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Clinical Policy Bulletin:
HIV Drug Susceptibility and Resistance Tests
Number: 0316


  1. Aetna considers HIV drug susceptibility and resistance tests (phenotypic or genotypic) medically necessary for any of the following groups:

    1. During acute (new onset) HIV infection to determine if a drug-resistant viral strain was transmitted and plan regimen accordingly; or
    2. Members with suboptimal suppression of viral load after initiation of anti-retroviral therapy to determine the role of resistance and maximize the number of active drugs in the new regimen if indicated; or
    3. Members with virologic failure during highly activated anti-retroviral therapy (HAART) to determine the role of resistance in drug failure and maximize the number of active drugs in the new regimen if indicated.

    Aetna considers HIV drug resistance and susceptibility tests experimental and investigational for all other indications becasue their effectiveness for indications other than the ones listed above has not been established.

  2. Aetna considers both HIV phenotypic and genotypic tests when performed at the same time not medically necessary because this approach is duplicative.  Upon review, the alternate type of HIV resistance assay (either phenotypic or genotypic) may be considered medically necessary on an exception basis for members with virologic failure (indicated by a rising plasma HIV RNA concentration (viral load) in HIV-infected individuals receiving adequate doses of antiretroviral therapy where other potential causes of virologic failure have been excluded) despite apparent lack of drug resistance by one type of HIV resistance assay (either phenotypic or genotypic).

  3. Aetna considers phenotypic recombinant virus assays/HIV tropism testing (i.e., Trofile) or genotypic HIV V3-loop assays medically necessary for determining virus tropism before commencement of a chemokine receptor 5 (CCR5) antagonist (e.g., maraviroc [Selzentry]).

    Aetna considers HIV tropism testing experimental and investigational for other indications (e.g., during or after failure of a CCR5 antagonist treatment, or for predicting disease progression) because its effectiveness has not been established.

  4. Aetna considers drug resistance testing experimental and investigational for members who have discontinued the use of anti-retroviral drugs because drug resistance mutations may become minor species in the absence of selective drug pressure.  Current tests may not detect minor drug resistant species.

  5. Aetna considers drug resistance testing for members who have HIV viral loads of less than 1,000 HIV RNA copies/ml experimental and investigational because available tests cannot reliably detect this low level of viral load.


Evidence suggests that HIV viral drug resistance is correlated with poor virological response to new therapy.  In-vitro phenotypic and genotypic tests for HIV drug resistance are now available.  A phenotypic test measures the drug susceptibility of the virus by determining the concentration of drug that inhibits viral replication in vitro.  A genotypic test identifies the presence of mutations that are known to confer reduced drug susceptibility.  Several studies have suggested that resistance testing may be useful in assessing the success of salvage anti-retroviral therapy, and improving short-term virological response.  Resistance testing is presently recommended to help guide the choice of new drugs for patients with HIV-1 infection after treatment has failed.  Guidelines also state that resistance testing should be considered in patients with acute HIV infection to assess whether a drug-resistant virus was transmitted.

Phenotypic and genotypic tests appear to provide similar results.  The latter is more commonly used because tests are more readily available and results are available more quickly.  Currently, there is insufficient information as to which approach is preferable in any particular clinical setting.  The Panel on Clinical Practices for Treatment of HIV Infection (2004) concluded that: “There are currently no prospective data to support the use of one type of resistance assay over the other (i.e., genotyping vs. phenotyping) in different clinical situations.  Therefore, one type of assay is generally recommended per sample; however, in the setting of a complex prior treatment history, both assays may provide important and complementary information.”

Current evidence for combined genotyping and phenotyping is limited to non-randomized studies; no randomized studies have compared the combination of genotyping and phenotyping directed therapy compared to either genotyping or phenotyping alone.

Commercially available HIV drug susceptibility and resistance tests include genotypic tests (e.g., ABI Gene Sequencing; TrueGene HIV Genotyping GeneKit; HIV-1 GeneSeek Test; Murex LiPA HIV-1 RT; ViroSeq Genotyping System, and Affymetrix GeneChip HIV PRT Assay)) and phenotypic tests (e.g., PhenoSense HIV, and Virco Antivirogram).

