I mostly agree with mgkrebbs (+1), but note that while viruses generally have some kind of RNA replicase subunit (RdRP) to help them out, viroids completely lack those, yet manage to reproduce:
While RNA viruses encode subunits of the enzymatic complex (RNA replicase) that catalyzes initiation and elongation of viral RNA strands, viroids must rely for this replication step on pre-existing host RNA polymerases. In principle, the best candidates would be RNA-dependent RNA polymerases, whose existence in plants has been known for a long time. However, viroids do not use these enzymes for their replication, but DNA-dependent RNA polymerases redirected to accept RNA templates.
The closest thing to a viroid in humans is Hepatitis D. Until last year, it was thought that it was mostly a human disease, but a 2019 survey found that HepD analogs are quite widespread in invertebrates, fish, snakes etc.
Viruses are "much more nasty" than viroids in that replication regard because
Positive-strand RNA viruses replicate by using virally encoded RNA-dependent RNA polymerases (RdRPs) that provide a direct RNA-to-RNA replication function not found in host cells.
Some recent research suggests that RdRPs have been independently lost in many animal clades. Ironically, the roles of these (former) host RdRPs was [most likely] to provide an anti-viral mechanism via RNA silencing (see [section] below for details), but evolution has provided with alternative host mechanisms for producing the same.
While it's possible to recognize the [core of the] viral RdRPs in software, it's not clear/known how to translate this into a general anti-viral strategy, as far as I know, due to their fairly substantial variation. (In general it's not enough to know the genetic sequence encoding the RdRP of some virus to even screen inhibitor drugs for it; additionally one must know the crystal structure of the RdRP complex for that virus.)
If you're curious about "intra-cell" (i.e. RNA-based) anti-viral defense... there exist mechanisms like that, but are substantially more complicated (that what you suggest), being based instead on RNA silencing:
In eukaryotic RNA-based antiviral immunity, viral double-stranded RNA is recognized as a pathogen-associated molecular pattern and processed into small interfering RNAs (siRNAs) by the host ribonuclease Dicer. After amplification by host RNA-dependent RNA polymerases in some cases, these virus-derived siRNAs guide specific antiviral immunity through RNA interference and related RNA silencing effector mechanisms.
Key steps in RNA-based antiviral immunity induced in Drosophila
melanogaster by infection of positive-strand RNA viruses such as flock house virus.
Following entry and uncoating of flock house virus (FHV) virions, the genomic
positive-strand RNA ((+)RNA) serves as both mRNA for the translation of viral
RNA-dependent RNA polymerase (RdRP) and as a template for the synthesis of
antigenomic negative-strand RNA ((–)RNA). Preferential production of (+)RNA by viral RdRP
is achieved by multiple rounds of initiation of RNA synthesis from the 3ʹ end of the low
abundant (–)RNA. The resulting double-stranded RNA (dsRNA) formed between the
5ʹ-terminal nascent progeny (+)RNA and the (–)RNA template is recognized by Dicer 2
(DCR2) and cleaved into small interfering RNAs (siRNAs), thereby triggering RNA-based
antiviral immunity. The viral siRNAs are assembled with Argonaute 2 (AGO2) into the
RNA-induced silencing complex (RISC), methylated at the 3ʹ end (depicted by a black
circle) by HEN1 and used to guide specific clearance of FHV RNAs. As a counter-defence,
FHV encodes a viral suppressor of RNA silencing, the B2 protein, which targets two
steps in this immune pathway: inhibition of viral siRNA production by binding to viral RdRP
and the viral dsRNA precursor, and sequestration of viral siRNAs by binding duplex siRNAs.
Loqs-PD, loquacious-isoform PD.
And yes, the RdRP of viruses (the most significant part of the self-copier machine they come with) is an important drug target, e.g.
CoVs employ a multi-subunit replication/transcription machinery. A set of non-structural proteins (nsp) produced as cleavage products of the ORF1a and ORF1ab viral polyproteins (5) assemble to facilitate viral replication and transcription. A key component, the RNA-dependent RNA polymerase (RdRp, also known as nsp12), catalyzes the synthesis of viral RNA and thus plays a central role in the replication and transcription cycle of COVID-19 virus, possibly with the assistance of nsp7 and nsp8 as co-factors (6). Nsp12 is therefore considered a primary target for nucleotide analog antiviral inhibitors such as remdesivir, which shows potential for the treatment of COVID-19 viral infections (7, 8). [...]
The efficacy of chain-terminating nucleotide analogs requires viral RdRps to recognize and successfully incorporate the active form of the inhibitors into the growing RNA strand.
So while it's not so simple to detect/fight viruses' as you suggested, some replication-targeting strategies involve either "jamming their own (RdRP) copier with fake parts" (as e.g. remdesivir does) or producing [hopefully] as many "copy cancelers" as possible, for which the RNA silencing machinery actually uses parts from the virus copies themselves.