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Phenotypic resistance of resistant strains of HIV type-1 subtype B in China.

BACKGROUND: This study was aim to explore the characteristics of phenotypic resistance of resistant strains of HIV type-1 (HIV-1) subtype B and to compare the concordance between the phenotypic resistance and genotypic resistance. METHODS: The genotypic resistance assay for the HIV-1 clinical isolates was performed. One isolate without resistance mutation was chosen as a drug-sensitive reference strain and seven subtype B isolates with resistance mutations were phenotypically tested. Fifty percent inhibitory concentrations (IC50) between resistant and sensitive viruses were compared. The resistance extent was determined by the folds of the increased IC50. The concordance between the phenotypic resistance and genotypic resistance was also analyzed. RESULTS: IC50 of resistant isolates were 0.0006 - 0.1300 micromol/L for zidovudine (AZT), 0.0016 - 0.0390 micromol/L for lamivudine (3TC), 0.0104 - 0.4234 micromol/L for nevirapine (NVP), and 0.0163 - 0.1142 micromol/L for indinavir (IDV), respectively. Genotypic and phenotypic resistance assays indicated that the resistant strains were intermediately and highly resistant to nucleotide analog reverse transcriptase inhibitors and non-nucleotide analog reverse transcriptase inhibitors. The phenotypic assay was consistent with the genotypic assay. For measuring the potential resistance, the genotypic assay was more sensitive than the phenotypic. In evaluating the resistance to protease inhibitors, these two assays were discrepant. CONCLUSIONS: Both the phenotypic and genotypic assays indicate that the resistant viruses exist in HIV-infected patients in China who have received treatment. Phenotypic and genotypic assays have high concordance, and the genotypic assay could replace the phenotypic assay to predict the HIV-1 resistance.

Anti-Retroviral Agents↗

A rational approach to the selection and sequencing of nucleoside/nucleotide analogues: a new paradigm.

While the value of highly active antiretroviral therapy (HAART) is unquestionable, its use as a life-long therapy will require a more structured and strategic approach to the sequential use of antiretroviral agents than has previously been the case. A complex cocktail of factors influences the durability of a given regimen, but the durability of HAART requires a carefully planned approach to the selection of agents across multiple regimens from first-line onwards, based on considerations of drug cross-resistance and sequenceability at regimen failure. Despite considerable ongoing interest in sequencing protease inhibitors and even non-nucleoside reverse transcriptase inhibitors, there has been little study into the optimal sequence of nucleoside reverse transcriptase inhibitor (NRTI) drugs in consecutive regimens. Historical practice, clinical experience and force of habit have all emphasized the use of thymidine analogue-based first-line combinations and the frequent retention of a thymdine analogue at all subsequent stages until a salvage situation is reached. Emerging data clearly associates thymidine analogue-derived reverse transcriptase mutations with loss of drug susceptibility and clinical response to other members of the NRTI class, particularly when present alongside other NRTI-associated mutations. Any approach to strategic therapy across multiple treatment lines will require, as a basic tenet, that agents with the greatest potential for cross-resistance be used later in therapy rather than earlier. To this end, a move away from the universal use of the thymidine analogues in first-line therapy is likely as strategic thinking becomes more integrated into clinical management in HIV disease. However, more clinical investigation is required into both the performance of alternative first-line

Anti-HIV Agents↗

Antibiotics from basidiomycetes. XLI. Clavicoronic acid, a novel inhibitor of reverse transcriptases from Clavicorona pyxidata (Pers. ex Fr.) Doty.

A novel inhibitor of RNA-directed DNA-polymerases was isolated from fermentations of Clavicorona pyxidata. Its structure was elucidated by spectroscopic methods. Clavicoronic acid (1) is a noncompetitive inhibitor of avian myeloblastosis virus (Ki 130 microM) and Moloney murine leukemia virus (Ki 68 microM) reverse transcriptases. In permeabilized cells and isolated nucleic DNA- and RNA-synthesis are not affected. Clavicoronic acid markedly inhibits the multiplication of vesicular stomatitis virus in baby hamster kidney cells by interfering with this virus's RNA-directed RNA-polymerase. 1 exhibits no cytotoxic and very weak antimicrobial activities.

Animals↗

Selective interaction of the human immunodeficiency virus type 1 reverse transcriptase nonnucleoside inhibitor efavirenz and its thio-substituted analog with different enzyme-substrate complexes.

