L5 - Viral Entry Flashcards
What is the significance of virus entry in the viral life cycle?
Virus entry is an essential step to establish infection as it allows the virus to bind, penetrate, and ultimately replicate within the host cell.
How do viruses achieve high local concentration on the cell surface?
They attach through multiple, low‐affinity receptor–virus interactions that stably concentrate virus particles on the cell surface.
What are the two general pathways a virus may follow after receptor binding?
Viruses may fuse directly at the plasma membrane or be internalised via endocytosis/macropinocytosis, remaining within a vesicle.
How does the virus escape from an endosomal compartment?
Escape occurs either by fusion of the viral and vesicular membranes or by disrupting the vesicle’s integrity.
What types of molecules serve as viral receptors and attachment factors?
They include proteins, glycoproteins, glycolipids, and sometimes carbohydrates such as heparan sulphate and sialic acids.
How do attachment factors differ from true viral receptors?
Attachment factors are non-essential, low-affinity, and serve primarily to concentrate virus particles, whereas receptors trigger entry via specific binding.
Why is multivalency important in virus–cell interactions?
Multivalent binding increases overall binding avidity, ensuring stable attachment despite individual low-affinity interactions.
In what way can receptor clustering influence viral uptake?
Clustering can induce signalling (e.g. via receptor tyrosine kinases) that promotes endocytosis or direct fusion.
Which uptake mechanisms allow viruses to enter host cells while enclosed in vesicles?
Clathrin-mediated endocytosis and macropinocytosis are key mechanisms for virus internalisation.
How does macropinocytosis differ from receptor-mediated endocytosis?
Macropinocytosis involves the non-specific “cell drinking” of extracellular fluid, while receptor-mediated endocytosis is a targeted, receptor-triggered process.
What role does the cellular environment (such as pH) play in viral uptake?
A drop in pH within endosomes can trigger conformational changes in viral proteins necessary for membrane fusion.
Why must viruses traffic to specific endosomal compartments?
Specific compartments provide the correct conditions—like low pH or particular enzymes—to facilitate viral fusion or uncoating.
What is the role of viral fusion proteins during entry?
Fusion proteins catalyse the merging of the viral envelope with the host cell membrane, enabling the delivery of the viral genome into the cytosol.
How is fusion at the plasma membrane initiated for enveloped viruses?
It is initiated by a dedicated fusion protein—often activated by receptor binding—that undergoes a conformational change exposing a fusion peptide.
What triggers fusion within the endosomal compartment?
A decrease in pH in the late endosome induces structural rearrangements in the fusion protein, exposing the fusion peptide.
What distinguishes Class I, II, and III fusion proteins?
They differ in structure and activation: Class I proteins are cleaved to expose an amino‐terminal fusion peptide; Class II proteins use an internal fusion peptide and form dimers that rearrange at low pH; Class III proteins combine features of both, often with reversible conformational changes.
How do non-enveloped viruses typically enter host cells without membrane fusion?
They rely on mechanisms such as endocytosis followed by the formation of membrane pores or disruption of the endosomal membrane.
What role does capsid reorganisation play in non-enveloped virus entry?
Reorganisation exposes hydrophobic domains or peptides that interact with and destabilise the host membrane to allow genome release.
Why is receptor-mediated attachment still critical for non-enveloped viruses?
It concentrates viruses on the cell surface and may trigger endocytic uptake despite the absence of a viral envelope.
What is a key difference between the entry mechanisms of enveloped and non-enveloped viruses?
Enveloped viruses use fusion proteins for membrane merging, whereas non-enveloped viruses typically form pores or cause mechanical disruption of the endosome.
What are the key steps involved in viral entry into host cells?
The key steps include attachment to host cell receptors, uptake via endocytosis or direct fusion, and genome release into the cytoplasm.
How does the specificity of receptor binding influence viral tropism?
Receptor binding determines which cells a virus can infect, influencing host and tissue specificity.
What distinguishes true viral receptors from attachment factors?
True receptors facilitate viral entry, while attachment factors merely enhance viral concentration on the cell surface.
How does receptor-mediated endocytosis facilitate viral entry?
Endocytosis allows viruses to enter vesicles, where pH changes trigger fusion with the endosomal membrane, releasing the genome.
