***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Abstract Genotypic and phenotypic characterization was performed of HIV-1 isolates from treatment-naive HIV-1–infected patients experiencing virologic failure ( VF ) during treatment with the nonnucleoside reverse transcriptase inhibitor ( NNRTIs ) rilpivirine or efavirenz in the pooled phase 3 studies ECHO and THRIVE . Among 686 patients receiving rilpivirine  , 72 ( 10 % ) experienced VF versus 39 of 682 ( 6 % ) receiving efavirenz . In patients with low baseline viral load ( VL ) ⩽100,000 copies per milliliter , the proportions of rilpivirine VFs ( 19 of 368 ) and efavirenz VFs ( 16 of 330 ) were the same ( 5 % ) . In patients with high baseline VL > 100,000 copies per milliliter , the proportion of VFs was higher with rilpivirine ( 53 of 318 ; 17 % ) than efavirenz ( 23 of 352 ; 7 % ) . The rate of rilpivirine VF was comparable between HIV-1 subtype B – infected ( 11 % ) and nonsubtype B – infected ( 8 % ) patients . The absolute number of VFs with treatment-emergent NNRTI resistance-associated mutations ( RAMs ) was higher for rilpivirine ( most commonly E138 K or K101E ) than efavirenz ( most commonly K103N ) , but relative proportions were similar [ 63 % ( 39 of 62 ) vs. 54 % ( 15 of 28 ) , respectively ] . More rilpivirine VFs had treatment-emergent nucleoside/nucleotide reverse transcriptase inhibitor RAMs than efavirenz VFs [ 68 % ( 42 of 62 ) versus 32 % ( 9 of 28 ) , respectively ] , most commonly M184I and M184V . The proportion of rilpivirine VFs with RAMs in patients with low baseline VL was lower than in those with high baseline VL [ 38 % ( 6 of 16 ) versus 72 % ( 33 of 46 ) for NNRTI RAMs and 44 % ( 7 of 16 ) versus 76 % ( 35 of 46 ) for nucleoside/nucleotide reverse transcriptase inhibitor RAMs , respectively ] . In summary , VF and treatment-emergent reverse transcriptase RAMs were similar at low baseline VL but more frequent at high baseline VL in rilpivirine-treated than in efavirenz-treated patients . The frequent emergence of E138 K , especially in combination with M184I , in rilpivirine VFs is a unique finding of these trials Highly active antiretroviral treatment is compromised by viral resistance mutations . Transmitted drug resistance ( TDR ) is therefore monitored closely , but follow-up studies of these patients are limited . Virus from 1405 individuals diagnosed with HIV-1 in Denmark between 2001 and 2009 was analyzed for TDR , and molecular-epidemiological links and progression of the infection were described based on data from st and ardized question naires , the prospect i ve Danish HIV Cohort Study , and by phylogenetic analysis . Eighty-five individuals were found to be infected with virus harboring mutations result ing in a prevalence of 6.1 % , with no changes over time . The main resistance mutations were nucleoside reverse transcriptase inhibitor ( NRTI ) mutation 215 revertants , as well as nonnucleoside reverse transcriptase inhibitor ( NNRTI ) mutation 103N/S and protease inhibitor ( PI ) mutations 90 M and 85V . Phylogenetic analysis confirmed 12 transmission chains involving 37 TDR individuals . Of these 21 were also documented epidemiologically . The virus included in the transmission chain carried similar resistance mutations to the TDR index case , whereas controls chains from index cases without TDR were generally without resistance mutations . We observed no difference in progression of the infection between individuals infected with TDR and individuals infected with wild-type HIV-1 . The prevalence of TDR is low in Denmark and transmission of dual-drug-resistant HIV-1 is infrequent . The TDR isolates were shown to originate from local patients failing therapy Objective : To assess the association between adherence to antiretroviral therapy and the presence of class-specific antiretroviral medication resistance . Design : Secondary analysis of prospect i ve clinical trial data . Methods : Participants r and omized to the protease inhibitor or nonnucleoside reverse