One Country Has Eliminated HIV Transmission to Newborns

  • Thailand has become the first Asian country to completely eliminate mother to child transmission of HIV
  • Since HIV is still a global pandemic, it is important for other countries to take note of the enormous success that Thailand has found through government support of health guidelines


While the virus existed earlier, the first case of HIV to be officially diagnosed in Thailand was in 1984. Since the first diagnosis in Thailand, the disease quickly spread, became epidemic throughout the country, and by the mid-90s, the rate of mother-to-child transmission (MTCT) had reached 20 to 40 percent.

A decade later, the country has managed to pull down these alarming numbers to 1.9 percent. Thailand has even lowered the annual number of women infected with HIV by 87 percent (from 2000 to 2014 ), and by 2016, Thailand became the first Asian country to eliminate MTCT of HIV.

Thailand’s success against MTCT transmission of HIV was recently published in the study: Elimination of mother-to-child transmission of HIV: lessons learned from success in Thailand.

Their success against the virus, experts believe, can be credited to their dedication to following a four-pronged approach to reduce MTCT transmissions recommended by the World Health Organization (WHO) and UNICEF:

  1. Primary prevention of HIV infection among women of childbearing age
  2. Prevent unintended pregnancies among women living with HIV
  3. Prevent HIV transmission from a woman living with HIV to her infant
  4. Provide appropriate treatment, care and support to mothers living with HIV and their children and families

Using these guidelines, the country implemented the 100% Condom Programme, which promotes 100% condom use with men soliciting commercial sex workers. This effort has significantly reduced HIV infection among women of reproductive age. Sustaining such initiatives is possible with guidance and support from Thailand’s government, who increased investment and focus for HIV/AIDS prevention and eradication. Voluntary HIV testing with same-day results, re-testing among pregnant HIV-negative women, and antiretroviral therapy (ART) for HIV-infected mothers are now accessible to women in Thailand thanks to stronger legislative support.


Thailand’s achievements can stand as a benchmark for other countries who are trying to address continued and rising HIV infection.

As UNAIDS Executive Director, Michel Sidibé points out in a statement:

Thailand has turned around its epidemic and transformed the lives of thousands of women and children affected by HIV. Thailand’s progress shows how much can be achieved when science and medicine are underpinned by sustained political commitment.

Around the world, there are 36.7 million people living with HIV. 78 million people have become infected since the epidemic began, and 35 million have already lost their lives due to AIDS-related complications. Barely half of those infected have access to treatment, and in 2015 alone, 2.1 million people became newly infected.

Women who are infected with HIV have a 15 to 45 percent chance of transmitting the virus to their children during pregnancy, labor, delivery, or through breastfeeding. These odds significantly drop to just a little over one percent once antiretroviral therapy is given to both mother and child. But because treatment isn’t 100 percent effective, a simultaneous preventative approach to lowering transmission is also important.

Hopefully, as the spread of HIV continues to be a global pandemic, other countries will take note of Thailand’s success. They have proven that proper government support and a clear set of guidelines can create enormous change, even in the most dire of situations.

Thailand is first country in Asia to eliminate mother-to-child transmission of HIV and syphilis

Thailand today received validation from WHO for having eliminated mother-to-child transmission of HIV and syphilis, becoming the first country in Asia and the Pacific region and also the first with a large HIV epidemic to ensure an AIDS-free generation. The Minister of Health of Thailand was presented with the certificate of validation during a ceremony which took place in New York on the eve of the United Nations General-Assembly High-Level Meeting on Ending AIDS.

“This is a remarkable achievement for a country where thousands of people live with HIV. Thailand’s unwavering commitment to core public health principles has made elimination of mother-to-child transmission of HIV and syphilis a reality, a critical step for rolling back the HIV epidemic. Thailand has demonstrated to the world that HIV can be defeated,” Dr Poonam Khetrapal Singh, Regional Director, WHO South-East Asia Region, said presenting the certificate of validation to Thailand in New York.

“Thailand has turned around its epidemic and transformed the lives of thousands of women and children affected by HIV,” said UNAIDS Executive Director, Michel Sidibé. “Thailand’s progress shows how much can be achieved when science and medicine are underpinned by sustained political commitment.”

“By investing in strong maternal and child health care and national AIDS prevention measures, Thailand has demonstrated there are ways to protect children from the global AIDS pandemic response,” said Karin Hulshof, Regional Director, UNICEF East Asia-Pacific Region. “Thailand’s achievement inspires its neighbours to greater action. There are still 21,000 infants who are born with HIV each year in the Asia-Pacific region, and more than 200,000 children who are growing up with HIV.”

Untreated, women living with HIV have a 15-45% chance of transmitting the virus to their children during pregnancy, labour, delivery or breastfeeding. However, that risk drops to just over 1% if antiretroviral medicines are given to both mothers and children throughout the stages when infection can occur.

According to Thailand’s Ministry of Public Health 98% of all pregnant women living with HIV have access to antiretroviral therapy and the rate of mother-to-child transmission of HIV has been reduced to less than 2%. In 2000, an estimated 1000 children became infected with HIV. In 2015, the number of children who became infected with HIV through mother to child transmission was reduced to 85, a decline of more than 90%, a significant achievement in a country where an estimated 450 000 people were living with HIV in 2014.

