Your favorite oblong fruit might be even healthier than you realized. According to The Gazette (Montreal) newspaper, a new study has found that chemicals commonly found in bananas are as potent in preventing HIV as two synthetic anti-HIV drugs.
Researchers say the findings could lead to a cheap new component for applied microbicides that prevent intimate transmission of HIV.
The miracle substance in bananas is called BanLec, a type of lectin, which are the sugar-binding proteins found in a variety of plants. Scientists have long been interested in lectins because of their ability to halt the chain reaction that leads to certain viral infections. In the case of BanLec, it works by binding naturally to the sugar-rich envelope that encases the HIV virus, thus blocking its entry into the body.
"The problem with some HIV drugs is that the virus can mutate and become resistant, but that's much harder to do in the presence of lectins," said lead author Michael D. Swanson. "Lectins can bind to the sugars found on different spots of the HIV-1 envelope, and presumably it will take multiple mutations for the virus to get around them."
Swanson and his colleagues noted that even modest success in developing BanLec into a womanly or BehindBased microbicide could save millions of lives. In fact, 20 percent coverage with a microbicide that is only 60 percent effective against HIV may prevent up to 2.5 million HIV infections in three years.
Furthermore, a BanLec ointment would be much cheaper to produce and distribute than most current anti-retroviral
One thing's for sure: new ways of stopping the transmission of HIV are desperately needed. Condoms are effective, but they are often used incorrectly or inconsistently,
The introduction of a cheap, long-lasting, self-applied ointment derived naturally from bananas could change all of that.
Current antiretroviral drugs can be divided into three classes: � Nucleoside analogue reverse transcriptase inhibitors (NRTIs) were the first type of drug available to treat HIV infection in 1987. When HIV infects a cell, it copies its own genetic code into the cell�s DNA, and the cell is then programmed to create new copies of HIV. To reproduce, HIV must first convert its RNA into DNA using the enzyme reverse transcriptase. Nucleoside analogue reverse transcriptase inhibitors act like false building blocks and compete with the cell�s nucleosides, thereby preventing DNA synthesis. This inhibits reverse transcriptase, which prevents HIV from infecting cells and duplicating itself. � Nonnucleoside reverse transcriptase inhibitors (NNRTIs) started to be approved in 1997. Like nucleoside analogue reverse transcriptase inhibitors, nonnucleosides also interfere with HIV�s ability to infect cells by targeting reverse transcriptase. In contrast to nucleoside analogue reverse transcriptase inhibitors, nonnucleosides bind directly to the enzyme. This blocks the binding site of the reverse transcriptase and inhibits the binding of nucleotides. � Protease inhibitors (PIs) were first approved in 1995. PIs interfere with viral replication by binding to the viral protease enzyme and preventing it from processing viral proteins into their functional forms and thereby rendering the resulting viral particles noninfectious (Peiperl, Coffey, and Volberding 2005). In recent years, the most volatile parameter in costeffectiveness analyses for HIV/AIDS has been the prices of antiretroviral drugs, which have dropped by about two orders of magnitude for some LMICs. Price reductions have not been consistent across countries, nor have they necessarily been larger for the poorest countries. This variability in pricing greatly complicates the establishment of national guidelines regarding which regimens to prescribe under which circumstances, because the ranking of regimens varies among and within countries as relative prices change. Box 18.6 discusses the three classes of drugs used in antiretroviral therapy. Because of their higher manufacturing costs and their more recent introduction into the market, protease inhibitors are more expensive than either nucleoside reverse transcriptase inhibitors or nonnucleoside reverse transcriptase inhibitors. They are also more difficult to manufacture, making them less attractive to generic manufacturers. Although the difference is less marked, nucleoside reverse transcriptase inhibitors tend to cost less than nonnucleoside reverse transcriptase inhibitors. Ranking different antiretroviral therapy regimens by their cost-effectiveness is more complex than doing so for most therapeutic situations, because a high proportion of patients will develop resistance to or intolerance of initial therapy and will need to stop their initial regimen and then initiate a second (and perhaps a subsequent) regimen, if available. One U.S. cohort study suggests that for 50 percent of patients the prescribed protease inhibitor�based regimen fails within a year (Deeks and others 1999). As a result, the cost-effectiveness of a regimen is a function not only of its effectiveness in isolation, but also of its impact on the effectiveness of future regimens. Thus, the comparative cost-effectiveness of different sequences of regimens needs to be considered. The effectiveness of antiretrovirals depends on not only the benefits conferred but also the associated side effects, the toxicity level of the drugs, and patients� adherence to the drug regimen. The ability of care providers to detect incipient toxicity at an early stage also influences the magnitude of side effects and toxicities. In low-income settings with limited laboratory capacity, a greater proportion of side effects will not be detected until they become severe. As a result, the relative costeffectiveness profiles will change depending on the availability of toxicity monitoring. Initiating antiretroviral therapy has a proven benefit for patients with a CD4 count of fewer than 350 cells per cubic millimeter (Palella and others 2003). In patients with a higher CD4 count, the benefits of