Potent Inhibition of Human Immunodeficiency Virus Type 1 in Primary T Cells and Alveolar Macrophages by a Combination Anti-Rev Strategy Delivered in an Adeno-Associated Virus Vector AUTHORS’ CORRECTION (5 articles) Nuclear Preservation and Cytoplasmic Degradation of Human Immunodeficiency Virus Type 1 Rev Protein SATOSHI KUBOTA, LINGXUN DUAN, RIKA A. FURUTA, MASAKAZU HATANAKA, AND ROGER J. POMERANTZ The Dorrance H. Hamilton Laboratories, Section of Molecular Retrovirology, Division of Infectious Diseases, Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania, and Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606-01, Japan Volume 70, no. 2, p. 1282–1287. Binding of Intracellular Anti-Rev Single Chain Variable Fragments to Different Epitopes of Human Immunodeficiency Virus Type 1 Rev: Variations in Viral Inhibition YONG WU, LINGXUN DUAN, MINGHUA ZHU, BAOCHENG HU, SATOSHI KUBOTA, OMAR BAGASRA, AND ROGER J. POMERANTZ The Dorrance H. Hamilton Laboratories, Center for Human Retrovirology, Division of Infectious Diseases, Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107 Volume 70, no. 5, p. 3290–3297. Targeting Human Immunodeficiency Virus Type 1 Reverse Transcriptase by Intracellular Expression of Single-Chain Variable Fragments To Inhibit Early Stages of the Viral Life Cycle FARIDA SHAHEEN, LINGXUN DUAN, MINGHUA ZHU, OMAR BAGASRA, AND ROGER J. POMERANTZ The Dorrance H. Hamilton Laboratories, Section of Molecular Retrovirology, Division of Infectious Diseases, Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107 Volume 70, no. 6, p. 3392–3400. Intracellular Expression of Single-Chain Variable Fragments To Inhibit Early Stages of the Viral Life Cycle by Targeting Human Immunodeficiency Virus Type 1 Integrase PNINA LEVY-MINTZ, LINGXUN DUAN, HUIZHONG ZHANG, BAOCHENG HU, GEETHANJALI DORNADULA, MINGHUA ZHU, JOSEPH KULKOSKY, DIANE BIZUB-BENDER, ANNA MARIE SKALKA, AND ROGER J. POMERANTZ Dorrance H. Hamilton Laboratories, Center for Human Virology, Division of Infectious Diseases, Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, and Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111 Volume 70, no. 12, p. 8821–8832. 3505 o n A p ril 5 , 2 0 2 1 a t C A R N E G IE M E L L O N U N IV L IB R h ttp ://jvi.a sm .o rg / D o w n lo a d e d fro m http://jvi.asm.org/ Potent Inhibition of Human Immunodeficiency Virus Type 1 in Primary T Cells and Alveolar Macrophages by a Combination Anti-Rev Strategy Delivered in an Adeno-Associated Virus Vector ROGER T. INOUYE, BIN DU, DEBORAH BOLDT-HOULE, ANTHONY FERRANTE, IN-WOO PARK, SCOTT M. HAMMER, LINGXUN DUAN, JEROME E. GROOPMAN, ROGER J. POMERANTZ, AND ERNEST F. TERWILLIGER Divisions of Experimental Medicine and Hematology/Oncology and Infectious Disease, Beth Israel Deaconess Medical Center and Harvard Institutes of Medicine, Boston, Massachusetts 02215, and Dorrance H. Hamilton Laboratories, Center for Human Virology, Division of Infectious Disease, Thomas Jefferson University, Philadelphia, Pennsylvania 19107 Volume 71, no. 5, p. 4071–4078. The following correction pertains to all of the above articles. The heavy chain of the D8 anti-Rev single-chain variable fragment (SFv) has been reanalyzed and demonstrated to be an aberrant heavy chain sequence. This heavy chain sequence is very close to the aberrant heavy chain sequence published by P. Thammana (Molecular Immunology 31:77–78, 1994), who derived it via RT-PCR directly from the RNA of the NS1 cell line which is commonly used as a fusion partner to construct mouse hybridomas. Therefore, it is likely that the aberrant D8SFv heavy chain was derived from a gene originating from the fusion partner cell line used to make the original D8 hybridoma and not from the heavy chain gene expressed by the B-cell precursor to this hybridoma. This aberrant heavy chain has a deletion in the framework region 3 (FR3) leading to a frameshift in CDR3 and downstream regions of the heavy chain gene. In addition, there were some individual nucleotide changes, on reanalysis, that brought the heavy chain sequence even closer to that described by Thammana. It should also be noted that the function of the aberrant heavy chain in the D8SFv is not known. As well, the initial 12 amino acids in the D8SFv represent a portion of the Vk leader sequence. The possible effects, if any, of this segment on subcellular localization and/or secretion have not been investigated. There was noted to be rather minimal binding data for the D8SFv available to be reevaluated at this time, including only a single ELISA for the D8SFv to recombinant Rev and a single binding study of the activation domain peptide of Rev. Comparisons to the original D8 monoclonal antibody are not obtainable since the characteristics of the original monoclonal antibody are not fully demonstrated at the present time. As well, complete original data dealing with anti-Rev D10SFv binding to peptides of Rev are not available at the present time. On reanalysis, inaccuracies in the D10SFv sequence were noted. D10SFv on resequencing showed the following differences compared to the published sequence: T58 to A (ACA to GCA), T106 to S (ACG to TCG), and G115 to A (GGT to GCT). Nucleotide changes which did not alter the amino acid sequence were: 81C to T, 315G to C, 354T to A, and 357T to A (numbering started at initial ATG codon). A nucleotide was demonstrated to be missing at position 771 (G) (L257), compared to the original sequence, altering the remaining amino acids (DYWGQGTSVTVSSAKTTPPPVYPLAPGS). On reevaluation, the originally reported D10 sequence would connote a frameshift in the CDR3 of Vh, but now, as resequencing revealed the missing nucleotide, the frameshift is shown not to be present. Thus, D10SFv is, in fact, an appropriate antibody sequence. Although further studies are planned, these additional findings do not alter the previous conclusions that intracellular D8 and D10 SFvs inhibit HIV-1. We regret any difficulties these inaccuracies in the original publications may have caused. 3506 AUTHORS’ CORRECTION J. VIROL. o n A p ril 5 , 2 0 2 1 a t C A R N E G IE M E L L O N U N IV L IB R h ttp ://jvi.a sm .o rg / D o w n lo a d e d fro m http://jvi.asm.org/