Accumulating data have brought the nonnucleoside reverse transcriptase (RT) inhibitors (NNRTIs) into the forefront of antiretroviral therapy. Among the emerging compounds in this class, a particularly attractive one is efavirenz (Sustiva), recently approved for clinical use by the U.S. Food and Drug Administration. In the present study, the equilibrium dissociation constants for efavirenz binding to the different catalytic forms of human immunodeficiency virus type 1 RT as well as the association and dissociation rates have been determined using a steady-state kinetic approach. In addition, the same enzymological analysis has been extended to the thio-substituted analog, sefavirenz, which showed comparable activity in vitro against RT. Both compounds have been found to act as purely uncompetitive inhibitors at low drug concentrations (5 to 50 nM) and as mixed noncompetitive inhibitors at higher doses (50 to 500 nM). This behavior can be interpreted in terms of the relative affinities for the different catalytic forms of the enzyme. Both efavirenz and sefavirenz showed increasing affinities for the different forms of RT in the following order: free enzyme < (i.e., bound with lower affinity) binary RT-template-primer (TP) complex < ternary RT-TP-deoxynucleoside triphosphate (dNTP) complex. The rate of binding of the two inhibitors to the different enzyme-substrate complexes was well below the diffusion limit (on the order of 10(4) M(-1) s(-1)); however, both inhibitors, when bound to the ternary RT-TP-dNTP complex, showed very low dissociation rates, on the order of 10(-4) s(-1) for both compounds, typical of tightly binding inhibitors. Thus, efavirenz and its thio-substituted derivative sefavirenz appear to be peculiar in their mechanism of action, being selective tightly binding inhibitors of the ternary RT-TP-dNTP complex. Efavirenz is the first clinically approved NNRTI to show this property.

Alkynes↗

A review of HIV-1 resistance to the nucleoside and nucleotide inhibitors.

The nucleoside reverse transcriptase inhibitors (NRTIs) were the first class of agents used for the treatment of HIV and remain an important component of combination antiretroviral therapy. Resistance to the NRTIs occurs by the acquisition of mutations in the reverse transcriptase gene that result in a structural change that either decreases the NRTI incorporation into the extending nucleotide chain or enhances removal of the NRTI from the terminated chain, also known as primer unblocking or pyrophosphorylysis. There are several major genetic mutational patterns of resistance and cross-resistance that evolve with the NRTIs including the thymidine analog mutations M41L, D67N, K70R, L210W, T215Y, and K219Q/E/W, the non-thymidine mutations M184V, L74V, and K65R, and the multidrug resistant Q151M complex, as well as others. Increasing knowledge of resistance and cross-resistance patterns that evolve on the NRTIs as well as the other antiretroviral classes will help optimize antiretroviral treatment strategies. Advancing knowledge of the biochemical and structural basis of resistance will aid in the design of newer compounds that are active against HIV resistant to the currently available drugs, ultimately prolonging virologic suppression and life in the millions of people who are infected with HIV.

Drug Resistance, Viral↗

[Changes in lipid tissue redistribution and metabolic disorders in HIV positive patients treated with protease inhibitors].

Significant decrease in AIDS mortality rate has been noted since 1996 when proteases inhibitors (PI) were introduced into vast use. Unfortunately they revealed major side effects of which lipodystrophy (L) turned out to be very serious due to various clinical implications consequently worsening prognosis of HIV-positive patients treated with HAART (highly active antiretroviral therapy). Redistribution of lipid tissue in many cases was a reason of switching the PI-therapy, though very effective, into PI-sparing therapy of non-nucleoside reverse transcriptase inhibitors (NNRTI) and nucleoside reverse transcriptase inhibitors (NRTI), doubtlessly confining future therapeutic options. This review presents our to date knowledge on clinical aspects, pathogenesis, treating and further consequences of these changes.

Acquired Immunodeficiency Syndrome↗

Highly potent oxathiin carboxanilide derivatives with efficacy against nonnucleoside reverse transcriptase inhibitor-resistant human immunodeficiency virus isolates.

