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. 2001 Jan;75(2):1092.

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 1, Lingxun Duan 1, Minghua Zhu 1, Baocheng Hu 1, Satoshi Kubota 1, Omar Bagasra 1, Roger J Pomerantz 1
PMCID: PMC114012

Volume 70, no. 5, p. 3290–3297, 1996.

The following correction applies to all of the above articles and to the Authors' Correction published in the April 1998 issue of the Journal of Virology (72:3505–3506):

In attempts to re-evaluate our previously reported data on inhibition of HIV-1 by intracellular single chain variable fragments (SFvs), some original data were not able to be located and some other data might not be fully consistent with certain previously published graphs. Therefore, we have now completed extensive new experimentation involving the anti-HIV-1 single chain variable fragments (SFvs), including Rev (D8), Integrase (IN33), and Reverse Transcriptase SFvs, described by our laboratories. In these repeat studies, the multiplicity of infections (mois) used in viral challenge studies were estimated by tissue culture infectious dose 50% (TCID50) per target cell, calculated via a described technique (Techniques in HIV Research, Eds. Aldovini, A. and Walker, B., 1990). The mois of viral input which led to complete or near complete protection of SUPT1 T-cells transduced with the anti-HIV-1-SFvs varied between 0.00004 to 0.00002. These were somewhat lower than those described in the initial reports (utilizing HIV-1NL4-3). Nevertheless, the levels of viral growth in control cultures, in the previously published reports and in the new studies, were very similar. Many of the new studies actually showed higher viral growth in control cultures, with complete viral suppression in the SFv-transduced cultures, as compared to the previously published data. As such, only the moi numbers seem to differ but not the robustness of protection against HIV-1 growth by these intracellular anti-HIV-1-SFvs. In addition, we have recently shown the specificity of post-integration inhibition of HIV-1 by the RevD8-SFv in latently infected cells (AIDS Res. & Human Retro. 14:1573, 1998). Binding studies for D8RevSFv against recombinant Rev protein were also repeated by ELISA and showed binding above the background and negative control levels. Intracellular specific binding was also demonstrated by another group utilizing our IN33SFv (PNAS 96:11723, 1999). Our recent results are consistent with our previously published studies in that they confirm that SFvs to HIV-1 Rev, Reverse Transcriptase and Integrase are able to specifically and significantly inhibit HIV-1 replication compared to control cultures. * Publisher's Note: The Authors' Correction for these three articles was published at the request of various governmental and nongovernmental bodies. Because it was submitted in a form specifically agreed upon by the requestors, ASM was not permitted to edit the Correction to confirm with the stylistic conventions set forth in the JVI Instructions to Authors or with the standards of English usage normally found in the Journal. In addition, signed letters of agreement to publish this Author's Correction were provided by some but not all authors of the original manuscripts.


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