Antiviral Drug Target
Antiviral Drug Target - Related Videos
02:48
Determining Antiviral Efficacy of Experimental Drugs Through a Plaque Assay
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2025
This video demonstrates the method to perform a plaque assay using a virus obtained from infected porcine cornea. The porcine cornea is used to test the antiviral efficacy of experimental drugs.
12:02
Assays for the Identification of Novel Antivirals against Bluetongue Virus
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Cited by 11 •
2013
Three assays, including the cytopathic effect (CPE)-based assay, dose-response assay and Time-of-Addition (ToA) assay have been developed, optimized, validated and utilized to identify novel antivirals against Bluetongue virus (BTV), as well as to determine the possible Mechanism-of-Action (MoA) for newly identified antivirals.
09:07
Using Zebrafish Models of Human Influenza A Virus Infections to Screen Antiviral Drugs and Characterize Host Immune Cell Responses
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Cited by 16 •
2017
Systemic and localized zebrafish infection models for human influenza A virus are demonstrated. Using a systemic infection model, zebrafish can be used to screen antiviral drugs. Using a localized infection model, zebrafish can be used to characterize host immune cell responses.
11:56
Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection
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Cited by 4 •
2013
Acquired resistance to antibiotics is a major public healthcare problem and is presently ranked by the WHO as one of the greatest threats to human life. Here we describe the use of cantilever technology to quantify antibacterial resistance, critical to the discovery of novel and powerful agents against multidrug resistant bacteria.
09:29
Early Viral Entry Assays for the Identification and Evaluation of Antiviral Compounds
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Cited by 45 •
2015
Here, we present a protocol that examines specific steps of the viral entry to identify and evaluate novel antiviral agents.
FAQs
Conserved viral enzymes are attractive candidates because they represent functions maintained across relevant viral forms and may be essential for replication. Disrupting one of these enzymes can interfere with a central step rather than a peripheral feature. Their conservation also helps researchers evaluate whether a compound could address diverse viruses or related viral variants.
Target selection depends on which viral process is most suitable for disruption. Attachment and entry targets act early, while genome replication, polyprotein processing, assembly, and release occur at later stages. Comparing these steps helps researchers identify where a drug can interrupt infection most effectively and whether the target represents an essential part of viral multiplication.
A compound may act by binding a viral or host-cell molecule, or by changing how that molecule functions. These mechanisms can prevent an essential process from proceeding even when the target remains present. The distinction matters because researchers must evaluate both the interaction with the target and the resulting effect on infection or viral replication.
Researchers first examine the viral life cycle to identify essential processes, then focus on components such as conserved viral enzymes or functions required for replication. Candidate compounds can be assessed for their ability to bind a target or alter its activity. The resulting effects on infection and replication help determine whether the target supports further therapy development.
Target analysis links a compound’s action to a specific viral process or host-cell function. Investigators can therefore evaluate whether treatment affects attachment, entry, genome replication, processing, assembly, or release. This framework helps interpret experimental outcomes, compare emerging therapies, and assess whether a proposed treatment interrupts a meaningful stage of the viral life cycle.
They provide a structured basis for developing treatments against existing infections and for studying therapies aimed at emerging viruses. Knowing the affected component or process also helps organize resistance monitoring around the relevant target. In biology research, this connection links molecular activity with changes in viral replication and supports comparisons among therapies directed at different life-cycle stages.