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https://www.readbyqxmd.com/read/29769087/replacement-of-feline-foamy-virus-bet-by-feline-immunodeficiency-virus-vif-yields-replicative-virus-with-novel-vaccine-candidate-potential
#1
Carmen Ledesma-Feliciano, Sarah Hagen, Ryan Troyer, Xin Zheng, Esther Musselman, Dragana Slavkovic Lukic, Ann-Mareen Franke, Daniel Maeda, Jörg Zielonka, Carsten Münk, Guochao Wei, Sue VandeWoude, Martin Löchelt
BACKGROUND: Hosts are able to restrict viral replication to contain virus spread before adaptive immunity is fully initiated. Many viruses have acquired genes directly counteracting intrinsic restriction mechanisms. This phenomenon has led to a co-evolutionary signature for both the virus and host which often provides a barrier against interspecies transmission events. Through different mechanisms of action, but with similar consequences, spumaviral feline foamy virus (FFV) Bet and lentiviral feline immunodeficiency virus (FIV) Vif counteract feline APOBEC3 (feA3) restriction factors that lead to hypermutation and degradation of retroviral DNA genomes...
May 16, 2018: Retrovirology
https://www.readbyqxmd.com/read/29760455/substrate-sequence-selectivity-of-apobec3a-implicates-intra-dna-interactions
#2
Tania V Silvas, Shurong Hou, Wazo Myint, Ellen Nalivaika, Mohan Somasundaran, Brian A Kelch, Hiroshi Matsuo, Nese Kurt Yilmaz, Celia A Schiffer
The APOBEC3 (A3) family of human cytidine deaminases is renowned for providing a first line of defense against many exogenous and endogenous retroviruses. However, the ability of these proteins to deaminate deoxycytidines in ssDNA makes A3s a double-edged sword. When overexpressed, A3s can mutate endogenous genomic DNA resulting in a variety of cancers. Although the sequence context for mutating DNA varies among A3s, the mechanism for substrate sequence specificity is not well understood. To characterize substrate specificity of A3A, a systematic approach was used to quantify the affinity for substrate as a function of sequence context, length, secondary structure, and solution pH...
May 14, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29746834/characterization-of-bk-polyomaviruses-from-kidney-transplant-recipients-suggests-a-role-for-apobec3-in-driving-in-host-virus-evolution
#3
Alberto Peretti, Eileen M Geoghegan, Diana V Pastrana, Sigrun Smola, Pascal Feld, Marlies Sauter, Stefan Lohse, Mayur Ramesh, Efrem S Lim, David Wang, Cinzia Borgogna, Peter C FitzGerald, Valery Bliskovsky, Gabriel J Starrett, Emily K Law, Reuben S Harris, J Keith Killian, Jack Zhu, Marbin Pineda, Paul S Meltzer, Renzo Boldorini, Marisa Gariglio, Christopher B Buck
BK polyomavirus (BKV) frequently causes nephropathy (BKVN) in kidney transplant recipients (KTRs). BKV has also been implicated in the etiology of bladder and kidney cancers. We characterized BKV variants from two KTRs who developed BKVN followed by renal carcinoma. Both patients showed a swarm of BKV sequence variants encoding non-silent mutations in surface loops of the viral major capsid protein. The temporal appearance and disappearance of these mutations highlights the intra-patient evolution of BKV. Some of the observed mutations conferred resistance to antibody-mediated neutralization...
May 9, 2018: Cell Host & Microbe
https://www.readbyqxmd.com/read/29720713/treatment-resistance-in-urothelial-carcinoma-an-evolutionary-perspective
#4
REVIEW
Panagiotis J Vlachostergios, Bishoy M Faltas
The emergence of treatment-resistant clones is a critical barrier to cure in patients with urothelial carcinoma. Setting the stage for the evolution of resistance, urothelial carcinoma is characterized by extensive mutational heterogeneity, which is detectable even in patients with early stage disease. Chemotherapy and immunotherapy both act as selective pressures that shape the evolutionary trajectory of urothelial carcinoma throughout the course of the disease. A detailed understanding of the dynamics of evolutionary drivers is required for the rational development of curative therapies...
May 2, 2018: Nature Reviews. Clinical Oncology
https://www.readbyqxmd.com/read/29716624/reconstruction-of-a-replication-competent-ancestral-murine-endogenous-retrovirus-l
#5
Daniel Blanco-Melo, Robert J Gifford, Paul D Bieniasz
BACKGROUND: About 10% of the mouse genome is composed of endogenous retroviruses (ERVs) that represent a molecular fossil record of past retroviral infections. One such retrovirus, murine ERV-L (MuERV-L) is an env-deficient ERV that has undergone episodic proliferation, with the most recent amplification occurring ~ 2 million years ago. MuERV-L related sequences have been co-opted by mice for antiretroviral defense, and possibly as promoters for some genes that regulate totipotency in early mouse embryos...
