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Literature summary for 3.1.26.13 extracted from

  • Delviks-Frankenberry, K.A.; Nikolenko, G.N.; Pathak, V.K.
    The connection between HIV drug resistance and RNase H (2010), Viruses, 2, 1476-1503.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.1.26.13

Protein Variants

Protein Variants Comment Organism
A360I mutation in the connection domain, the mutation significantly contributes to zidovudine resistance Human immunodeficiency virus 1
A360K naturally occuring mutation in HIV infection patients, the mutation increases zidovudine resistance and decreased reverse trancriptase template switching Human immunodeficiency virus 1
A360V mutation in the connection domain, the mutation significantly contributes to zidovudine resistance Human immunodeficiency virus 1
A371V mutation in the connection domain Human immunodeficiency virus 1
A376S mutation in the connection domain, the mutation significantly contributes to zidovudine resistance Human immunodeficiency virus 1
A400T mutation in the connection domain Human immunodeficiency virus 1
A554K naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
A554L naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
A554T naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
D67N thymidine analogue mutation, TAMs, arising with zidovudine and stavudine treatment, take the TAM-2 pathway Human immunodeficiency virus 1
E312Q mutation in the connection domain, the mutation significantly contributes to zidovudine resistance Human immunodeficiency virus 1
E396A naturally occuring mutation in HIV infection patients, the mutation increases zidovudine resistance and decreased reverse trancriptase template switching Human immunodeficiency virus 1
E399D mutation in the connection domain Human immunodeficiency virus 1
G333D mutation in the connection domain Human immunodeficiency virus 1
G333E mutation in the connection domain Human immunodeficiency virus 1
G335C mutation in the connection domain, the mutation significantly contributes to zidovudine resistance Human immunodeficiency virus 1
G335D mutation in the connection domain, the mutation significantly contributes to zidovudine resistance Human immunodeficiency virus 1
G359A naturally occuring mutation in HIV infection patients, the mutation increases zidovudine resistance and decreased reverse trancriptase template switching Human immunodeficiency virus 1
I505A naturally occuring mutation in HIV infection patients, the mutation increases zidovudine resistance and decreased reverse trancriptase template switching Human immunodeficiency virus 1
K219E thymidine analogue mutation, TAMs, arising with zidovudine and stavudine treatment, take the TAM-2 pathway Human immunodeficiency virus 1
K219N thymidine analogue mutation, TAMs, arising with zidovudine and stavudine treatment, take the TAM-2 pathway Human immunodeficiency virus 1
K219Q thymidine analogue mutation, TAMs, arising with zidovudine and stavudine treatment, take the TAM-2 pathway Human immunodeficiency virus 1
K390A naturally occuring mutation in HIV infection patients, the mutation increases zidovudine resistance and decreased reverse trancriptase template switching Human immunodeficiency virus 1
K395A naturally occuring mutation in HIV infection patients, the mutation increases zidovudine resistance and decreased reverse trancriptase template switching Human immunodeficiency virus 1
K476A naturally occuring mutation in HIV infection patients, the mutation increases zidovudine resistance and decreased reverse trancriptase template switching Human immunodeficiency virus 1
K558E naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, associated with an increase in thymidine analogue mutations, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
K558G naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, associated with an increase in thymidine analogue mutations, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
K558R naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, associated with an increase in thymidine analogue mutations, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
K65R naturally occuring mutation in HIV infection patients, arises with abacavir, didanosine, emtricitabine, lamivudine, or tenofovir disoproxil fumarate treatment Human immunodeficiency virus 1
K70R naturally occuring mutation in HIV infection patients, is common to stavudine, tenofovir disoproxil fumarate, and zidovudine therapy Human immunodeficiency virus 1
K70R thymidine analogue mutation, TAMs, arising with zidovudine and stavudine treatment, take the TAM-2 pathway Human immunodeficiency virus 1
L210W thymidine analogue mutation, TAMs, arising with zidovudine and stavudine treatment, take the TAM-1 pathway Human immunodeficiency virus 1
L469H naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
L469I naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
L469M naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
L469T naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
M184V naturally occuring mutation in HIV infection patients, arises with abacavir, emtricitabine, or lamivudine treatment Human immunodeficiency virus 1
M41L thymidine analogue mutation, TAMs, arising with zidovudine and stavudine treatment, take the TAM-1 pathway Human immunodeficiency virus 1
N348I mutation in the connection domain, the mutation significantly contributes to zidovudine resistance Human immunodeficiency virus 1
Q475A naturally occuring mutation in HIV infection patients, the mutation increases zidovudine resistance and decreased reverse trancriptase template switching Human immunodeficiency virus 1
Q509L mutation in the RNase H domain, the mutation significantly contributes to zidovudine resistance Human immunodeficiency virus 1
T215F thymidine analogue mutation, TAMs, arising with zidovudine and stavudine treatment, take the TAM-2 pathway Human immunodeficiency virus 1
T215Y thymidine analogue mutation, TAMs, arising with zidovudine and stavudine treatment, take the TAM-1 pathway Human immunodeficiency virus 1
T369I mutation in the connection domain Human immunodeficiency virus 1
T470E naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
T470K naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
T470P naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
T470S naturally occuring mutation in HIV infection patients, the mutation renders the patient more prevalent amongst treatment-experienced patients, treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors Human immunodeficiency virus 1
T473M naturally occuring mutation in HIV infection patients, the mutation increases zidovudine resistance and decreased reverse trancriptase template switching Human immunodeficiency virus 1
V365I mutation in the connection domain, the mutation significantly contributes to zidovudine resistance Human immunodeficiency virus 1
Y318F mutation in the connection domain Human immunodeficiency virus 1
Y501A naturally occuring mutation in HIV infection patients, the mutation increases zidovudine resistance and decreased reverse trancriptase template switching Human immunodeficiency virus 1

