8.2
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Q1: What are the main differences between RNA and DNA viral genomes?
RNA viruses typically have smaller genomes than DNA viruses and lack proofreading mechanisms, leading to higher mutation rates. RNA viruses can be positive-sense, functioning directly as messenger RNA, or negative-sense, requiring transcription before translation. DNA viruses generally have larger, more stable genomes and employ distinct replication strategies to ensure genome stability and prolonged persistence within host cells.
Q2: How do positive-sense RNA viruses differ from negative-sense RNA viruses?
Positive-sense RNA viruses, like Poliovirus, function directly as messenger RNA and allow immediate translation of viral proteins upon host cell entry. Negative-sense RNA viruses, such as Rabies virus, must first undergo transcription to produce complementary mRNA before translation can occur. Both rely on different mechanisms to initiate protein synthesis within the host.
Q3: What role does RNA-dependent RNA polymerase play in viral replication?
RNA-dependent RNA polymerase is essential for negative-sense RNA viruses and double-stranded RNA viruses to transcribe their genomes into positive-sense RNA before translation. Host cells lack enzymes capable of directly processing double-stranded RNA, making this viral enzyme critical for replication. This polymerase enables these viruses to convert their genomic RNA into a form that can be translated into viral proteins.
Q4: How do single-stranded DNA viruses prepare their genomes for replication?
Single-stranded DNA viruses, such as Parvoviruses, must first be converted into a double-stranded replicative intermediate before transcription can occur. The positive-sense DNA strand shares the same sequence as mRNA, but transcription proceeds using the complementary strand as the template. This intermediate formation is essential for establishing a functional template for gene expression and genome replication.
Q5: What makes double-stranded DNA viruses capable of establishing persistent infections?
Double-stranded DNA viruses, including Herpesviruses, often have larger genomes and can encode their own polymerases or rely on host-cell polymerases for genome replication. This capability allows them to establish latent infections, persisting within the host for extended periods before reactivating under favorable conditions. Their genome stability and replication flexibility support long-term persistence.
Q6: How do retroviruses like HIV achieve long-term persistence in host cells?
Retroviruses such as HIV utilize reverse transcriptase to convert their RNA genome into DNA, which is subsequently integrated into the host genome. This integration allows the virus to persist within host cells, remaining latent or actively replicating depending on cellular conditions. This strategy facilitates long-term infection and immune evasion by becoming part of the host's genetic material.
Q7: Why do viral genomes vary in size and structure across different virus types?
Viral genomes vary in size and structure because they consist of either DNA or RNA, can be linear or circular, and exist as single- or double-stranded molecules. These variations influence replication strategies and interactions with host cells. RNA viruses generally have smaller genomes contributing to higher mutation rates, while DNA viruses employ distinct mechanisms ensuring genome stability and persistence.