May 2, 2018: Retrovirology
https://www.readbyqxmd.com/read/29716522/the-cytidine-deaminase-under-representation-reporter-cdur-as-a-tool-to-study-evolution-of-sequences-under-deaminase-mutational-pressure
#6
Maxwell Shapiro, Stephen Meier, Thomas MacCarthy
BACKGROUND: Activation induced deaminase (AID) and apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3 (APOBEC3) are deaminases that mutate C to U on single-stranded DNA (ssDNA). AID is expressed primarily in germinal center B-cells, where it facilitates affinity maturation and class-switch recombination. APOBEC3 are a family of anti-viral proteins that act as part of the intrinsic immune response. In both cases, there are particular sequence motifs, also known as "mutation motifs", to which these deaminases prefer to bind and mutate...
May 2, 2018: BMC Bioinformatics
https://www.readbyqxmd.com/read/29693745/human-apobec3b-interacts-with-the-heterogenous-nuclear-ribonucleoprotein-a3-in-cancer-cells
#7
Nawneet Mishra, K Sony Reddy, Uddhav Timilsina, Deepak Gaur, Ritu Gaur
Human APOBEC3B (A3B), like other APOBEC3 members, is a cytosine deaminase which causes hypermutation of single stranded genome. Recent studies have shown that A3B is predominantly elevated in multiple cancer tissues and cell lines such as the bladder, cervix, lung, head and neck, and breast. Upregulation and activation of A3B in developing tumors can cause an unexpected cluster of mutations which promote cancer development and progression. The cellular proteins which facilitate A3B function through direct or indirect interactions remain largely unknown...
April 25, 2018: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/29677220/hiv-1-adaptation-studies-reveal-a-novel-env-mediated-homeostasis-mechanism-for-evading-lethal-hypermutation-by-apobec3g
#8
Terumasa Ikeda, Menelaos Symeonides, John S Albin, Ming Li, Markus Thali, Reuben S Harris
HIV-1 replication normally requires Vif-mediated neutralization of APOBEC3 antiviral enzymes. Viruses lacking Vif succumb to deamination-dependent and -independent restriction processes. Here, HIV-1 adaptation studies were leveraged to ask whether viruses with an irreparable vif deletion could develop resistance to restrictive levels of APOBEC3G. Several resistant viruses were recovered with multiple amino acid substitutions in Env, and these changes alone are sufficient to protect Vif-null viruses from APOBEC3G-dependent restriction in T cell lines...
April 20, 2018: PLoS Pathogens
https://www.readbyqxmd.com/read/29653302/jembrana-disease-virus-vif-antagonizes-the-inhibition-of-bovine-apobec3-proteins-through-ubiquitin-mediate-protein-degradation
#9
Xing Su, Hong Wang, Xiaohong Zhou, Zhaolong Li, Baisong Zheng, Wenyan Zhang
Viral infectivity factor (Vif) encoded by lentiviruses is essential for viral replication and escaping from antiviral activity of host defensive factors APOBEC3. Jembrana disease virus (JDV) causes an acute disease syndrome with approximately 20% case fatality rate in Bali cattle. However, the interplay mechanism between JDV Vif and Bos taurus APOBEC3 (btA3) is poorly understood. In this study, we determined that JDV Vif recruits ElonginB, ElonginC(ELOB/C), Cul2 and RBX1 but without the need of CBF-β to form E3 ubiquitin ligase and induces the degradation of btA3 proteins...
April 10, 2018: Virology
https://www.readbyqxmd.com/read/29642583/feline-apobec3s-barriers-to-cross-species-transmission-of-fiv
#10
REVIEW
Zeli Zhang, Qinyong Gu, Daniela Marino, Kyeong-Lim Lee, Il-Keun Kong, Dieter Häussinger, Carsten Münk
The replication of lentiviruses highly depends on host cellular factors, which defines their species-specific tropism. Cellular restriction factors that can inhibit lentiviral replication were recently identified. Feline immunodeficiency virus (FIV) was found to be sensitive to several feline cellular restriction factors, such as apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3 (APOBEC3) and tetherin, but FIV evolved to counteract them. Here, we describe the molecular mechanisms by which feline APOBEC3 restriction factors inhibit FIV replication and discuss the molecular interaction of APOBEC3 proteins with the viral antagonizing protein Vif...
