Questions: Viral Replication Cycle

Question 1

During the lysogenic cycle in a bacteriophage infection, what happens to the viral genome immediately after it enters the host cell?

• A. It is immediately replicated and new virions are assembled
• B. It integrates into the host chromosome as a prophage and replicates passively with cell division
• C. It remains in the cytoplasm as an autonomous episome
• D. It is degraded by host restriction enzymes

Answer: (B)

In the lysogenic cycle, the phage genome integrates into the bacterial chromosome as a prophage. It then replicates silently with every cell division — the host does all the work. The phage can persist this way for many generations until an inducing signal (such as UV damage) triggers excision and entry into the lytic cycle. Options A describes the lytic cycle, C is incorrect (integration into the chromosome is the defining feature), and D would prevent lysogeny from occurring.

Question 2

Most viruses should kill their host cell as part of their replication cycle in order to release new virions.

• T. True
• F. False

Answer: False

Lysis is only one release mechanism. Many enveloped viruses (including HIV and influenza) exit by budding — the virus acquires a membrane envelope as it pushes through the host cell membrane, and the host cell survives the process, at least initially. Lysogenic phages can persist indefinitely in the host chromosome without killing the cell at all. Killing the host is the lytic strategy, not a universal feature of viral replication.

Question 3

Why can a human virus not infect a plant cell, even if the viral particles were artificially injected directly into the plant's cytoplasm?

Model answer: Attachment depends on specific receptor-ligand binding between viral surface proteins and host cell receptors. Plant cells lack the receptors that human viruses recognize, so the attachment step fails. However, if particles were injected past this step, replication might partly proceed — the deeper constraint is that the host replication machinery must also be compatible.

Receptor specificity is the primary determinant of host range and tissue tropism. This is why HIV only infects cells expressing CD4 receptors, why influenza targets cells with specific sialic acid residues, and why most viruses cannot cross species barriers without mutations to their attachment proteins. The injection caveat is important for teaching: if you bypassed attachment, some replication factors might work, but viruses are also adapted to exploit species-specific cellular machinery throughout the replication cycle.