Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease

Human APOBEC3H has several haplotypes and splice variants with distinct anti-HIV-1 activities, but the genetics underlying the expression of these variants are unclear. Here, the authors identify an intronic deletion in A3H haplotype II resulting in production of the most active splice variant, whic...

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Main Authors:	Diako Ebrahimi, Christopher M. Richards, Michael A. Carpenter, Jiayi Wang, Terumasa Ikeda, Jordan T. Becker, Adam Z. Cheng, Jennifer L. McCann, Nadine M. Shaban, Daniel J. Salamango, Gabriel J. Starrett, Jairam R. Lingappa, Jeongsik Yong, William L. Brown, Reuben S. Harris
Format:	Article
Language:	English
Published:	Nature Publishing Group 2018-10-01
Series:	Nature Communications
Online Access:	https://doi.org/10.1038/s41467-018-06594-3

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spelling	doaj-ea3b48a2ed974a7c8e6b38190a93470e2021-05-11T10:16:10ZengNature Publishing GroupNature Communications2041-17232018-10-019111110.1038/s41467-018-06594-3Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 proteaseDiako Ebrahimi0Christopher M. Richards1Michael A. Carpenter2Jiayi Wang3Terumasa Ikeda4Jordan T. Becker5Adam Z. Cheng6Jennifer L. McCann7Nadine M. Shaban8Daniel J. Salamango9Gabriel J. Starrett10Jairam R. Lingappa11Jeongsik Yong12William L. Brown13Reuben S. Harris14Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartments of Global Health, Medicine and Pediatrics, University of WashingtonDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaDepartment of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of MinnesotaHuman APOBEC3H has several haplotypes and splice variants with distinct anti-HIV-1 activities, but the genetics underlying the expression of these variants are unclear. Here, the authors identify an intronic deletion in A3H haplotype II resulting in production of the most active splice variant, which is counteracted by HIV-1 protease.https://doi.org/10.1038/s41467-018-06594-3
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Diako Ebrahimi Christopher M. Richards Michael A. Carpenter Jiayi Wang Terumasa Ikeda Jordan T. Becker Adam Z. Cheng Jennifer L. McCann Nadine M. Shaban Daniel J. Salamango Gabriel J. Starrett Jairam R. Lingappa Jeongsik Yong William L. Brown Reuben S. Harris
spellingShingle	Diako Ebrahimi Christopher M. Richards Michael A. Carpenter Jiayi Wang Terumasa Ikeda Jordan T. Becker Adam Z. Cheng Jennifer L. McCann Nadine M. Shaban Daniel J. Salamango Gabriel J. Starrett Jairam R. Lingappa Jeongsik Yong William L. Brown Reuben S. Harris Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease Nature Communications
author_facet	Diako Ebrahimi Christopher M. Richards Michael A. Carpenter Jiayi Wang Terumasa Ikeda Jordan T. Becker Adam Z. Cheng Jennifer L. McCann Nadine M. Shaban Daniel J. Salamango Gabriel J. Starrett Jairam R. Lingappa Jeongsik Yong William L. Brown Reuben S. Harris
author_sort	Diako Ebrahimi
title	Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease
title_short	Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease
title_full	Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease
title_fullStr	Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease
title_full_unstemmed	Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease
title_sort	genetic and mechanistic basis for apobec3h alternative splicing, retrovirus restriction, and counteraction by hiv-1 protease
publisher	Nature Publishing Group
series	Nature Communications
issn	2041-1723
publishDate	2018-10-01
description	Human APOBEC3H has several haplotypes and splice variants with distinct anti-HIV-1 activities, but the genetics underlying the expression of these variants are unclear. Here, the authors identify an intronic deletion in A3H haplotype II resulting in production of the most active splice variant, which is counteracted by HIV-1 protease.
url	https://doi.org/10.1038/s41467-018-06594-3
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Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease

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