Inhibitors

Inhibitors Comment Organism Structure
Abacavir a nucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1
delaviridine a nonnucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1
didanosine a nucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1
efavirenz a nonnucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1
Emtricitabine a nucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1
Etravirine a nonnucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1
lamivudine a nucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1
additional information C-terminal domain mutations reduce RNase H activity either directly by affecting the RNase H cleavage activity of the enzyme, or indirectly by affecting the overall positioning of the template/primer strand, which in turn affects RNase H activity, template switching, polymerization and/or nucleotide excision. Effects of enzyme mutations on treatment with nucleoside reverse transcriptase inhibitors and nonnucleoside reverse transcriptase inhibitors, detailed overview. Nucleoside reverse transcriptase inhibitors are nucleoside analogues that lack the 3' OH on the sugar ring and competitively block reverse transcription by causing chain termination during DNA polymerization. Nucleoside reverse transcriptase inhibitors are prodrugs that require intracellular phosphorylation to the 5'-triphosphate formed by host cell kinases in order to become active. Nonnucleoside reverse transcriptase inhibitors in general are non-competitive inhibitors of RT that bind to a hydrophobic pocket near the polymerase active site, inducing conformational changes that inhibit RT enzymatic activity. Inhibition mechanisms of the two inhibitor classes, overview Human immunodeficiency virus 1
nevirapine a nonnucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1
stavudine a nucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1
tenofovir disoproxil a nucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1
zalcitabine a nucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1
zidovudine a nucleoside reverse transcriptase inhibitor Human immunodeficiency virus 1

Organism

Organism UniProt Comment Textmining
Human immunodeficiency virus 1
-
 HIV-1
-
Human immunodeficiency virus 1 HXB2
-
 HIV-1
-

Synonyms

Synonyms Comment Organism
RNase H
-
 Human immunodeficiency virus 1

General Information

General Information Comment Organism
malfunction patients treated with nucleoside reverse transcriptase inhibitors develop classical patterns of resistance-associated mutations in the pol domain. Thymidine analogue mutations, TAMs, arise with zidovudine and stavudine treatment, which encompass M41L, D67N, K70R, L210W, T215F/Y, and K219Q/E/N. Different patterns of thymidine analogue mutations accumulate in patients, which segregate into two distinct pathways named TAM-1 and TAM-2. The TAM-1 pathway includes M41L, L210W and T215Y, whereas the TAM-2 pathway includes D67N, K70R, T215F and K219Q/E/N Human immunodeficiency virus 1
additional information RT is a unique viral protein containing two enzymatic properties, i.e. RNase H cleavage activity and RNA- and DNA-dependent DNA polymerase activity Human immunodeficiency virus 1