transcriptase inhibitor ( NNRTI ) strategies of the Community Programs for Clinical Research on AIDS ( CPCRA ) Flexible Initial Retrovirus Suppressive Therapies ( FIRST ) Study were included . Adherence was measured by 7-day self-report . Virological failure was defined as an HIV-RNA more than 1000 at or after 4 months . The association between cumulative adherence and the development of class-specific genotypic resistance was assessed by Cox regression analysis . Results : Included were 457 and 446 antiretroviral-naive participants on the protease inhibitor and NNRTI strategies , respectively . The median time to initial virological failure in the protease inhibitor strategy was 1.2 years ; 135 ( 30 % ) individuals failed with resistance . The median time to initial virological failure in the NNRTI strategy was 3.0 years ; 127 ( 28 % ) failed with resistance . No association was found between cumulative adherence and protease inhibitor resistance [ hazard ratio 1.1 , 95 % confidence interval ( CI ) 0.9–1.4 per 10 % lower adherence ] . However , lower cumulative adherence was associated with an increased risk of NNRTI resistance at initial virological failure ( hazard ratio 1.2 , 95 % CI 1.1–1.3 per 10 % lower adherence ) . In both strategies , lower cumulative adherence was associated with an increased risk of nucleoside reverse transcriptase inhibitor ( NRTI ) resistance at initial virological failure . Conclusion : Adherence – resistance relationships are class-specific . For NRTIs and NNRTIs , initial virological failure with resistance is more likely at lower levels of cumulative adherence BACKGROUND Primary HIV drug resistance ( PDR ) is associated with poor treatment outcome of first-line highly active antiretroviral therapy ( HAART ) . The aim of the study was to observe the trend of prevalence of PDR between 2001 and 2005 . METHODS In a prospect i ve multicentre study in the state of Nordrhein-Westfalen , Germany , 831 treatment-naive chronically HIV-infected patients underwent genotypic resistance testing .  RESULTS Six hundred and forty ( 77 % ) of them were male . Two-thirds of the patients ( 558 , 67 % ) were infected with HIV subtype B. PDR was found in 75 of 831 [ 9 % ; 95 % confidence interval ( CI ) 7.1 - 10.9 ] cases entering the study between January 2001 and December 2005 . An increasing trend of PDR was found from 2001 ( 4.8 % ; CI 2.1 - 9.4 ) to 2005 ( 9.0 % ; CI 5.4 - 12.6 ; P = 0.08 ) . A significant tendency to higher PDR was observed for ethnicity other than Caucasian ( P = 0.04 ) , HIV subtypes other than B ( P = 0.02 ) and transmission routes other than homosexual ( P = 0.03 ) . CONCLUSIONS A non-significant increase in prevalence of PDR was observed from 2001 to 2005 . A significant trend to higher PDR rate was detected in non-Caucasian patients , patients infected with non-B subtypes , and in patients with risk factors for acquisition of HIV other than homosexual transmission . Based on the fact that there is a trend to higher PDR rate , resistance testing in untreated HIV-infected patients starting HAART becomes more important in clinical routine . The identification of patient subgroups with a remarkable risk of PDR makes continuous monitoring of PDR m and atory Objective To evaluate the virologic responses and mutational profiles in antiretroviral-experienced patients adding tenofovir DF once-daily to their existing regimens . Design Resistance analyses were performed for patients in a phase II placebo-controlled clinical trial of tenofovir DF . Methods HIV-1 reverse transcriptase and protease genes from plasma sample s were analyzed genotypically and phenotypically at baseline , week 24 , and week 48 . Results Of 184 patients , 173 ( 94 % ) had baseline HIV-1 expressing one or more nucleoside reverse transcriptase inhibitor-associated resistance mutation . Protease inhibitor and non-nucleoside reverse transcriptase inhibitor ( NNRTI ) resistance mutations were observed in 57 % and 32 % of patients , respectively . Compared to placebo , significant reductions in HIV-1 RNA were observed for tenofovir DF-treated patients who had thymidine analog- ( TAM ) , lamivudine- ( M184V ) , NNRTI- or protease inhibitor-associated mutations . Patients with phenotypic susceptibility to tenofovir within 4-fold of wild-type responded durably to tenofovir DF 300 mg therapy with a decline in plasma HIV-1 RNA of ⩾ 0.5 log10 copies/ml ; few patients had a more than 4-fold reduced susceptibility to tenofovir at baseline . Four patients ( 2 % ) developed the K65R mutation ( selected by tenofovir in vitro ) and showed 3- to 4-fold reductions in tenofovir susceptibility but no evidence of rebound viremia . Thirty-four percent of patients developed additional TAMs , coincident with concurrent zidovudine or stavudine therapy , but also showed durable HIV-1 reductions . There was no evidence of novel resistance to tenofovir . Conclusions Adding tenofovir DF 300 mg to an existing regimen in patients with ongoing viral replication and a wide range of genotypic resistance patterns result ed in significant and durable HIV-1 RNA reductions . In addition , there was a low incidence of genotypic or phenotypic resistance  to tenofovir DF arising during 48 weeks of therapy Background : The NEFA Study was a r and omized study comparing nevirapine ( NVP ) , efavirenz ( EFV ) or abacavir ( ABC ) as substitutes for protease inhibitors in a large group of HIV-1-infected patients successfully treated with antiretroviral regimens containing protease inhibitors . Objective : To evaluate genotype and phenotype resistance patterns among patients who have experienced virological failure under one of the three study arms . Methods : Patients with virological failure , defined as two consecutive determinations of HIV-1 RNA > 200 copies/ml , were analysed for phenotypic susceptibility and HIV-1 mutations . Results : Of the 460 patients included in the study , 51 ( 11 % ) experienced virological failure after 24 months of follow-up while on assigned study medication . A higher proportion of patients in the ABC [ 25 ( 17 % ) ] than in the NVP [ 14 ( 9 % ) ] or EFV [ 12 ( 8 % ) ] arms selected resistance to the study drug ( P = 0.04 ) . Moreover , a much higher number of resistance mutations to one or more of the backbone nucleoside reverse transcriptase inhibitor drugs contained in the failing regimen were observed in the ABC than in the EFV or NVP arms . In general , there was a good concordance among genotype and phenotype resistance testing , except for ABC , stavudine and didanosine , where phenotypic resistance testing added valuable information ( fold change in the median inhibitory concentration ) . Conclusions : Cross-resistance involving nucleoside reverse transcriptase inhibitor drugs might explain the higher risk of virological failure in patients switched to ABC-containing antiretroviral therapy . Phenotypic resistance testing may be helpful in interpreting unclear genotypic results OBJECTIVES To investigate the interplay between resistance and adherence in the virological failure of three fundamentally different highly active antiretroviral therapy ( HAART ) regimens . METHODS We retrospectively identified 56 verified primary virological failures ( viral load > 400 HIV-1 RNA copies/mL ) among 293 patients r and omized to two nucleoside reverse transcriptase inhibitors (NRTIs)+ritonavir+saquinavir ( RS-arm ) ( n=115 ) , two NRTIs+nevirapine+nelfinavir ( NN-arm ) ( n=118 ) , or abacavir+stavudine+didanosine ( ASD-arm ) ( n=60 ) followed up for a median of 90 weeks . Data on adherence were collected from patient files , and genotyping was performed on plasma sample s collected at time of failure . RESULTS Treatment interruption or poor adherence was mainly caused by side effects and accounted for 74 % of failures , and 
    Output:
    
Trends in NNRTI resistance among TN patients show an increased burden in the US and some EU countries compared to others .
These findings signify a need for alternate first-line treatments in some regions