Baseline resistance testing should include the polymerase and protease genes. Testing for susceptibility to integrase and entry inhibitors is not recommended SB431542 order routinely in naïve patients at present, although this area is kept under active review (IIb). The most appropriate sample is the one closest to the time of diagnosis (Ia) and this should preferably be tested at the time of initial presentation (IV). The possibility exists that the resistance profile obtained at diagnosis may change in patients who acquire a new infection. The true risk of HIV-1 superinfection

remains to be determined but may be significant in persons who continue to be exposed to new sources of the virus [27], especially in early stages of the initial infection [28]. Triggers to repeat resistance testing prior to starting ART may include a sudden increase in viral load, a sudden drop in the CD4 T-cell count, and a recurrence of symptoms of acute HIV infection [29, 30]. It should be noted,

however, that most patients with sudden changes in viral load and CD4 T-cell counts do not have evidence DNA Synthesis inhibitor of superinfection [29, 30]. In a London cohort study of 47 homosexual men who showed an increase in viral load of greater than 0.5 log10 copies/mL during routine monitoring, two (4%) showed evidence of superinfection and a change in the initial drug susceptibility profile as determined by repeat sequencing of the reverse transcriptase and protease genes [30]. For patients who have not undergone resistance testing at the

time of diagnosis, testing is recommended before starting therapy (Ia). Whenever possible, a plasma sample collected as close as possible to the time Cyclooxygenase (COX) of diagnosis should be retrieved for retrospective testing (Ia). When a stored sample is not available a current sample should be tested (IV). Following resistance testing at the time of diagnosis, repeat testing is not routinely recommended prior to starting therapy, although it should be considered in selected persons who may have experienced reinfection (IIb). In patients without evidence of drug resistance by routine methods, a suboptimal virological response to first-line therapy (a viral load reduction of less than 1 log10 copies/mL by 4 weeks) may signal the emergence of drug-resistant variants that were initially present at low frequency and therefore undetectable by routine testing. In patients without evidence of drug resistance at diagnosis by routine genotypic methods, a suboptimal virological response to first-line therapy (a viral load reduction of less than 1 log10 copies/mL by 4 weeks) should prompt resistance testing at that time (IV). The prevalence of drug resistance has declined among treatment-experienced patients in the UK as a result of improved management of ART and treatment failure.