Final answer:
Viruses are more susceptible to nucleotide analogs due to their rapid nucleic acid replication and more error-prone enzymes lacking proofreading capabilities, which leads to the incorporation of analogs and ineffective replication.
Step-by-step explanation:
Viruses are generally more susceptible to nucleotide analogs than their host cells due to the unique characteristics of their replication enzymes and rapid replication cycles. When considering why viruses are more affected by nucleotide analogs than host cells, the most accurate statement is that viruses replicate their nucleic acid more rapidly than host cells do. This is because viruses must rapidly synthesize new viral genomes to produce new virions. Viral DNA polymerases and RNA polymerases, especially those from RNA viruses, are typically more prone to incorporating nucleotide analogs because they lack the proofreading capabilities of host cell polymerases. This makes viral replication machinery more error-prone and more likely to incorporate nucleotide analogs into the viral genome, leading to ineffective viral replication.
Moreover, since many viruses, particularly RNA viruses, require their own specific enzymes to replicate, drugs that mimic the normal nucleotides can target these enzymes without affecting the host’s normal cellular processes as much. As mentioned, the genomes of RNA viruses code for enzymes that are not found in host cells, like the virus-specific RNA-dependent RNA polymerase. The fact that retroviruses also produce their own unique enzyme, reverse transcriptase, has allowed for the development of drugs that inhibit these enzymes without significantly impacting normal host cell functions.