The structure-activity relationships of a series of compounds related to the nonnucleoside reverse transcriptase (RT) inhibitor (NNRTI) oxathiin carboxanilide have been described (R. W. Buckheit, Jr., T. L. Kinjerski, V. Fliakas-Boltz, J. D. Russell, T. L. Stup, L. A. Pallansch, W. G. Brouwer, D. C. Dao, W. A. Harrison, R. J. Schultz, J. P. Bader, and S. S. Yang, Antimicrob. Agents Chemother. 39:2718-2727, 1996). From these studies, the furanyl-containing analog UC10 was identified as the most potent inhibitor of human immunodeficiency virus type 1 (HIV-1) replication and a promising candidate for further development. Three new UC analogs (UC040, UC82, and UC781) have been determined to inhibit laboratory-derived and low-passage-number, primary virus isolates at low nanomolar concentrations in both established and fresh human cells. Each of the compounds synergistically interacted with the nucleoside analogs zidovudine, dideoxyinosine, dideoxycytosine, and lamivudine to inhibit HIV-1 replication. As a group, the UC compounds were found to be less active against viruses with the L100I, K103N, and Y181C amino acid changes in the RT and, upon in vitro selection, yielded resistant virus with the Y181C mutation in the RT. The most potent of the three new compounds, UC781, contains a furanyl side chain, similar to UC10, but differs in having an extended ether side chain instead of an oxime chain. The broad therapeutic index of UC781 (>62,000) resulted in effective inhibition of NNRTI-resistant virus isolates at high nanomolar concentrations. Furthermore, UC781 and the NNRTI costatolide were able to synergistically inhibit HIV-1 replication when used in combination, suggesting that UC781 may interact with the RT differently than the other UC analogs. The favorable anti-HIV properties of the UC compounds suggest they should be considered for further clinical development.

Anti-HIV Agents↗

Hyphodontal, a new antifungal inhibitor of reverse transcriptases from Hyphodontia sp. (Corticiaceae, Basidiomycetes).

In a search for inhibitors of RNA-directed DNA polymerases a new isolactarane sesquiterpenoid, hyphodontal (1), was isolated from fermentations of a Canadian Hyphodontia species. Its structure was elucidated by spectroscopic methods. Hyphodontal strongly inhibits the growth of several yeasts and is a non-competitive inhibitor of avian myeloblastosis virus (Ki 346 microM) and Moloney murine leukemia virus (Ki 112 microM) reverse transcriptases. In addition, cytotoxic and antifungal activities were observed.

Avian Myeloblastosis Virus↗

Determination of antiretroviral agents in human serum by capillary electrophoresis.

In this work, a simple and rapid electrokinetic chromatography method for the simultaneous separation of different protease inhibitors (indinavir, ritonavir, saquinavir, nelfinavir), nucleoside reverse transcriptase inhibitors (stavudine, zidovudine, didanosine) and non-nucleoside reverse transcriptase inhibitors (nevirapine, efavirenz) was developed. The analyses were performed in a 75 microm i.d. uncoated fused-silica capillary with 48.5 cm length (effective length of 40 cm) using a running buffer consisting of 20 mmol L(-1) sodium dodecyl sulfate, 10 mmol L(-1) sodium tetraborate, 30% acetonitrile and 5% ethanol. Samples were injected hydrodynamically by applying 50 mbar pressure during 6 s. All analytes were separated within 10 min with a voltage of 20 kV. The proposed method was validated for zidovudine, didanosine and efavirenz in human serum. Serum samples were prepared using a solid-phase extraction procedure (Waters Oasis HLB cartridges). For quantitative purposes, stavudine was chosen as the internal standard (IS). Method validation parameters were determined revealing good migration time repeatability (<0.7% RSD) and peak area repeatability (<1.2% RSD). Intra- and inter-day precisions were less than 1.7% and 4.4% RSD, respectively. Matrix matching analytical curves for each drug were linear in the 1.0-20.0 microg mL(-1) interval (r > 0.998). Limits of detection (LOD) were in range of 0.3-0.5 microg mL(-1). The extraction recoveries were higher than 90% with exception of efavirenz, which was 77.4%. Based on the performance characteristics, the proposed method was found suitable for the determination of zidovudine, didanosine and efavirenz in serum samples.

Acetonitriles↗

Delavirdine: a review of its use in HIV infection.