Napravnik et al (2010) examined the suitability of the ExaVir Load and ExaVir Drug assays for use in patient monitoring.  Specimens from 108 adults were used to compare ExaVir Load HIV-1 RT to Amplicor HIV-1 Monitor HIV-1 RNA, and ExaVir Drug phenotype to HIV GenoSure genotype.  HIV-1 RT and HIV-1 RNA levels were comparable (Pearson correlation coefficient 0.83).  Most (94 %) had detectable results in both assays.  The mean difference (HIV-1 RT minus HIV-1 RNA) was -0.21 log(10)cps/mLequiv.  Relationship between HIV-1 RT and HIV-1 RNA was not affected by RT mutations, CD4 cell count, or efavirenz (EFV) or nevirapine (NVP) use.  Phenotypes were generally consistent with genotype findings for EFV, but not for NVP.  Most patients (93.9 %) with phenotypic EFV resistance had at least 1 EFV mutation, while 78.0 % of patients with phenotypic NVP resistance had at least 1 NVP mutation.  Eleven of 49 samples tested for EFV susceptibility were found resistant (n = 2) or with reduced susceptibility (n = 9) despite the absence of genotypic resistance.  Eleven of 45 samples tested for NVP susceptibility were found resistant (n = 9) or with reduced susceptibility (n = 2) with no evidence of genotypic mutations.  The authors concluded that the ExaVir Load assay performed well and may be an alternative to amplification based techniques for HIV-1 RNA quantification.  On the other hand, the ExaVir Drug assay for phenotypic resistance testing requires further evaluation, especially for NVP.

Maraviroc (Selzentry) is indicated for use in combination with other anti-retroviral agents, for treatment-experienced adult patients infected with only chemokine receptor 5 (CCR5)-tropic HIV-1 detectable, who have evidence of viral replication and HIV-1 strains resistant to multiple anti-retroviral agents.  Tropism and treatment history should guide the use of maraviroc (Mueller and Bogner, 2007).

According to the manufacturer of maraviroc (Pfizer, 2008), the following points should be considered when initiating therapy with Selzentry:

  • The safety and efficacy of Selzentry have not been established in treatment-naive adult patients or pediatric patients.
  • Tropism testing and treatment history should guide the use of Selzentry.
  • Use of Selzentry is not recommended in patients with dual/mixed or CXCR4-tropic HIV-1 as efficacy was not demonstrated in a phase 2 study of this patient group.

Also, there are no study results demonstrating the effect of Selzentry on clinical progression of HIV-1 (Pfizer, 2008).

Whitcomb et al (2007) stated that most HIV-1 strains require either the CXCR4 or CCR5 chemokine receptor to efficiently enter cells.  Blocking viral binding to these co-receptors is an attractive therapeutic target.  Currently, several co-receptor antagonists are being evaluated in clinical trials that require characterization of co-receptor tropism for enrollment.  These researchers described the development of an automated and accurate procedure for determining HIV-1 co-receptor tropism (Trofile) and its validation for routine laboratory testing.  HIV-1 pseudoviruses are generated using full-length env genes derived from patient virus populations.  Co-receptor tropism is determined by measuring the abilities of these pseudovirus populations to efficiently infect CD4+/U87 cells expressing either the CXCR4 or CCR5 co-receptor.  Viruses exclusively and efficiently infecting CXCR4+/CD4+/U87 cells are designated X4-tropic.  Conversely, viruses exclusively and efficiently infecting CCR5+/CD4+/U87 cells are designated R5-tropic.  Viruses capable of infecting both CXCR4+/CD4+/U87 and CCR5+/CD4+/U87 cells are designated dual/mixed-tropic.  Assay accuracy and reproducibility were established by evaluating the tropisms of well-characterized viruses and the variability among replicate results from samples tested repeatedly.  The viral subtype, hepatitis B virus or hepatitis C virus co-infection, and the plasma viral load did not affect assay performance.  Minority sub-populations with alternate tropisms were reliably detected when present at 5 to 10 %.  The plasma viral load above which samples can be amplified efficiently in the Trofile assay is 1,000 copies per ml of plasma.  Trofile has been automated for high-throughput use; it can be used to identify patients most likely to benefit from treatment regimens that include a co-receptor inhibitor and to monitor patients on treatment for the emergence of resistant virus populations that switch co-receptor tropism.

