained with the 'method of small changes'. This method compares pairwise the 2D 15N-1H NMR spectra of APOBEC3A bearing a deactivating mutation E72A in the presence of 36 slightly different DNA substrates...
March 22, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28336404/mapping-region-of-human-restriction-factor-apobec3h-critical-for-interaction-with-hiv-1-vif
#7
Masaaki Nakashima, Shinya Tsuzuki, Hiroaki Awazu, Akiko Hamano, Ayaka Okada, Hirotaka Ode, Masami Maejima, Atsuko Hachiya, Yoshiyuki Yokomaku, Nobuhisa Watanabe, Hirofumi Akari, Yasumasa Iwatani
The APOBEC3 (A3) family of cellular cytidine deaminases comprises seven members (A, B, C, D, F, G, and H) that potently inhibit retroviral replication. Human immunodeficiency virus type 1 (HIV-1) Vif is a small pleiotropic protein that specifically inactivates these enzymes, targeting them for ubiquitin-mediated proteasomal degradation. A3 Vif-interaction sites are presumed to fall into three distinct types: A3C/D/F, A3G, and A3H. To date, two types of A3G and A3C/D/F sites have been well characterized, whereas the A3H Vif-binding site remains poorly defined...
March 21, 2017: Journal of Molecular Biology
https://www.readbyqxmd.com/read/28331087/feline-immunodeficiency-virus-evolutionarily-acquires-two-proteins-vif-and-protease-capable-of-antagonizing-feline-apobec3
#8
Rokusuke Yoshikawa, Junko S Takeuchi, Eri Yamada, Yusuke Nakano, Naoko Misawa, Yuichi Kimura, Fengrong Ren, Takayuki Miyazawa, Yoshio Koyanagi, Kei Sato
The interplay between viral and host proteins has been well studied to elucidate virus-host interactions and their relevance to virulence. Mammalian genes encode apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3) proteins, which act as intrinsic restriction factors against lentiviruses. To overcome APOBEC3-mediated anti-viral actions, lentiviruses have evolutionarily acquired an accessory protein, viral infectivity factor (Vif), and Vif degrades host APOBEC3 proteins via a ubiquitin/proteasome-dependent pathway...
March 22, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28315663/enhancing-the-catalytic-deamination-activity-of-apobec3c-is-insufficient-to-inhibit-vif-deficient-hiv-1
#9
Ananda Ayyappan Jaguva Vasudevan, Henning Hofmann, Dieter Willbold, Dieter Häussinger, Bernd W Koenig, Carsten Münk
The retroviral restriction factors of the APOBEC3 (A3) cytidine deaminase family catalyze the deamination of cytidines in single-stranded viral DNA. APOBEC3C (A3C) is a strong antiviral factor against viral infectivity factor (vif)-deficient simian immunodeficiency virus Δvif, which is, however, a weak inhibitor against human immunodeficiency virus (HIV)-1 for reasons unknown. The precise link between the antiretroviral effect of A3C and its catalytic activity is incompletely understood. Here, we show that the S61P mutation in human A3C (A3C...
March 16, 2017: Journal of Molecular Biology
https://www.readbyqxmd.com/read/28302150/identification-of-a-tripartite-interaction-between-the-n-terminus-of-hiv-1-vif-and-cbf%C3%AE-that-is-critical-for-vif-function
#10
Belete A Desimmie, Jessica L Smith, Hiroshi Matsuo, Wei-Shau Hu, Vinay K Pathak
BACKGROUND: HIV-1 Vif interacts with the cellular core-binding factor β (CBFβ) and counteracts the protective roles of certain human APOBEC3 (A3) proteins by targeting them for proteasomal degradation. Previous studies have identified some amino acids important for Vif-CBFβ interactions, and recently a co-crystal structure of a pentameric complex of HIV-1 Vif, CBFβ, Cul5, EloB, and EloC was resolved. However, a comprehensive analysis of Vif-CBFβ interactions that are important for Vif function has not been performed...