April 10, 2018: Viruses
https://www.readbyqxmd.com/read/29620931/prevalence-of-drug-resistance-mutations-in-protease-reverse-transcriptase-and-integrase-genes-of-north-central-mexico-hiv-isolates
#11
Pedro G Hernandez-Sanchez, Sandra E Guerra-Palomares, Jose Luis Ramirez-GarciaLuna, J Rafael Arguello, Daniel E Noyola, Christian Alberto Garcia-Sepulveda
This study set out to determine the frequency of antiretroviral drug resistance mutations in treatment-naïve subjects of the north central Mexican state of San Luis Potosí. Mexican studies of antiretroviral drug resistance mutations have focused mainly on large metropolitan areas and border towns subjected to intense international migrations. This study set forth to describe the frequency of these mutations in a Mexican region less subjected to such migratory influences and more representative of smaller Mexican cities...
March 12, 2018: AIDS Research and Human Retroviruses
https://www.readbyqxmd.com/read/29618650/siv-mac239-vif-and-human-apobec3b-interactions-resemble-those-between-hiv-1-vif-and-human-apobec3g
#12
Jiayi Wang, Nadine M Shaban, Allison M Land, William L Brown, Reuben S Harris
Several members of the APOBEC3 DNA cytosine deaminase family can potently inhibit Vif-deficient HIV-1 by catalyzing cytosine deamination in viral cDNA and impeding reverse transcription. HIV-1 counteracts restriction with the virally encoded Vif protein, which targets relevant APOBEC3 proteins for proteasomal degradation. HIV-1 Vif is optimized for degrading the restrictive human APOBEC3 repertoire and, in general, lentiviral Vif proteins specifically target the restricting APOBEC3 enzymes of each host species...
April 4, 2018: Journal of Virology
https://www.readbyqxmd.com/read/29617834/differential-evolution-of-antiretroviral-restriction-factors-in-pteropid-bats-as-revealed-by-apobec3-gene-complexity
#13
Joshua A Hayward, Mary Tachedjian, Jie Cui, Adam Z Cheng, Adam Johnson, Michelle Baker, Reuben S Harris, Lin-Fa Wang, Gilda Tachedjian
Bats have attracted attention in recent years as important reservoirs of viruses deadly to humans and other mammals. These infections are typically nonpathogenic in bats raising questions about innate immune differences that might exist between bats and other mammals. The APOBEC3 gene family encodes antiviral DNA cytosine deaminases with important roles in the suppression of diverse viruses and genomic parasites. Here we characterize pteropid APOBEC3 genes and show that species within the genus Pteropus possess the largest and most diverse array of APOBEC3 genes identified in any mammal reported to date...
March 29, 2018: Molecular Biology and Evolution
https://www.readbyqxmd.com/read/29611801/a-naturally-occurring-feline-apobec3-variant-that-loses-anti-lentiviral-activity-by-lacking-two-amino-acid-residues
#14
Yoriyuki Konno, Shumpei Nagaoka, Izumi Kimura, Mahoko Takahashi Ueda, Ryuichi Kumata, Jumpei Ito, So Nakagawa, Tomoko Kobayashi, Yoshio Koyanagi, Kei Sato
Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3) is a mammalian protein that restricts lentiviral replication. Various polymorphisms of mammalian APOBEC3 genes have been observed in humans, Old World monkeys and domestic cats; however, the genetic diversity of APOBEC3 genes in other mammals remains unaddressed. Here we identify a novel haplotype of the feline APOBEC3Z3 gene, an APOBEC3 gene that restricts feline immunodeficiency virus (FIV) replication, in a Eurasian lynx (Lynx lynx)...
April 3, 2018: Journal of General Virology
https://www.readbyqxmd.com/read/29609878/a-new-class-of-antiretroviral-enabling-innate-immunity-by-protecting-apobec3-from-hiv-vif-dependent-degradation
#15
REVIEW
Ryan P Bennett, Jason D Salter, Harold C Smith
The infectivity of HIV depends on overcoming APOBEC3 (A3) innate immunity, predominantly through the expression of the viral protein Vif, which induces A3 degradation in the proteasome. Disruption of the functional interactions of Vif enables A3 mutagenesis of the HIV genome during viral replication, which can result in a broadly neutralizing antiviral effect. Vif function requires self-association along with interactions with A3 proteins, protein chaperones, and factors of the ubiquitination machinery and these are described here as a potential platform for novel antiviral drug discovery...