UNLABELLED: Delavirdine, a bisheteroarylpiperazine derivative, is a non-nucleoside reverse transcriptase inhibitor (NNRTI) that allosterically binds to HIV-1 reverse transcriptase, inhibiting both the RNA- and DNA-directed DNA polymerase functions of the enzyme. Delavirdine in combination with nucleoside reverse transcriptase inhibitors (NRTIs) produced sustained reductions in plasma viral loads and improvements in immunological responses in large randomised, double-blind, placebo-controlled studies of 48 to 54 weeks' duration. In patients with advanced HIV infection, triple therapy with delavirdine, zidovudine and lamivudine, didanosine or zalcitabine for 1 year significantly prolonged the time to virological failure compared with dual therapy (delavirdine plus zidovudine or 2 NRTIs; p < 0.0001). After 50 weeks' treatment, plasma HIV RNA levels were below the limit of detection (LOD; <50 copies/ml) for 40% of patients receiving triple therapy but for only 6% of those receiving dual NRTI therapy. Preliminary results suggest that delavirdine also has beneficial effects on surrogate markers as a component of protease inhibitor-containing triple or quadruple regimens. At 16 to 48 weeks, the minimum mean reduction in plasma viral load from baseline was 2.5 log10 copies/ml and mean CD4+ counts increased by 100 to 313 cells/microl. The proportion of patients with plasma HIV RNAlevels below the LOD (usually 200 to 500 copies/ml) ranged from 48 to 100% after > or = 16 weeks. Delavirdine was also effective as a component of saquinavir soft gel capsule-containing salvage regimens. Since delavirdine shares a common metabolic pathway (cytochrome P450 3A pathway) with other NNRTIs, HIV protease inhibitors and several drugs used to treat opportunistic infections in patients infected with HIV, the drug is associated with a number of pharmacokinetic interactions. Some of these drug interactions are clinically significant, necessitating dosage adjustments or avoidance of co-administration. Delavirdine is not recommended for use with lovastatin, simvastatin, rifabutin, rifampicin, sildenafil, ergot derivatives, quinidine, midazolam, carbamazepine, phenobarbital or phenytoin. Importantly, the drug favourably increases the plasma concentration of several protease inhibitors. Delavirdine is generally well tolerated. Skin rash is the most frequently reported adverse effect, occurring in 18 to 50% of patients receiving delavirdine-containing combination therapy in clinical trials. Although a high proportion of patients developed a rash, it was typically mild to moderate in intensity, did not result in discontinuation or adjustment of treatment in most patients and resolved quickly. The occurrence of Stevens-Johnson syndrome was rare (1 case in 1,000 patients). A retrospective analysis of pooled clinical trial data indicated that there was no significant difference in the incidence of liver toxicity, liver failure or noninfectious hepatitis between delavirdine-containing and non-delavirdine-containing antiretroviral treatment groups. In addition, the incidence of lipodystrophy, metabolic lipid disorders, hyperglycaemia and hypertriglyceridaemia was not significantly different between these 2 treatment groups. CONCLUSIONS: In combination with NRTIs. delavirdine produces sustained improvements in surrogate markers of HIV disease and prolongs the time to virological failure in adult patients with HIV infection. Preliminary data of delavirdine as a component of protease inhibitor-containing triple or quadruple highly active antiretroviral therapy regimens indicate that patients achieve marked improvements in virological and immunological markers. The drug is generally well tolerated, with a transient skin rash, typically of mild to moderate intensity, being the most common adverse effect. Delavirdine is an effective component of recommended antiretroviral treatment strategies for adult patients with HIV infection and, in combination with 2 NRTIs as a first-line therapy, the drug has the advantage of sparing protease inhibitors for subsequent use. Since delavirdine favourably increases plasma concentrations of several protease inhibitors, the drug may also be beneficial as a component of salvage therapy in combination with protease inhibitors.

Anti-HIV Agents↗

Nelfinavir plus nevirapine plus two NRTIS as salvage therapy for HIV-infected patients receiving long-term antiretroviral treatment.

PURPOSE: To evaluate a rescue therapy involving nevirapine plus nelfinavir plus two nucleoside reverse transcriptase inhibitors (NRTIs) in patients with prior extensive antiretroviral therapy (AT) including protease inhibitors (PIs) but not nonnucleoside reverse transcriptase inhibitors (NNRTIs). METHOD: Patients with failing regimens were prospectively enrolled. According to genotypic profile at baseline, two groups were identified: a highly resistant (HR) group, which included strains resistant to PI and NRTI, and a moderate nonresistant group (MR), which showed resistance only to PI or NRTI or no resistance. RESULTS: Twenty-two individuals were included. Average time of AT prior to enrollment was 3.7 years (range 1.4-7.6), median viral load 4.92 log(10) (interquartile range [IQR] 1.63 log(10)), and median CD4 cell count 64 cells/microL (IQR 94). After 16 weeks of treatment, seven patients (31%) achieved virological response, five of them (22.7%) with <500 c/mL (bDNA). Fourteen patients were studied for resistance. The HR group showed a poorer response than the MR group (0 vs. 7 responses; p =.034). CONCLUSION: We found a virological response in 31% of our patients, and mainly in those of the MR group some presented previous intolerance. These two factors probably reflect the number of drugs included in the rescue therapy to which the patient is sensitive. Treatment history as well as genotypic resistance assays are useful in identifying patients with the best chance of responding.

