HIV | Reverse transcriptase | Pseudoknot; RNA | 25 pM | Inhibition of polymerase activity; 95% reduction of HIV particle formation by transient expression of aptamers | [42,63,64] |
HIV | Drug resistant Reverse transcriptase mutant 3 | M302; N-methyl-isatoicanhydride modified RNA | 30 nM | No inhibition of polymerase and RNase H activities | [65] |
HIV | Reverse transcriptase | ODN112; G-quadruplex DNA | N.A. | Inhibition of RNase H and polymerase activities with IC50 = 500 nM; Reduction of viral infectivity in cell culture with IC50 < 100 nM | [66] |
HIV | RNase H domain of Reverse transcriptase | R12-2; Thiolated DNA aptamer | 70 nM | Inhibition of RNase H activity; Reduction of viral infectivity in cell culture with IC50 < 100 nM | [67] |
HIV | Reverse transcriptase | 37NT; DNA | 660 pM | Inhibition of primer-template binding and polymerase activity | [68] |
HIV | Reverse transcriptase | RT1t49; DNA | ~1 nM | Inhibition of polymerase activity with IC50 = 0.3 nM | [69,70] |
HIV | Reverse transcriptase | PF1; DNA | 82 nM | Inhibition of polymerase activity with IC50 = 60 nM | [71] |
HIV | Reverse transcriptase | RU25-80; | N.A. | Inhibition of primer extension with IC50 = 60 nM and viral replication. Dependent on the nonpseudoknot UCAA motif | [72] |
RNA |
HIV | Reverse transcriptase | 6/5 asymmetric loop; | N.A. | Inhibition of primer extension in vitro. | [73] |
RNA | Inhibition of viral replication in cell culture |
HIV | Integrase | 93del; G-quadruplex DNA | N.A. | Inhibition of viral entry, reverse transcriptase and integration activities; Inhibition of cell fusion in cell at 1 µM | [74,75] |
HIV | Integrase | T30695; G-quadruplex DNA | N.A. | Inhibition of integrase activities with IC50 < 100 nM | [76] |
HIV | DP6 truncated Gag lacking p6 and the | DP6-22; RNA | 100 nM | Inhibition of Gag-genomic interactions that negatively affects RNA transcription, processing or stability | [77] |
N-terminal myristate |
HIV | Nucleocapsid | N70-13; RNA | 0.6 nM | Inhibition of nucleocapsid and HIV psi-RNA interaction | [78] |
HIV | Nucleocapsid | N50-20; RNA | 0.5 nM | Not Determined | [79] |
HIV | Gp120 of HIV strain HXB2 | J58; 2' Fluoro modified RNA | 210 nM | No neutralization of infection | [80] |
HIV | Gp120 of HIV-1BAL | B40; 2' Fluoro modified RNA | 21 nM | Inhibition of gp120-CCR5 interactions | |
HIV | Gp120 of HIV-1BAL | UCLA1 (truncated B40); modified RNA with an inverted thymine at 3' end and a dimethoxyltrityloxy-(CH2)6-SS-(CH2)6-phospholinker at 5' end | 150 pM | Neutralization of isolated of R5 strains with IC50 < 100 nM; | [81] |
Synergistic effect with a gp41 fusion inhibitor |
and an anti-CD4 antibody |
HIV | Gp120 of HIV-1BAL | A-1; 2' Fluoro modified RNA | 52 nM | Conjugation with siRNAs targeting HIV tat/rev and TNPO3 to inhibit HIV-1 infection in primary human peripheral blood mononuclear cells and humanized mice | [82,83] |
HIV | Tat-1- derived peptide | RNA Tat; RNA | 120 pM | Competition with TAR for sequestering Tat-1 in cell culture | [84] |
HIV | Rev | RBE(apt); RNA | N.A. | Conjugation with ribozyme targeting HIV Env for gene therapy | [85] |
HIV | TAR | IV04; 2'-O-Methyl modified DNA | 20 nM | Disruption of TAR secondary structure by formation of RNA-DNA kissing complexes | [86] |
HIV | TAR | R-0624; RNA | 32 nM | Formation of TAR RNA-aptamer complexes by 8-nt complementary base-pairing | [87] |
HIV | TAR | a1.16; RNA | 17 nM | Formation of TAR RNA-aptamer complexes by 5-nt complementary base-pairing | [88] |
HIV | TAR | B22; DNA | 50 nM | No inhibition of TAR function | [89] |
HCV | NS3 | G6-16; RNA | 238 nM | Inhibition of protease activity with IC50 = 3 µM | [90] |
HCV | Truncated protease domain of NS3 | G9-I; RNA | 10 nM | Inhibition of protease activity with IC50 = 100 nM | [91] |
HCV | Helicase domain of NS3 | G5; RNA | 25 nM | Inhibition of helicase activity with IC50 = 50 nM | [92] |
