Print this page    •   Back to Web version of article

The Body Covers: The 13th Conference on Retroviruses and Opportunistic Infections

Emtricitabine and Lamivudine May Be Similar, but They Differ in Important Ways

Coverage provided by Benjamin Young, M.D., Ph.D.

February 6, 2006

Two of the most frequently prescribed components of combination therapy for HIV are the cytidine nucleoside reverse transcriptase inhibitors lamivudine (3TC, Epivir) and emtricitabine (FTC, Emtriva). They are nearly identical in atomic structure, although they differ somewhat in their pharmacokinetic properties. Both drugs also select for the M184V mutation in reverse transcriptase -- leading to high-level resistance to both drugs.

Previous descriptive studies have suggested that the M184V mutation emerged less frequently with emtricitabine failure than with lamivudine failure. We'll have to wait for head-to-head studies of emtricitabine and lamivudine to be able to answer this important question. The susceptibility (or sensitivity) of lamivudine and emtricitabine can also be affected by other drug resistance mutations in reverse transcriptase. The question asked in this study is a critical one: To what extent do these mutations affect the two drugs -- are the two drugs similarly affected or not?

The current poster presentation by virologist Lisa Ross from GlaxoSmithKline and collaborators from Monogram Bioscience reviewed the effect of different reverse transcriptase drug resistance mutations on the fold change in susceptibility to lamivudine and emtricitabine. Because the M184 mutations cause very high-level resistance to both drugs (thereby negating the ability to measure additional influence on fold change), viruses with M184V or M184I were excluded from the study.

A fold change of 3.5 was used as the cutoff to determine resistance to both drugs. Viruses that harbored thymidine analog mutations (TAMs) had different fold changes for the two drugs, with more viral isolates with fold changes for emtricitabine that were greater than the cutoff. By contrast, viruses with the mutations K65R (associated with exposure to tenofovir [TDF, Viread]) or L74V (or I) had similar fold changes to lamivudine and emtricitabine.

While this study was well designed (and used state-of-the-art resistance tests to measure fold change[s]), these data probably don't have a far-reaching impact for the typical HIV-infected patient or his/her doctors -- most viruses that have TAMs probably also have mutations at 184. However, the ability of phenotypic assays to discriminate between lamivudine and emtricitabine tells us that while the drugs are very similar in many aspects, the two drugs differ in other aspects. Data like these enrich our understanding of the complex relationship between drug resistance mutations and the potential for cross resistance to other drugs.

Copyright Body Health Resources Corporation. All rights reserved.

You can find this article online by typing the following address into your Web browser:

Please Note: Knowledge about HIV changes rapidly. Note the date of this article's publication, and before treating patients or employing any therapies described in these materials, verify all information independently. If you are a patient, please consult a doctor or other medical professional before acting on any of the information presented in this article.

General Disclaimer: The Body is designed for educational purposes only and is not engaged in rendering medical advice or professional services. The information provided through The Body should not be used for diagnosing or treating a health problem or a disease. It is not a substitute for professional care. If you have or suspect you may have a health problem, consult your healthcare provider.