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Related Concept Videos

Indirect-Acting Cholinergic Agonists: Pharmacokinetics01:22

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Indirect-acting cholinergic agonists, or anticholinesterases, enhance the body's cholinergic activity by inhibiting acetylcholine's breakdown. They are categorized as reversible or irreversible agents based on their mechanism of action. They are further classified into short-acting, intermediate-acting, and long-acting agents based on their duration of action.
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Indirect-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:29

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Indirect-acting cholinergic agonists are agents that interact with the acetylcholinesterase enzyme in the synaptic cleft, preventing the breakdown of acetylcholine into choline and acetate. Consequently, the concentration of acetylcholine in the synaptic cleft increases. These agonists can be classified into reversible and irreversible inhibitors based on their duration of action.
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All neuromuscular blocking agents are injected intravenously because they are poorly absorbed from the GI tract. Rapid onset is achieved with intravenous administration, although absorption is also adequate from an intramuscular injection. Since these agents are highly ionized, they do not readily penetrate cell membranes or cross the blood-brain barrier.
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Local Anesthetics: Mechanism of Action01:23

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Local anesthetics (LAs) block sensory and motor impulses by inhibiting the sodium channels on the nerve cell membranes. This induces temporary loss of sensation, relieving pain in a specific body area.
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Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
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Depolarizing Blockers: Mechanism of Action01:28

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Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
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Latency-reversing agents: where are we now?

Maryam Bendoumou1, Carine Van Lint

  • 1Université Libre de Bruxelles (ULB), Service of Molecular Virology, Department of Molecular Biology (DBM), Gosselies, Belgium.

Current Opinion in HIV and AIDS
|November 20, 2025
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Summary

Latency-reversing agents (LRAs) show promise for HIV-1 remission by reactivating latent virus. Combining LRAs with immune modulators enhances viral clearance and immunological control, moving towards ART-free remission.

Keywords:
HIV-1 latencylatency-reversing agentsshock and kill strategiesviral reservoirs

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Area of Science:

  • Immunology
  • Virology
  • Infectious Diseases

Background:

  • Effective antiretroviral therapy (ART) suppresses HIV-1 but does not eradicate the virus.
  • HIV-1 persists in latent reservoirs, evading immune responses and enabling viral rebound upon treatment cessation.
  • The "shock and kill" strategy aims to eliminate latent HIV-1 reservoirs.

Purpose of the Study:

  • To review the efficacy of latency-reversing agents (LRAs) in reactivating HIV-1.
  • To evaluate the potential of combining LRAs with immune modulators for HIV-1 reservoir eradication.
  • To explore strategies for achieving durable, ART-free remission from HIV-1.

Main Methods:

  • Review of ex vivo and in vivo studies on LRAs for HIV-1 latency reversal.
  • Analysis of clinical trial data for LRAs and LRA-immune modulator combinations.
  • Assessment of LRA efficacy, safety, and impact on viral reservoirs and immune responses.

Main Results:

  • Various LRAs can reactivate HIV-1 ex vivo, but many cause excessive T-cell activation, limiting in vivo use.
  • Clinical trials show LRAs safely trigger HIV-1 transcription and modestly reduce reservoir size but not eradicate it.
  • Limited in vivo efficacy is attributed to posttranscriptional blocks and off-target cellular effects of LRAs.
  • Recent trials combining LRAs with immune modulators show promise in reducing reservoir size and improving immune control.

Conclusions:

  • Combining LRAs with immune modulators is a promising strategy to expose HIV-1 reservoirs for immune clearance.
  • This combination approach offers a potential pathway toward durable, scalable, ART-free remission from HIV-1.