Integrase Strand Transfer Inhibitors
Integrase Strand Transfer Inhibitors - Related Videos
05:46
Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
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Cited by 15 •
2014
Here we describe cellular cytotoxicity and single round infectivity assays that allow for the rapid and accurate screening of compounds to determine their cellular cytotoxicity (CC50) and IC50 values against WT and drug resistant HIV-1.
03:45
Purification of Viral Integrase Using Affinity Chromatography
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2026
Source: Lopez Jr., M. A., et al. Detection and Removal of Nuclease Contamination During Purification of Recombinant Prototype Foamy Virus Integrase. J. Vis. Exp. (2017)This video demonstrates the purification of polyhistidine-tagged viral integrase using nickel affinity chromatography. The protocol uses imidazole gradient elution to selectively isolate the integrase based on its affinity for nickel-charged resin.
02:21
Purification of Viral Integrase Using Heparin Affinity Chromatography
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2026
Source: Lopez Jr., M. et al. Detection and Removal of Nuclease Contamination During Purification of Recombinant Prototype Foamy Virus Integrase. J. Vis. Exp. (2017)This video demonstrates the procedure for purifying viral integrase from bacterial nuclease contamination using heparin Sepharose column chromatography followed by SDS-PAGE analysis to confirm protein purity.
07:50
Detection and Removal of Nuclease Contamination During Purification of Recombinant Prototype Foamy Virus Integrase
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Cited by 10 •
2017
Recombinant prototype foamy virus integrase protein is often contaminated with a bacterial nuclease during purification. This method identifies nuclease contamination and removes it from the final preparation of the enzyme.
08:21
Site-specific Bacterial Chromosome Engineering: ΦC31 Integrase Mediated Cassette Exchange (IMCE)
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Cited by 11 •
2012
A quick and efficient method to integrate foreign DNA of interest into pre-made acceptor strains, termed landing pad strains, is described. The method allows site-specific integration of a DNA cassette into the engineered landing pad locus of a given strain, through conjugation and expression of the ΦC31 integrase.
FAQs
Integrase strand transfer inhibitors act at HIV integrase’s catalytic site, where they chelate essential magnesium ions. This metal-ion interaction prevents the strand-transfer reaction from joining viral DNA to cellular DNA. Blocking that reaction interrupts a required molecular transition in infection, so the virus cannot proceed normally toward stable integration within the host-cell genome.
Strand transfer is a strategic target because it links the viral replication process to the host-cell genome. Preventing this joining reaction acts before infection becomes established in that genomic form, rather than merely addressing later consequences. This explains why inhibiting integrase can contribute to rapid suppression of HIV replication when the inhibitor is included in combination antiretroviral therapy.
Drug resistance, adherence, pharmacokinetics, and interactions with host immune responses are distinct variables that guide treatment strategies. Together, they help explain why a regimen’s ability to suppress HIV replication cannot be judged from its molecular target alone. These considerations are especially important when evaluating treatment performance across patients or experimental settings.
Use of these agents is framed within combination antiretroviral therapy rather than as an isolated intervention. A treatment strategy therefore pairs integrase inhibition with other antiretroviral activity, then considers factors such as adherence, pharmacokinetics, resistance, and immune interactions. This combination-based approach is relevant when the goal is effective and sustained control of HIV replication.
Rapid viral suppression is the principal treatment outcome associated with these agents in combination therapy. Its importance extends beyond virologic control: suppression is linked in the overview to reduced risk of disease progression and transmission. Consequently, investigators can assess these drugs both as antiviral interventions and as tools for studying broader immunology and infection questions.
Their subject-specific value comes from connecting a viral enzyme target with host-level consequences. Studies can examine how blocking integration and suppressing replication relates to disease progression, transmission risk, and host immune responses. This makes the drugs relevant not only to antiretroviral treatment, but also to research on infection control and the relationship between viral replication and immunity.