March 17, 2017: Retrovirology
https://www.readbyqxmd.com/read/28299671/cbf%C3%A3-and-hiv-infection
#11
Dong Young Kim, John D Gross
In order to achieve a persistent infection, viruses must overcome the host immune system. Host restriction factors dominantly block virus transmission, but are subject to down regulation by viral accessory proteins. HIV encodes several accessory factors that overcome different cellular restriction factors. For example, the HIV-1 protein Vif down regulates the human APOBEC3 family of restriction factors by targeting them for proteolysis by the ubiquitin-proteasome pathway. Recently, this function was shown to require the transcription cofactor CBFβ, which acts as a template to assist in Vif folding and allow for assembly of an APOBEC3-targeting E3 ligase complex...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28289235/correction-for-baig-et-al-determinants-of-efficient-degradation-of-apobec3-restriction-factors-by-hiv-1-vif
#12
Tayyba T Baig, Yuqing Feng, Linda Chelico
No abstract text is available yet for this article.
April 1, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28182305/hepatitis-b-virus-covalently-closed-circular-dna-homeostasis-is-independent-of-the-lymphotoxin-pathway-during-chronic-hbv-infection
#13
Marie-Anne Meier, Aleksei Suslov, Sylvia Ketterer, Markus H Heim, Stefan F Wieland
Current treatment options for patients with chronic hepatitis B virus (HBV) infection are not curative as they are not effective in eliminating covalently closed circular DNA (cccDNA). cccDNA is a stable template for HBV transcription in the nucleus of hepatocytes and is thought to be one of the main factors responsible for HBV persistence. Recently, activation of the lymphotoxin beta receptor (LTβR) has been shown to trigger degradation of cccDNA through induction of cytidine deaminases of the APOBEC3 family in HBV cell culture model systems...
February 9, 2017: Journal of Viral Hepatitis
https://www.readbyqxmd.com/read/28122978/conserved-interaction-of-lentiviral-vif-molecules-with-hiv-1-gag-and-differential-effects-of-species-specific-vif-on-virus-production
#14
Wenwen Zheng, Limian Ling, Zhaolong Li, Hong Wang, Yajuan Rui, Wenying Gao, Shaohua Wang, Xing Su, Wei Wei, Xiao-Fang Yu
The virion infectivity factor (Vif) open reading frame is conserved among most lentiviruses. Vif molecules contribute to viral replication by inactivating host antiviral factors, the APOBEC3 cytidine deaminases. However, various species of lentiviral Vif proteins have evolved different strategies for overcoming host APOBEC3. Whether different species of lentiviral Vif proteins still preserve certain common features has not been reported. Here, we show for the first time that diverse lentiviral Vif molecules maintain the ability to interact with the human immunodeficiency virus type 1 (HIV-1) Gag precursor (Pr55(Gag)) polyprotein...
April 1, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28100701/self-cytoplasmic-dna-upregulates-the-mutator-enzyme-apobec3a-leading-to-chromosomal-dna-damage
#15
Rodolphe Suspène, Bianka Mussil, Hélène Laude, Vincent Caval, Noémie Berry, Mohamed S Bouzidi, Valérie Thiers, Simon Wain-Hobson, Jean-Pierre Vartanian
Foreign and self-cytoplasmic DNA are recognized by numerous DNA sensor molecules leading to the production of type I interferons. Such DNA agonists should be degraded otherwise cells would be chronically stressed. Most human APOBEC3 cytidine deaminases can initiate catabolism of cytoplasmic mitochondrial DNA. Using the human myeloid cell line THP-1 with an interferon inducible APOBEC3A gene, we show that cytoplasmic DNA triggers interferon α and β production through the RNA polymerase III transcription/RIG-I pathway leading to massive upregulation of APOBEC3A...
April 7, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28031368/the-structural-interface-between-hiv-1-vif-and-human-apobec3h
#16
Marcel Ooms, Michael Letko, Viviana Simon
Human APOBEC3H (A3H) is a cytidine deaminase that inhibits HIV-1 replication. To evade this restriction, the HIV-1 Vif protein binds A3H and mediates its proteasomal degradation. To date, little information on the Vif-A3H interface has been available. To decipher how both proteins interact, we first mapped the Vif-binding site on A3H by functionally testing a large set of A3H mutants in single-cycle infectivity and replication assays. Our data show that the two A3H α-helixes α3 and α4 represent the Vif-binding site of A3H...