HCV | NS5B∆C55 | B.2; RNA | 1.5 nM | Inhibition of HCV RNA polymerase in a non-competitive manner; IC50 = 10 nM | [93] |
HCV | NS5B | 27v; DNA | 132 nM | Competition with the RNA template for binding to the RNA polymerase and blocked both the initiation and the elongation of RNA synthesis; IC50 = 190 nM | [94] |
HCV | NS5B | R-F t1; 2' Fluoro modified RNA | 8 nM | Competition with the RNA template for binding to the RNA polymerase and blocked both the initiation and the elongation of RNA synthesis | [95] |
HCV | NS5B | P-58; RNA | 570 nM | Interference with HCV replication by targeting the essential 5BSL3.2 domain within the cis-acting replication element; IC50 =185 nM | [96] |
HCV | Domain II of IRES | 2-02; RNA | 11 nM | Inhibition of IRES-dependent translation | [97] |
HCV | Domain III-IV of IRES | 3-07; RNA | 9 nM | Inhibition of IRES-dependent translation | [98] |
HCV | Entire IRES | AP50; RNA | 5 nM | Inhibition of IRES-dependent translation | [99,100] |
HBV | Surface antigen | HBs-A22;RNA | N.A. | Inhibition of receptor binding | [101] |
HBV | Truncated polymerase protein | S9; RNA | N.A. | Competition with RNA to inhibit P protein binding to | [102] |
ε signal on pgRNA |
SCoV | Helicase | NG8; Modified DNA | 5 nM | Inhibition of nucleic acid unwinding activity; IC50 = 91.0 nM | [103] |
SCoV | Helicase | ES15; RNA | N.A. | Inhibition of nucleic acid unwinding activity; IC50 = 1.2 nM | [104] |
Influenza A virus | Hemagglutinin [HA-(91-261) from H3N2] | A22; DNA | N.A. | Inhibition of receptor binding; 95% reduction of viruses in mice | [105] |
Influenza A virus | Hemagglutinin | A10; DNA | Strong binding | Inhibition of receptor binding, dose-dependent inhibition demonstrated | [106] |
(HA from H5N1) | measured by ELISA |
Influenza A virus | Whole H3N2 virus | P30-10-16; | 0.2 nM | Inhibition of receptor binding; 95% inhibition of viral fusion efficiencies in the presence of 5 µM aptamers | [107,108] |
[A/Panama(H3N2) strain] | RNA |
Influenza A virus | Hemagglutinin | HA68; DNA | 7 nM | Inhibition of receptor binding; complete inhibition of the agglutination of RBC in the presence of 2.5 µM aptamers | [109] |
(HA from H3N2) |
Influenza A virus | Hemagglutinin | C7; DNA | Strong binding | Inhibition of receptor binding; 55% inhibition of the viral infection | [110] |
[HA-(101-257) from H9N2] | measured by ELISA |
at 1nmol in the cell viability assay |
Influenza A virus | Hemagglutinin | HAS15-5; RNA | Strong binding | Inhibition of receptor binding | [111] |
(HA from H5N1) | using RT-PCR |
Influenza A virus | Hemagglutinin | D-26, 2' Fluoro modified RNA | 67 fM | Inhibition of receptor binding, Complete inhibition of the agglutination of RBC in the presence of 200 nM aptamer | |
(HA from H1N1) |
Influenza B virus | Hemagglutinin (HA from B/Johannesburg strain) | A20; RNA | 0.7 nM | Inhibition of receptor binding; 93% inhibition of viral fusion efficiencies in the presence of 25 µM aptamers | [112] |
Rabies virus | Rabies virus (CVS-11) infected BHK-21 cells | F34; DNA | 28 nM | Inhibition of CVS-11 infectivity with a dose-dependent manner | [113] |
Rabies virus | Rabies virus (CVS-11) infected BHK-21 cells | PEG-FO24; PEGylated DNA | N.A. | 87.5% survival rate of mice inoculated with aptamers for 24 h prior to challenge with rabies virus | [114] |
HPV | HPV16 E7 | G5α3N.4; RNA | 1.9 µM | N.A. | [115] |
HPV | HPV transformed HeLa cells | Aptamer 20, DNA | 1 nM | N.A. | [116] |
HPV | HPV16 E7 | A2; RNA | 107 nM | Induction of apoptosis in HPV infected cancer cells | [117,118] |
HSV-1 | Glycoprotein D protein | Aptamer-1; 2' Fluoro modified RNA | 170 nM | Inhibition of gD protein and HSV-1 | [119] |
target cell receptor (HVEM) interactions, EC50 = 60 nM |
HSV-2 | Glycoprotein D protein | G7a; 2' Fluoro modified RNA | N.A. | Inhibition of receptor binding, IC50 = 20 nM | [120] |