Final answer:
Adenovirus uses the E1A protein to prevent host cell differentiation by disrupting regulatory pathways, keeping cells in a state viable for viral replication. Influenza, on the other hand, exits host cells through budding without killing them, allowing prolonged viral production and spread.
Step-by-step explanation:
The E1A protein of adenovirus plays a crucial role in preventing the differentiation of host cells, effectively keeping them in a state conducive to proliferation. E1A achieves this by interfering with the regulatory pathways of the host cell, particularly those involved in controlling the cell cycle and initiating differentiation.
By binding to and modulating the function of retinoblastoma protein (Rb), p300/CBP, and other factors that are pivotal in the regulation of the cell cycle and gene expression, E1A ensures that the cells remain in an undifferentiated and proliferative state. This activity is significant for the adenovirus lifecycle as it allows for the efficient production of new viral particles by exploiting the host cell's machinery.
Similarly, influenza virus has a mechanism to exit the host cell without killing it, ensuring viral replication and propagation without immediate host cell death.
The influenza virus is packaged in a viral envelope that fuses with the plasma membrane, allowing virions to exit through budding while keeping the host cell alive and functioning. By maintaining the viability of the host cell, the virus can continue to replicate and spread, ultimately infecting more cells and hosts.