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Antibiotics have a very broad spectrum because they attack the metabolism pathways many bacteria share. For example, penicillin inhibits peptidoglycan synthesis, which is vital for formation of cell wall of gram-positive bacteria, so penicillin can be used to treat gram-positive bacteria infections. Streptomycin inhibits protein synthesis of bacteria. Because all the bacteria need protein synthesis, streptomycin has a very broad spectrum.

Why doesn't such strategy work on viruses? For example, nucleos(t)ide analogues can inhibit the RNA synthesis of RdRp. Most riboviruses (except hepatitis D virus) require a viral RdRp to replicate their genome. But why can't nucleos(t)ide analogues be used as broad spectrum anti-riboviral drugs even we have found very good drugs such as Sovaldi?

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One of the main issues with nucleotide analogs is that they can also affect the host replication and transcription (though they have a higher affinity to the viral polymerase), and can therefore have adverse side effects. On the other hand, the broad spectrum anti-bacterial antibiotics specifically affect prokaryotic cellular machinery.

(Note that some antibiotics like streptomycin do affect the host mitochondria and thereby cause toxicity. Ototoxicity and nephrotoxicity are known side effects of streptomycin.)

Nucleotide analogs are actually used as broad spectrum anti-virals: For example, Lamivudine is used for both HBV and HIV, which are different types of viruses.

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