The Panel on Anti-retroviral Guidelines for Adults and Adolescents' guidelines on the use of anti-retroviral agents in HIV-1-infected adults and adolescents (DHHS, 2013) recommends that a co-receptor tropism assay should be performed whenever the use of a CCR5 co-receptor antagonist is being considered. The Panel also recommends that co-receptor tropism testing for patients who exhibit virologic failure on a CCR5 antagonist. The Panel stated that a phenotypic tropism assay is preferred to determine HIV-1 co-receptor usage, but that a genotypic tropism assay should be considered as an alternative test to predict HIV-1 co-receptor usage. The guideline explained that, compared to genotypic testing, phenotypic testing has more evidence supporting its usefulness. Therefore, a phenotypic test for co-receptor usage is generally preferred. However, because phenotypic testing is more expensive and requires more time to perform, a genotypic test to predict HIV-1 co-receptor usage should be considered as an alternative test

A European consensus panel on HIV tropism testing (Vandekerckhove et al, 2010; Vandekerckhove et al, 2011) concluded that both the phenotypic Trofile assay and genotypic population sequencing of the V3-loop are recommended for use in clinical practice.  Although the panel did not recommend one methodology over another, the panel stated that it anticipated that genotypic testing will be used more frequently because of its greater accessibility, lower cost and shorter turnaround time.

Perez-Olmeda and Alcami (2013) stated that assessment of HIV co-receptor tropism assay is recommended before starting therapy with CCR5 co-receptor antagonists.  So far, only maraviroc (MVC) has been approved for clinical use and a tropism assay is mandatory for patients with virologic failure or patients in which MVC is considered into future treatment options.  Viral tropism can be assessed with either genotypic or phenotypic methods and to this aim different techniques have been developed.  However, it is unclear which assay is more appropriate for routine testing.  In fact, although phenotypic assays are considered the gold standard as they directly measure the viral tropism and current versions allow detection of a lower threshold of minor CXCR4-dependent variants, the genotypic assays present major practical advantages for their use in the clinical setting.

The Department of Health and Human Services’ Panel on Antiretroviral Guidelines for Adults and Adolescents’ guidelines on “The use of antiretroviral agents in HIV-1-infected adults and adolescents” (2013) provided the following recommendations:

  • A co-receptor tropism assay should be performed whenever the use of a CCR5 co-receptor antagonist is being considered (AI).
  • Co-receptor tropism testing is also recommended for patients who exhibit virologic failure on a CCR5 antagonist (BIII).
  • A phenotypic tropism assay is preferred to determine HIV-1 co-receptor usage (AI).
  • A genotypic tropism assay should be considered as an alternative test to predict HIV-1 co-receptor usage (BII).

Mortier et al (2013) noted that determination of HIV-1 co-receptor use is a necessity before initiation of a CCR5 antagonist; but the longevity of a CCR5-use prediction remains unknown.  Genotypic co-receptor tropism determination was performed in 225 newly diagnosed individuals consulting an AIDS Reference Center.  Samples were collected at diagnosis and at initiation of anti-retroviral therapy or just before closure of the study for patients who did not initiate therapy.  For individuals with a discordant tropism prediction on the 2 longitudinal samples, analysis of intermediate samples and single genome sequencing of pro-viral DNA was performed to confirm the tropism switch.  Deep sequencing was done to identify minor CXCR4 or CCR5-using populations in the initial sample.  Overall, tropism switches were rare (7.6 %).  Only a geno2pheno false positive rate of less than 50 % at baseline was retained as predictive for a subsequent switch from CCR5-use only to predicted CXCR4-use.  Minor CXCR4-using virus populations were detected in the first sample of 9 of the 14 R5-to-X4 switchers, but the subsequent outgrowth of these minor populations was documented in only 3.  The authors concluded that with the current guidelines for treatment initiation at CD4(+) T cell counts of less than 500 cells/mm(3), co-receptor switch between diagnosis and starting anti-retroviral therapy is rare.  Patients with R5 viruses and a geno2pheno FPR of less than 50 % are more prone to subsequent co-receptor switch than patients with an FPR of greater than 50 % and will need repeat tropism testing if initiation of maraviroc is considered and previous testing dates from more than 1 year before.

CPT Codes / HCPCS Codes / ICD-9 Codes
CPT codes covered if selection criteria are met:
81400 - 81408
+ 87904
ICD-9 codes covered if selection criteria are met:
042 Human immunodeficiency virus [HIV] disease
079.53 Human immunodeficiency virus, type 2 [HIV-2]
V08 Asymptomatic human immunodeficiency virus [HIV] infection status

The above policy is based on the following references:
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Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to change.
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