March 30, 2018: Trends in Molecular Medicine
https://www.readbyqxmd.com/read/29605684/mouse-apobec3-expression-in-nih-3t3-cells-mediates-hypermutation-of-akv-murine-leukemia-virus
#16
Stefano Boi, Morgan E Ferrell, Ming Zhao, Kim J Hasenkrug, Leonard H Evans
Mouse APOBEC3 (mA3) is a cytidine deaminase that can act on the single-stranded DNA reverse transcripts of retroviruses resulting in G→A hypermutation of proviral DNA. Many mA3 studies have used NIH 3T3 cells assuming that endogenous mA3 production was negligible. We developed a monoclonal antibody specific for mA3 that reveals detectable mA3 in NIH 3T3 cells and we demonstrate that AKV released from the cells undergoes G→A hypermutation. Inactivation of the mA3 gene abolished the deamination confirming that AKV hypermutation was mediated by mA3...
March 29, 2018: Virology
https://www.readbyqxmd.com/read/29593034/deaminase-dead-mouse-apobec3-is-an-in-vivo-retroviral-restriction-factor
#17
Spyridon Stavrou, Wenming Zhao, Kristin Blouch, Susan R Ross
The apolipoprotein B editing complex 3 (APOBEC3) proteins are potent retroviral restriction factors that are under strong positive selection, both in terms of gene copy number and sequence diversity. A common feature of all the members of the APOBEC3 family is the presence of one or two cytidine deamination domains, essential for cytidine deamination of retroviral reverse transcripts as well as packaging into virions. Several studies have indicated that human and mouse APOBEC3 restrict retrovirus infection via cytidine deaminase (CD)-dependent and -independent means...
March 28, 2018: Journal of Virology
https://www.readbyqxmd.com/read/29555777/expansions-diversification-and-interindividual-copy-number-variations-of-aid-apobec-family-cytidine-deaminase-genes-in-lampreys
#18
Stephen J Holland, Lesley M Berghuis, Justin J King, Lakshminarayan M Iyer, Katarzyna Sikora, Heather Fifield, Sarah Peter, Emma M Quinlan, Fumiaki Sugahara, Prashant Shingate, Inês Trancoso, Norimasa Iwanami, Elena Temereva, Christine Strohmeier, Shigeru Kuratani, Byrappa Venkatesh, Guillaume Evanno, L Aravind, Michael Schorpp, Mani Larijani, Thomas Boehm
Cytidine deaminases of the AID/APOBEC family catalyze C-to-U nucleotide transitions in mRNA or DNA. Members of the APOBEC3 branch are involved in antiviral defense, whereas AID contributes to diversification of antibody repertoires in jawed vertebrates via somatic hypermutation, gene conversion, and class switch recombination. In the extant jawless vertebrate, the lamprey, two members of the AID/APOBEC family are implicated in the generation of somatic diversity of the variable lymphocyte receptors (VLRs). Expression studies linked CDA1 and CDA2 genes to the assembly of VLRA /C genes in T-like cells and the VLRB genes in B-like cells, respectively...
March 19, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29550589/non-lytic-lymphocytes-engineered-to-express-virus-specific-t-cell-receptors-limit-hbv-infection-by-activating-apobec3
#19
Sarene Koh, Janine Kah, Christine Y L Tham, Ninghan Yang, Erica Ceccarello, Adeline Chia, Margaret Chen, Atefeh Khakpoor, Andrea Pavesi, Anthony T Tan, Maura Dandri, Antonio Bertoletti
BACKGROUND & AIMS: Strategies to develop virus-specific T cells against hepatic viral infections have been hindered by safety concerns. We engineered non-lytic human T cells to suppress replication of hepatitis B virus (HBV) and hepatitis C virus (HCV) without overt hepatotoxicity, and investigated their antiviral activity. METHODS: We electroporated resting T cells or T cells activated by anti-CD3 with mRNAs encoding HBV or HCV-specific T-cell receptors (TCRs) to create 2 populations of TCR-reprogrammed T cells...
March 14, 2018: Gastroenterology
https://www.readbyqxmd.com/read/29491387/understanding-the-structure-multimerization-subcellular-localization-and-mc-selectivity-of-a-genomic-mutator-and-anti-hiv-factor-apobec3h
#20
Fumiaki Ito, Hanjing Yang, Xiao Xiao, Shu-Xing Li, Aaron Wolfe, Brett Zirkle, Vagan Arutiunian, Xiaojiang S Chen
APOBEC3H (A3H) is a member of the APOBEC3 subfamily of DNA cytosine deaminases that are important for innate immune defense and have been implicated in cancer biogenesis. To understand the structural basis for A3H biochemical function, we determined a high-resolution structure of human A3H and performed extensive biochemical analysis. The 2.49 Å crystal structure reveals a uniquely long C-terminal helix 6 (h6), a disrupted β5 strand of the canonical five-stranded β-sheet core, and a long loop 1 around the Zn-active center...
February 28, 2018: Scientific Reports
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