Viruses with RNA Genomes

Positive-sense RNA viruses have genomes that function directly as messenger RNA upon entering host cells, enabling immediate translation of viral proteins. Bacteriophage MS2 and poliovirus exemplify this strategy, producing viral proteins including RNA replicase and polyproteins that are cleaved into structural and enzymatic components necessary for virion assembly and genome amplification.

Antigenic shift occurs when two different influenza virus strains co-infect the same cell and their segmented genomes randomly reassort, producing new viral strains with pandemic potential. This process differs from antigenic drift, which results from gradual mutation accumulation causing seasonal variations. Understanding size and structure of viral genomes helps explain how segmentation enables this genetic exchange mechanism.

Double-stranded RNA viruses like rotavirus replicate within the viral nucleocapsid, which shields their RNA from host immune detection and aids immune evasion. During replication, the virus transcribes positive-strand RNA from its double-stranded genome, serving as a template for protein synthesis and genome replication while minimizing host immune responses.

Negative-sense RNA viruses cannot be directly translated because their genomes are complementary to mRNA. Instead, they require viral RNA-dependent RNA polymerases to transcribe their genomes into mRNA, which is then translated into viral proteins necessary for replication and virion assembly. Rabies and influenza viruses exemplify this mechanism.

Retroviruses like HIV use reverse transcriptase to synthesize complementary DNA from their RNA genome, converting RNA into DNA as part of their life cycle. This cDNA integrates into the host genome, enabling persistent infection and lifelong latency. This reverse transcription strategy distinguishes retroviruses from other RNA viruses.

Although hepatitis B virus is classified as a DNA virus, it employs a unique replication pathway utilizing reverse transcription to convert an RNA intermediate into a partially double-stranded DNA genome. This mechanism differentiates hepadnaviruses from classical DNA viruses, highlighting their distinct reverse-transcribing replication strategy.

Poliovirus enters human cells by binding to the poliovirus receptor on the cell surface, then synthesizes a large polyprotein that is cleaved by viral proteases into structural and enzymatic components. In contrast, bacteriophage MS2 infects E. coli by attaching to F pili and injecting its RNA genome, demonstrating diverse host cell entry mechanisms across positive-strand RNA viruses.