Virus mutation
A resistance mutation is a mutation in a virus gene that allows the virus to become resistant to treatment with a particular antiviral drug. The term was first used in the management of HIV, the first virus in which genome sequencing was routinely used to look for drug resistance. At the time of infection, a virus will infect and begin to replicate within a preliminary cell. As subsequent cells are infected, random mutations will occur in the viral genome. When these mutations begin to accumulate, antiviral methods will kill the wild type strain, but will not be able to kill one or many mutated forms of the original virus. At this point a resistance mutation has occurred because the new strain of virus is now resistant to the antiviral treatment that would have killed the original virus. Resistance mutations are evident and widely studied in HIV due to its high rate of mutation and prevalence in the general population. Resistance mutation is now studied in bacteriology and parasitology.
Mechanisms.
Resistance mutations can occur through several mechanisms from single nucleotide substitutions to combinations of amino acid substitutions, deletions and insertions. Over time, these new genetic lines will persist if they become resistant to treatments being used against them. It has been shown that pathogens will favor and become more resistant to treatment in common host genotypes through frequency-dependent selection. Further, strict adherence to a retroviral regimen correlates to a strong decrease in retroviral resistance mutations. There are five classes of drug that are used to treat HIV infection, and resistance mutations can effect the efficacy of these treatments as well.
In Other Viruses.
Resistance mutations are found and become problematic in many viruses other than HIV. Notable examples of such viruses include the herpes simplex virus and hepatitis B virus. In the herpes virus, drugs mainly target the viral DNA polymerase. As a result, mutations in the viral DNA polymerase that make it resistant to these drugs are selected for, which ultimately can cause complete resistance of the treatment. In hepatitis B, nucleoside and nucleotide analogs are used to cause early termination of viral transcription. Mutations in viral reverse transcriptase can cause the enzyme to not incorporate these nonfunctional analogs, in favor for their natural counterparts. If this mutation occurs, transcription will not be halted, and viral proteins can be created.
References.
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