antiretroviral therapy are believed to be outweighed by the toxicities that may accrue from continued drug exposure (Mallal and others 2000). Concerted research efforts are needed to gauge both the average costs of care and the survival benefits of identifying patients and initiating antiretroviral therapy while their immune function is still competent, compared with the costs and survival benefits associated with starting care late, on presentation of an opportunistic infection�as is currently the norm in LMICs. Drug Resistance. Drug resistance occurs as the virus evolves to escape the inhibitory effects of antiretroviral drugs. The capacity of HIV to mutate is extraordinary, as the wide diversity of HIV variants that occurs worldwide demonstrates. Viral diversification is driven by low-fidelity enzymes (which have a high rate of mutation) that carry out replication of the viral genome. Drug resistance resulting from being infected by a drugresistant HIV strain is known as primary drug resistance. Secondary drug resistance develops as a consequence of treatment. Primary HIV drug resistance to nucleoside reverse transcriptase inhibitors, nonnucleoside reverse transcriptase inhibitors, and protease inhibitors has been reported (Salomon and others 2000;Wegner and others 2000). The first reports of transmission of drug resistance have typically occurred within a few years of a drug�s introduction into clinical practice. The proportion of newly infected people who acquire drug-resistant HIV has implications for the choice of first-line regimen. Primary resistance in recently infected individuals in high-income countries is stable or has been in decline since 2000, following a rise between 1996 and 1999. Almost nothing is known regarding primary drug resistance among those recently infected in low-income countries, although this question will become more important with the increased availability of antiretroviral therapy in resource-limited settings. Drug resistance is associated with increases in plasma viral RNA levels and attenuation of the responses of CD4 counts to therapy.Nonetheless, clinical and epidemiological observations suggest that drug resistance does not completely offset the benefits of therapy (Deeks and others 1999; Ledergerber and others 1999). Individuals with drug-resistant HIV typically have plasma viral RNA levels that remain 3- to 10-fold lower than pretreatment levels. Furthermore, patients with drug resistance experience more rapid immunological decline and disease progression if they discontinue their drugs (Nijhuis, Deeks, and Boucher 2001). Importance of Adherence to Prescribed Therapy. With certain drugs, resistance can develop in as little as two weeks if therapy is suboptimal (which can be less than 90 percent adherence). Conversely, patients who adhere to therapy can obtain continued viral suppression for many years without the need for second- or third-line options. Research has shown that drug adherence is one of the most important predictors of continued treatment response (Mannheimer and others 2002). Patients in resource-limited countries are likely to be subjected to a number of influences that challenge their ability to adhere to the prescribed therapy, including limited education and the consequent poorer understanding of their disease state, unstable housing and financial circumstances, a limited number of treatment options, and clinicians with limited antiretroviral therapy treatment experience (Kitahata and others 1996). Those factors, in addition to the toxicity of the therapy, influence adherence and future disease progression rates (Duran and others 2001) and lead to an increase in drug resistance. Thus, poorly coordinated scale-up of antiretroviral therapy in some developing countries has the potential to jeopardize both the duration of clinical benefit for the first wave of patients who receive substandard care and future response rates as the prevalence of drug resistance increases (Harries and others 2001). Studies in India,Mexico, Senegal, and Uganda point to poor adherence (which for some classes of drugs can be adherence of less than 95 percent), inadequate doses and regimes, and poor monitoring as factors that contribute to more rapid development of antiretroviral therapy resistance (Oyugi and Bangsberg 2004, Laniece and others 2004, Bautista and others 2003, Liechty and Bangsberg 2003). By contrast, experiences in Haiti and Uganda suggest that it is possible to achieve adherence rates in developing countries equal to or better than those observed in high-income countries (Farmer and others 2001; Mitty and others 2002). Second-Line and Subsequent Therapies. Studies from highincome countries have unequivocally demonstrated that the probability that an antiretroviral therapy regimen will achieve viral suppression diminishes with each subsequent regimen (Deeks and others 1999). Similarly, the mean duration of viral suppression for those who achieve suppression is also lower for subsequent regimens (Deeks and others 1999). This finding is entirely expected because failing a previous regimen is associated with lower adherence, higher toxicity, or side effects and increased resistance, all of which increase the probability of similar problems occurring with subsequent regimens. Thus, the expected survival benefit per month of antiretroviral therapy declines with each change of regimen. In contrast, the monthly cost of therapy rises as a patient moves from first-line to more expensive protease inhibitor�based second-line and subsequent therapies. Given this steadily declining costeffectiveness, wealthier countries are likely to offer a greater number of regimen changes than poorer countries. Laboratory Monitoring of Immune Function to Guide Therapy Laboratory monitoring determines when antiretroviral therapy should be initiated and when it should be changed because of toxicity, lack of efficacy, or resistance. The optimal frequency and precision of monitoring depends on numerous factors, principally the