Adult↗

Antiviral drug discovery and development: where chemistry meets with biomedicine.

The successful development of antiviral drugs is highly dependent on a close interaction and collaboration between the chemist and the biologist (biomedic). This is illustrated by a number of representative examples: S-adenosylhomocysteine (SAH) hydrolase inhibitors which display broad-spectrum antiviral activity, bromovinyldeoxyuridine (BVDU) and derivatives thereof, that are highly selective inhibitors of varicella-zoster virus (VZV), (dideoxy)nucleoside reverse transcriptase inhibitors (NRTIs) and non-nucleoside reverse transcriptase inhibitors (NNRTIs) which are now widely used in the treatment of HIV infections (AIDS), the bicyclams (i.e. AMD3100) which were originally discovered as anti-HIV agents, then found to be potent CXCR4 antagonists and now being pursued for a number of indications such as stem cell mobilization, and the acyclic nucleoside phosphonates which have heralded a new strategy for the treatment of various DNA virus (herpes-, adeno-, pox-, papillomavirus) infections (cidofovir), hepatitis B (adefovir) and AIDS (tenofovir).

Animals↗

Human immunodeficiency virus type 1: drug resistance in treated and untreated Brazilian children.

Twenty-two vertically human immunodeficiency virus type 1 (HIV-1) infected Brazilian children were studied for antiretroviral drug resistance. They were separated into 2 groups according to the administration of antiretroviral therapy into those who presented disease symptoms or without symptoms and no therapy. Viral genome sequencing reactions were loaded on an automated DNA sampler (TruGene, Visible Genetics) and compared to a database of wild type HIV-1. In the former group 8 of 12 children presented isolates with mutations conferring resistance to protease inhibitors (PIs), 7 presented isolates resistant to nucleoside reverse transcriptase inhibitors (NRTIs) and 2 presented isolates resistant to non-nucleoside reverse transcriptase inhibitors (NNRTIs). Ten children were included in the antiretroviral na ve group. Eight were susceptible to NRTIs and all of them were susceptible to PIs; one presented the V108I mutation, which confers low-level resistance to NNRTIs. The data report HIV mutant isolates both in treated and untreated infants. However, the frequency and the level of drug resistance were more frequent in the group receiving antiretroviral therapy, corroborating the concept of selective pressure acting on the emergence of resistant viral strains. The children who presented alterations at polymorphism sites should be monitored for the development of additional mutations occurring at relevant resistance codons.

Adolescent↗

Determination of serum levels of thirteen human immunodeficiency virus-suppressing drugs by high-performance liquid chromatography.

Two high-performance liquid chromatographic methods using UV detection are presented for the determination of two different groups (A and B) of drugs used in the suppression of human immunodeficiency virus (HIV). Group A is comprised of six nucleosidic reverse transcriptase inhibitors, viz. zalcitabine, lamivudine, stavudine, didanosine, zidovudine and ziagen. Group B consists of seven drugs four of which are protease inhibitors (PIs) and three of which are non-nucleosidic reverse transcriptase inhibitors (NNRTIs). The PIs are: indinavir, nelfinavir, saquinavir and ritonavir. The NNRTIs are: nevirapine, delavirdine and efavirenz. Groups A and B require separate aliquots of serum for extraction and must be chromatographed separately.

Anti-HIV Agents↗

Are all non-thymidine analogue backbones appropriate for treating antiretroviral-naïve patients?

An increasing number of antiretroviral agents are available for the treatment of HIV infection. Many clinicians and patients prefer once-daily therapy, and this, in addition to accumulating evidence of toxicity associated with thymidine analogues, means many individuals commence a non-thymidine analogue-based regimen. Stavudine (d4T) is no longer recommended for initial therapy, and zidovudine (AZT) may also be associated with lipoatrophy. Despite investigations into nucleoside-sparing options, triple agent therapy with two nucleoside analogues [nucleoside reverse transcriptase inhibitors (NRTIs)] and a ritonavir-boosted protease inhibitor (PI) or a non-nucleoside reverse transcriptase inhibitor (NNRTI) remains the mainstay. In this article, we review the advantages, and drawbacks, of different non-thymidine NRTI backbones.