March 1, 2017: Journal of Virology
https://www.readbyqxmd.com/read/27907174/evolutionary-paradigms-from-ancient-and-ongoing-conflicts-between-the-lentiviral-vif-protein-and-mammalian-apobec3-enzymes
#17
Reuben S Harris, Brett D Anderson
No abstract text is available yet for this article.
December 2016: PLoS Pathogens
https://www.readbyqxmd.com/read/27890786/heat-increases-the-editing-efficiency-of-human-papillomavirus-e2-gene-by-inducing-upregulation-of-apobec3a-and-3g
#18
Yang Yang, Hexiao Wang, Xinrui Zhang, Wei Huo, Ruiqun Qi, Yali Gao, Gaofeng Zhang, Bing Song, Hongduo Chen, Xinghua Gao
Apolipoprotein B mRNA-editing catalytic polypeptide (APOBEC) 3 proteins have been identified as potent viral DNA mutators and have broad antiviral activity. In this study, we demonstrated that apolipoprotein B mRNA-editing catalytic polypeptide 3A (A3A) and A3G expression levels were significantly upregulated in human papillomavirus (HPV)-infected cell lines and tissues. Heat treatment resulted in elevated expression of A3A and A3G in a temperature-dependent manner in HPV-infected cells. Correspondingly, HPV-infected cells heat-treated at 44 °C showed accumulated G-to-A or C-to-T mutation in HPV E2 gene...
November 24, 2016: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/27881650/mechanism-of-enhanced-hiv-restriction-by-virion-coencapsidated-cytidine-deaminases-apobec3f-and-apobec3g
#19
Anjuman Ara, Robin P Love, Tyson B Follack, Khawaja A Ahmed, Madison B Adolph, Linda Chelico
The APOBEC3 (A3) enzymes, A3G and A3F, are coordinately expressed in CD4(+) T cells and can become coencapsidated into HIV-1 virions, primarily in the absence of the viral infectivity factor (Vif). A3F and A3G are deoxycytidine deaminases that inhibit HIV-1 replication by inducing guanine-to-adenine hypermutation through deamination of cytosine to form uracil in minus-strand DNA. The effect of the simultaneous presence of both A3G and A3F on HIV-1 restriction ability is not clear. Here, we used a single-cycle infectivity assay and biochemical analyses to determine if coencapsidated A3G and A3F differ in their restriction capacity from A3G or A3F alone...
February 1, 2017: Journal of Virology
https://www.readbyqxmd.com/read/27825961/repression-of-microrna-function-mediates-inflammation-associated-colon-tumorigenesis
#20
Takeshi Yoshikawa, Jianfeng Wu, Motoyuki Otsuka, Takahiro Kishikawa, Nobumi Suzuki, Akemi Takata, Motoko Ohno, Rei Ishibashi, Mari Yamagami, Ryo Nakagawa, Naoya Kato, Masaaki Miyazawa, Jiahuai Han, Kazuhiko Koike
BACKGROUND & AIMS: Little is known about the mechanisms by which chronic inflammation contributes to carcinogenesis, such as the development of colon tumors in patients with inflammatory bowel diseases. Specific microRNA (miRNAs) can function as suppressors or oncogenes, and widespread alterations in miRNA expression have been associated with tumorigenesis. We studied whether alterations in miRNA function contribute to inflammation-associated colon carcinogenesis. METHODS: We studied the effects of inflammatory cytokines, such as tumor necrosis factor, interleukin-1α (IL1A), and IL1β (IL1B), on miRNA function, measured by activity of reporter constructs containing miRNA-binding sites in their 3' untranslated regions, in human 293T embryonic kidney, Caco-2, HT29, and HCT116 colon carcinoma cells, as well as dicer(+/+) and dicer(-/-), and Apobec3(+/+) and Apobec3(-/-) mouse embryonic fibroblasts...
November 5, 2016: Gastroenterology
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