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Related Concept Videos

Inhibitors of Virion Maturation and Assembly01:19

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...
Antiviral Nucleoside Inhibitors01:22

Antiviral Nucleoside Inhibitors

Antiviral Nucleoside InhibitorsAntiviral nucleoside inhibitors are structural analogs of natural nucleosides that interfere with viral DNA or RNA synthesis. These compounds selectively target viral polymerases due to their resemblance to host nucleosides, thereby disrupting viral genome replication.Mechanism of Acyclovir ActionAcyclovir is a guanosine analog with a three-carbon acyclic side chain. It selectively targets herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2),...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Inhibitors of Bacterial DNA Synthesis01:28

Inhibitors of Bacterial DNA Synthesis

Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...
Inhibitors Of Virion Release01:25

Inhibitors Of Virion Release

Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
Retrovirus Life Cycles01:10

Retrovirus Life Cycles

Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...

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Related Experiment Video

Updated: Jun 22, 2026

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
05:46

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors

Published on: April 9, 2014

[Resistance to integrase inhibitors].

Carolina Garrido1, Carmen de Mendoza, Vicente Soriano

  • 1Servicio de Enfermedades Infecciosas, Hospital Carlos III, Madrid, España.

Enfermedades Infecciosas Y Microbiologia Clinica
|July 3, 2009
PubMed
Summary

Integrase inhibitors for HIV treatment can lead to drug resistance mutations. Cross-resistance between raltegravir and elvitegravir limits treatment options due to selected mutations in the integrase gene.

Area of Science:

  • Infectious Diseases
  • Virology
  • Pharmacology

Background:

  • Integrase inhibitors are a recent class of antiretroviral drugs for HIV treatment.
  • Incomplete viral suppression under drug pressure can lead to the selection of HIV resistance mutations.
  • Mutations in the integrase gene, particularly near the catalytic center, confer resistance.

Purpose of the Study:

  • To review and summarize the limited clinical information on resistance mutations associated with integrase inhibitors.
  • To identify common resistance mutations and patterns for raltegravir and elvitegravir.
  • To assess the degree of cross-resistance between these two integrase inhibitors.

Main Methods:

  • Literature review of clinical data on integrase inhibitor resistance.

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Measurement of In Vitro Integration Activity of HIV-1 Preintegration Complexes
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Measurement of In Vitro Integration Activity of HIV-1 Preintegration Complexes

Published on: February 22, 2017

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Last Updated: Jun 22, 2026

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
05:46

Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors

Published on: April 9, 2014

A Protocol for the Production of Integrase-deficient Lentiviral Vectors for CRISPR/Cas9-mediated Gene Knockout in Dividing Cells
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A Protocol for the Production of Integrase-deficient Lentiviral Vectors for CRISPR/Cas9-mediated Gene Knockout in Dividing Cells

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Measurement of In Vitro Integration Activity of HIV-1 Preintegration Complexes
10:34

Measurement of In Vitro Integration Activity of HIV-1 Preintegration Complexes

Published on: February 22, 2017

  • Analysis of reported mutations in the integrase gene following virologic failure.
  • Comparison of resistance patterns between raltegravir and elvitegravir.

    • Main Results:

    • Raltegravir failure is associated with N155H (40%) and Q148 (28%) mutations.
    • Elvitegravir failure commonly involves E92Q, E138K, Q148R/K/H, and N155H.
    • A frequent elvitegravir resistance pattern is E138K + E147G + Q148R.
    • High cross-resistance exists between raltegravir and elvitegravir, precluding sequential use.

    Conclusions:

    • HIV integrase inhibitors can rapidly select for resistance mutations.
    • Specific mutations like N155H and Q148 are key in raltegravir resistance.
    • Elvitegravir resistance involves a broader set of mutations, including E138K + E147G + Q148R.
    • Significant cross-resistance between raltegravir and elvitegravir necessitates careful treatment sequencing.