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A woman with influenza is treated with zanamivir. Which step in viral replication is prevented by this drug? (A) entry into host cells (B) uncoating of viral nucleic acid (C) replication of viral nucleic acid (D) maturation of viral proteins (E) release of progeny virions

Short Answer

Expert verified
Zanamivir prevents the release of progeny virions (option E).

Step by step solution

01

Understanding the Question

The question asks us to identify which step in the viral replication process is hindered or blocked by the drug zanamivir when treating influenza.
02

List Viral Replication Steps

Various steps in viral replication include entry into host cells, uncoating of viral nucleic acid, replication of viral nucleic acid, maturation of viral proteins, and release of progeny virions.
03

Role of Zanamivir in Influenza Treatment

Zanamivir is known as a neuraminidase inhibitor. Neurominidases are enzymes that help in the release of progeny virions from infected cells. By inhibiting this enzyme, zanamivir prevents the final step in the viral replication cycle.
04

Identifying the Correct Step

Given that zanamivir inhibits neuraminidase, it specifically blocks the release of progeny virions, which corresponds to option (E) release of progeny virions.

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Key Concepts

These are the key concepts you need to understand to accurately answer the question.

Viral Replication Steps
The viral replication process is a series of crucial steps that viruses must complete to reproduce and infect new host cells. These steps give viruses the ability to spread within the host organism. Here’s a simplified breakdown of these steps:
  • Entry into Host Cells: This is the initial phase where the virus binds to surface receptors on the host cell, gaining entry into it.
  • Uncoating of Viral Nucleic Acid: Once inside, the viral particle sheds its outer coating, releasing its genetic material, usually DNA or RNA.
  • Replication of Viral Nucleic Acid: The viral genome is replicated using the host cell's machinery, allowing the production of multiple copies of the viral genome.
  • Maturation of Viral Proteins: Proteins required for new viruses are produced and assembled, preparing them for the final assembly of new viral particles.
  • Release of Progeny Virions: New viral particles exit the host cell, ready to infect additional cells, typically involving the cleavage of host cell structures through specific enzymes like neuraminidase.
Understanding these steps is vital for developing antiviral strategies, as each step presents a potential target for drug action.
Neuraminidase Inhibitors
Neuraminidase inhibitors are a class of antiviral drugs that specifically target the enzyme neuraminidase, which plays a crucial role in the life cycle of influenza viruses. What is Neuraminidase? Neuraminidase is an enzyme found on the surface of influenza viruses. It facilitates the release of newly formed viral particles from the host cell by cleaving sialic acid residues. How do Neuraminidase Inhibitors Work? These inhibitors act by binding to the active site of the neuraminidase enzyme, effectively blocking its function. This action prevents the release of progeny viruses, thereby stopping further infection of other cells. Drugs in This Category: Zanamivir and oseltamivir are the most well-known neuraminidase inhibitors, widely used in treating influenza. Their action is most effective when taken early in the infection cycle. Neuraminidase inhibitors are essential tools in managing and controlling influenza outbreaks by limiting the spread and severity of the disease.
Influenza Treatment
Influenza, commonly known as the flu, is a viral infection that can cause mild to severe symptoms. Treatment depends on antiviral medications, symptomatic relief, and preventive measures. Antiviral Medications: These drugs target specific stages of the viral life cycle to prevent the spread and severity of the disease.
  • Neuraminidase Inhibitors: As discussed earlier, drugs like zanamivir and oseltamivir prevent the release of new viruses, reducing the spread of the virus within the body.
  • Timing of Treatment: For maximum efficacy, antiviral treatment should commence within the first 48 hours of symptom onset.
Symptomatic Relief: Although antivirals are important, addressing symptoms like fever, sore throat, and body aches is equally vital. Over-the-counter medications, rest, and fluids help manage these. Preventive Measures: Vaccination is the most effective method to prevent influenza, along with good hygiene practices like hand-washing and avoiding close contact with infected individuals. These treatment strategies aim to manage symptoms, reduce complications, and prevent the spreading of the virus.
Viral Life Cycle Inhibition
Inhibition of the viral life cycle is a key strategy in antiviral therapy, focused on disrupting the synthesis, assembly, or release of viruses. Each step in the viral replication process represents a potential target for intervention. Why Inhibit Viral Life Cycle? By blocking specific stages, we prevent the virus from reproducing and spreading, thus reducing infection severity and transmission. Examples of Inhibition Points:
  • Entry Inhibitors: These block the virus from attaching or entering the host cell. Although not directly linked to neuraminidase inhibitors, they represent another method of life cycle interruption.
  • Replication Inhibitors: These target the replication of viral genetic material, halting viral reproduction.
  • Assembly Inhibitors: By preventing the assembly of new viral particles, these inhibitors halt the production of mature virions.
  • Release Inhibitors: Drugs like neuraminidase inhibitors fall into this category, blocking the release of newly formed viruses from the host cell.
Targeting these specific stages allows for innovative treatment approaches, providing a comprehensive method to combat viral infections effectively.

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