Deletion mutagenesis within the dimerization initiation site of human immunodeficiency virus type 1 results in delayed processing of the p2 peptide from precursor proteins.

@article{Liang1999DeletionMW,
  title={Deletion mutagenesis within the dimerization initiation site of human immunodeficiency virus type 1 results in delayed processing of the p2 peptide from precursor proteins.},
  author={Chen Liang and Liwei Rong and Elizabeth Cherry and Lawrence S. Kleiman and M. Laughrea and Mark A. Wainberg},
  journal={Journal of virology},
  year={1999},
  volume={73 7},
  pages={
          6147-51
        }
}
Previous work has shown that deletions of genomic segments at nucleotide (nt) positions +238 to +253, i.e., construct BH10-LD3, or nt positions +261 to +274, i.e., construct BH10-LD4, within the human immunodeficiency virus type 1 (HIV-1) dimerization initiation site (DIS) destroyed DIS secondary structure and dramatically reduced viral replication capacity. Surprisingly, two point mutations located within the viral peptide 2 (p2) and nucleocapsid (NC) protein termed MP2 and MNC, respectively… CONTINUE READING
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