following: � the expected rate of change of variables of interest � the expected frequency of events, such as development of resistance, adherence failure, and side effects � the relative cost of monitoring versus the cost of providing ineffective treatment � the magnitude of the secondary effects of monitoring (motivating prevention, motivating adherence). WHO has suggested a pragmatic approach to monitoring, with inexpensive, easy-to-measure parameters (bodyweight or body mass index, body temperature, hemoglobin, liver enzymes, and clinical symptoms) for monitoring in lowincome countries. More specialized markers�namely, CD4 count, viral load, and resistance genotyping�would be restricted to sentinel sites and tertiary care services (Gutierrez and others 2004), at least initially. The large price reductions for antiretroviral drugs are only now starting to be mirrored in the costs of monitoring tests as new technologies are introduced, collective bargaining is undertaken, and international pressure mounts on diagnostic manufacturers to provide more favorable pricing for LMICs. Commercial cytometric CD4 measurements are now available to some developing countries at less than US$5 per test (R. G�hde, personal communication, 2004).Viral load testing is still significantly more expensive, but even those prices have dropped to US$20 following negotiations on behalf of lowincome countries by theWilliam Jefferson Clinton Foundation. Even when the potential savings become an operational reality in developing countries, the costs of laboratorymonitoring will still represent an important proportion of the costs of providing antiretroviral therapy. Monitoring to Guide Initiation of Antiretroviral Therapy. If laboratory monitoring is performed, its optimal frequency must be determined. The closer patients get to an antiretroviral therapy threshold, the more often they must be tested to detect a CD4 decline that falls within a specific CD4 range. As use of antiretroviral therapy expands in LMICs and as the costs of drugs fall relative to the costs of laboratory monitoring, collecting empirical data and constructing models to compare different monitoring strategies is becoming increasingly urgent. In the absence of capacity to perform CD4 counts, several studies suggest that total lymphocyte count can be used as a proxy because of the correlation between the two counts (Badri andWood 2003).Research has also shown that falling body mass index is highly predictive of disease progression (Pistone and others 2002). In light of those findings, the cost-effectiveness of CD4 monitoring in developing countries must be considered in terms of its incremental improvement over total lymphocyte monitoring or body mass index monitoring rather than being compared with no monitoring at all. Testing for Primary Resistance. Testing for resistance in individual patients is still costly, because of both the cost of the diagnostic kit and the sophisticated laboratory capacity required to perform the tests. Because primary resistance is far less prevalent in LMICs than in high-income countries, no serious consideration is being given at this time to initiating individual resistance testing in the developing world. However, the choice of optimal first-line and subsequent treatment strategies should be guided by information about the prevalence of primary resistance to different antiretroviral drugs in a particular country, which indicates that populationlevel monitoring of the prevalence of resistance among antiretroviral-naive people living with HIV/AIDS is important. Monitoring Response to Therapy. Ideally, therapeutic failure should be detected as soon as possible to permit the implementation of clinical strategies to address toxicity, drug resistance, or poor adherence. Therapeutic failure leads to rising viral load and falling immune competence and to the subsequent development of opportunistic infections. Unfortunately, earlier detection comes at a price: testing for increases in viral load, which can be detected soonest, is more expensive than CD4 testing, which in turn is more expensive than the less sensitive monitoring of total lymphocyte count, which is more expensive than monitoring body mass index or waiting until clinical signs of failure appear. Where facilities for detecting early failure are absent, first-line therapy should be replaced by a completely new combination at failure, usually a protease inhibitor�based combination. Monitoring Toxicity. Available antiretroviral drugs have significant toxicity. Such toxicity is often insidious, progressing unnoticed until the patient�s health has been seriously impaired. Examples include zidovudine-associated anemia, nevirapine-associated impaired liver function, and didanosineassociated pancreatitis. Fortunately, the most commonly encountered serious toxicities can be detected either on clinical examination or with inexpensive laboratory tests. Data on the relative cost-effectiveness of different toxicity monitoring regimens are unavailable. Current guidelines identify what monitoring should be conducted in conjunction with specific antiretroviral drugs, depending on whether laboratory capacity is available (WHO 2004). Unfortunately, in the absence of a quantitative analysis of the costs of monitoring and the benefits associated with early detection of toxicity, it is difficult to provide guidance on the minimum laboratory capacity that should accompany the delivery of specific treatment combinations. Clearly, extremely low-cost monitoring tests are warranted for toxicities that occur frequently. The preeminent example is anemia monitoring for patients receiving zidovudine. Hemoglobin levels can be monitored for less than US$0.02 per test, which is almost certainly cost-effective given that the incidence of anemia with zidovudine therapy is approximately 10 percent in advanced-stage patients and that anemia frequently progresses to life-threatening levels if not detected.
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