Viral resistance testing should be performed at baseline to ensure selection of a fully active regimen and should be repeated if the viral load increases during antiretroviral treatment. The most common reason for breakthrough viremia is poor medication adherence. In general, plasma levels of HIV RNA must be greater than 500 copies/mL to provide enough virus for resistance testing. Viral resistance testing can be genotypic (looking for mutations associated with drug resistance) or phenotypic (assessing whether virus can replicate in the presence of the drug). Genotypic testing is faster and cheaper, but phenotypic testing may be better in the presence of multiple mutations or for drugs such as protease inhibitors in which the correlation of specific mutations and resistance is less straightforward. Resistance testing results are used to guide selection of a new regimen in the event resistant virus develops, but previous resistance testing results as well as previous regimens and responses must also be considered. Resistance testing may not be reliable if performed while the patient is not taking an antiretroviral regimen because resistance may not be detectable without the selective pressure of the antiretrovirals. Once selected for, previous mutations are generally archived in the viral population and may re-emerge even if resistance testing does not demonstrate the mutation. A regimen may also be switched because of adverse effects or to ease adherence or avoid drug interactions. Laboratory monitoring tests should be repeated 1 month after switching regimens to assess effectiveness and toxicity.
This patient needs baseline genotypic HIV resistance testing. Because of the possibility of transmitted virus having resistance mutations, it is recommended to obtain baseline resistance testing before starting an antiretroviral regimen. If the patient is ready, antiretrovirals can be started the same day, while waiting for resistance testing results, with regimen modification if necessary based on results. Virologic failure of a regimen (rebound of a suppressed viral load or failure to achieve undetectable viral load with therapy) is also an indication for resistance testing to guide the change in regimen. Genotypic testing looks for mutations in the viral genome associated with antiviral drug resistance. Phenotypic testing actually tests the virus's ability to grow in the presence of differing concentrations of the drug and is therefore more useful in the presence of multiple interacting mutations or unclear correlations of mutation and resistance, such as occurs with resistance to protease inhibitors. Genotypic testing is faster and less expensive because all that is necessary is sequencing of the respective genes for the patient's viral isolate. When significant resistance is not expected and information is needed more quickly, genotypic testing would be preferred over phenotypic testing.
Some antiretroviral agents have been associated with increased insulin resistance and risk for hyperglycemia, and assessing for this at baseline and during therapy is recommended. This patient, however, already has a normal glucose level at baseline testing, so measuring the glycohemoglobin is not necessary at this time.
All patients with HIV should begin antiretroviral therapy as soon as they are ready. Prompt initiation of therapy benefits the patient and reduces the risk of transmission to others, so waiting for repeat viral load and CD4 cell count is inappropriate and unnecessary.