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Literature summary for 3.1.26.13 extracted from

  • Nikolenko, G.; Palmer, S.; Maldarelli, F.; Mellors, J.; Coffin, J.; Pathak, V.
    Mechanism for nucleoside analog-mediated abrogation of HIV-1 replication: Balance between RNase H activity and nucleotide excision (2005), Proc. Natl. Acad. Sci. USA, 102, 2093-2098.
    View publication on PubMedView publication on EuropePMC
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Application

Application Comment Organism
pharmacology mutations in RNase H can significantly contribute to drug resistance either alone or in combination with nucleoside reverse transcriptase inhibitor-resistance mutations in reverse transcriptase. There exists an equilibrium between nucleoside reverse transcriptase inhibitor incorporation, nucleoside reverse transcriptase inhibitor excision, and resumption of DNA synthesis and degradation of the RNA template by RNase H activity, leading to dissociation of the template-primer and abrogation of HIV-1 replication Human immunodeficiency virus 1

Protein Variants

Protein Variants Comment Organism
D549N mutation increases the 3'-azido-3'-deoxythymidine concentration needed to inhibit viral replication by 50% 12fold by increasing the time available for excision of incorporated nucleoside reverse transcriptase inhibitors from terminated primers and results in 5- to 10fold reduction in viral titers in a single-replication cycle assay Human immunodeficiency virus 1
H539N increases the 3'-azido-3'-deoxythymidine concentration needed to inhibit viral replication by 50% 180fold relative to wild-type by increasing the time available for excision of incorporated nucleoside reverse transcriptase inhibitors from terminated primers Human immunodeficiency virus 1

Organism

Organism UniProt Comment Textmining
Human immunodeficiency virus 1
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