Antiretroviral Therapy, Highly Active↗

Pharmacological considerations in antiretroviral therapy.

Suboptimum drug exposure arising from pharmacological and pharmacokinetic factors is an important reason that combination antiretroviral therapy fails in patients with human immunodeficiency virus type 1 infection. With all three available drug classes, the major causes are drug-drug interactions and interpatient pharmacokinetic variability. Inadequate concentrations of protease inhibitors and non-nucleoside reverse transcriptase inhibitors occur when concurrently administered drugs interfere with their metabolism by the hepatic cytochrome P450 enzyme system, the major metabolic pathway for these drugs. Combined therapy with certain nucleoside reverse transcriptase inhibitors can reduce systemic drug exposure by interfering with the intracellular conversion of administered drugs to their active metabolites. Important causes of interpatient variability in pharmacokinetic parameters include low oral drug bioavailability and individual differences in drug disposition and metabolism. Careful selection and monitoring of combination drug therapy along with individualized rather than standard dosage regimens may minimize these pharmacological problems and help ensure optimum antiviral activity.

Anti-HIV Agents↗

Risk of severe hepatotoxicity associated with antiretroviral therapy in the HIV-NAT Cohort, Thailand, 1996-2001.

OBJECTIVE: To examine rates and predictors of severe hepatotoxicity with combination antiretroviral therapy in a developing country setting: the eight HIV-NAT randomized controlled trials in Thailand. METHODS: All patients (n = 692) received at least two nucleoside reverse transcriptase inhibitors; 215 also received a non-nucleoside reverse transcriptase inhibitor (NNRTI) and 135 also received a protease inhibitor. Severe hepatotoxicity was defined as an increase in alanine aminotransferase (ALT) level to five times the upper limit of normal and an increase of at least 100 U/l from baseline. Liver function tests were available at baseline and weeks 4, 8, 12, 24, 36 and 48. Hepatitis B virus (HBV) and hepatitis C virus (HCV) testing was performed on stored serum. RESULTS: Mean age was 32.3 years; 52% were male, 11% had Centers for Disease Control and Prevention category C HIV disease at baseline, and 22% had received prior antiretroviral therapy. Prevalence of HBV, HCV and HBV/HCV coinfection was 8.7%, 7.2%, and 0.4%, respectively. Incidence of severe hepatotoxicity was 6.1/100 person-years [95% confidence interval (CI), 4.3-8.3/100]. In multivariate analysis, predictors of severe hepatotoxicity were HBV or HCV coinfection, and NNRTI-containing therapy. Incidence of severe hepatotoxicity was particularly high among patients receiving nevaripine (18.5/100 person-years; 95% CI, 11.6-27.8) and nevirapine/efavirenz (44.4/100 person-years; 95% CI, 12.1-113.7). CONCLUSIONS: Incidence and risk factors for severe hepatotoxicity appear similar among these Thai patients to those in other racial groups. Development of standardized antiretroviral therapy regimens for developing country settings should consider potential toxicity and capabilities for monitoring of toxicity.

Adult↗

[Antiretroviral agents in HIV-infected patients with cirrhosis].

Since highly active antiretroviral therapies became available, the future of HIV-infected patients has been transformed. However, 20 to 25% of HIV patients are co-infected with hepatitis B or C viruses, and the course of these diseases has worsened, since these patients have an enhanced sensitivity to the hepatic toxicity of antiretrovirals. The relation between high antiretroviral concentrations and toxicity has been clearly demonstrated with certain protease inhibitors and non-nucleoside reverse transcriptase inhibitors (NNRTI) that have a predominantly hepatic metabolism (CYP4503A4). The nucleoside reverse transcriptase inhibitors (NRTI) are not predominantly metabolized by the liver, but may nevertheless be toxic for the liver through mitochondrial involvement. The hepatic toxicity observed in a patient treated with early or delayed antiretrovirals may be due to a cytolytic, cholestatic or mixed, direct or indirect, mechanism. Before initiating antiretroviral treatments, hepatic fibrosis must be explored (punch biopsy, biological fibrosis test, and Child-Pugh's score). It is recommended that the most hepatotoxic drugs be avoided, notably didanosine, didanosine+stavudine, nevirapine, and full-dose ritonavir. Although it is possible to initiate an antiretroviral at the standard dose in patients with cirrhosis (the therapeutic margin with antiretrovirals is wide), early assays are essential, particularly with PI and NNRTI, to adjust the dose and avoid adverse events. In any event rigorous monitoring is a must.

Anti-Retroviral Agents↗