At the same time, sustained efforts and success in preventing new HIV infections have helped reduce HIV among women of childbearing age. According to Thailand’s health authorities, between 2000 and 2014, the annual number of women newly infected with HIV fell from 15 000 to 1 900 – a 87% reduction. Thailand’s Universal Health Coverage framework ensured essential health services were available to both rich and poor. The country’s commitment to equitable access has ensured that both Thai citizens and migrants are covered for HIV treatment.

Thailand’s commitment to the UNAIDS-led ‘Global Plan towards the elimination of new HIV Infections among children by 2015 and keeping their mothers alive’, combined with the Government’s decision to provide all pregnant women – including documented and undocumented migrant workers – free antenatal care, delivery and services for HIV and syphilis pushed treatment coverage rates up, culminating in validation of elimination of mother-to-child transmission.

Thailand’s pioneering success and leadership demonstrates how countries can make real change when good policy is followed up with high-level commitment. WHO, UNAIDS and UNICEF will continue to work with other countries in the region, along with partners to replicate Thailand’s success.

WHO validation process

In 2014, WHO and key partners published the guidance on global processes and criteria for the validation of the elimination of mother-to-child transmission of HIV and syphilis, which outlines the validation process and the different indicators countries need to meet.

As treatment for prevention of mother-to-child-transmission is not 100% effective, elimination of transmission is defined as a reduction of transmission to such a low level that it no longer constitutes a public health problem.

An international expert mission convened by WHO visited Thailand in April 2016 to validate the progress toward the elimination of mother-to-child transmission of HIV and syphilis. The members visited health centres, laboratories, and government offices, and interviewed health officials and other key actors. The mission included experts from Australia, Cambodia, China, Philippines, India, Indonesia, Nepal, Thailand, United States and representatives from WHO, UNICEF and UNAIDS.

Resistance to Malaria Drugs Has Spread in SE Asia.

International experts raised the alarm Tuesday over the spread of drug-resistant malaria in several Southeast Asian countries, saying it endangers major global gains in fighting the mosquito-borne disease that kills more than 600,000 people annually.

While the disease wreaks its heaviest toll in Africa, it’s in nations along the Mekong River where the most serious threat to treating it has emerged.

The availability of therapies using the drug artemisinin has helped cut global malaria deaths by a quarter in the past decade. But over the same period, resistance to the drug emerged on Thailand’s borders with Myanmar and Cambodia and has spread. It has been detected in southern Vietnam and likely exists in southern Laos, said Prof. Nick White of the Thailand-based Mahidol Oxford Tropical Medicine Research Unit.

White, a leading authority on the subject, said that while there’s no confirmed evidence of resistance in Africa, there’s plenty of risk of transmission by air travelers from affected countries, such as construction laborers, aid workers or soldiers serving on peacekeeping missions.

“We have to take a radical approach to this. It’s like a cancer that’s spreading and we have to take it out now,” White told a conference at the Center for Strategic and International Studies think tank in Washington. He said no alternative anti-malarial drug is on the horizon.

The U.N. World Health Organization, or WHO, is also warning that what seems to be a localized threat could easily get out of control and have serious implications for global health.

Mosquitoes have developed resistance to antimalarial drugs before.

It happened with the drug chloroquine, which helped eliminate malaria from Europe, North America, the Caribbean and parts of Asia and South-Central America during the 1950s. Resistance first began appearing on the Thai-Cambodia border, and by the early 1990s it was virtually useless as an antimalarial in much of the world.

Resistance to artemisinin is caused by various factors, such as use of substandard or counterfeit drugs, or prescribing artemisinin on its own rather than in combination with another longer-acting drug to ensure that all malaria-carrying parasites in a patient’s bloodstream are killed off.

Scientists have been working for decades to develop a malaria vaccine, but none is yet available.

Nowhere are the challenges to countering drug resistance greater than in Myanmar, also known as Burma, which accounts for most of malaria deaths in the Mekong region, according to a report for the conference by Dr. Christopher Daniel, former commander of the U.S. Naval Medical Research Center.

Myanmar’s public health system is ill-equipped to cope, although once-paltry government spending on it has increased significantly under the quasi-civilian administration that took power in 2011.

Dr. Myat Phone Kyaw, assistant director of the Myanmar Medical Research Center, said malaria drug resistance first emerged in the country’s east where migrant workers cross between Myanmar and Thailand, and is assumed to have spread to other regions. Death rates have dropped as effective treatments have become more available, but more aid and research is needed as transient workers in industries like mining and logging pose a continuing transmission risk, he said.

White said it is critical to prevent drug resistance creeping across Myanmar’s northwestern border with densely populated India. “In my view, once it gets into the northeast part of India, that’s it, it’s too late, you won’t be able to stop it,” he said.

The Center for Strategic and International Studies is advocating greater U.S. involvement and aid for health and fighting malaria in the Mekong region, particularly in Myanmar, where Washington has been in the vanguard of ramping up international aid. The think tank says that can increase America’s profile in Southeast Asia in a way that will benefit needy people and not be viewed as threatening to strategic rival, China.

But securing more funds won’t be easy at a time when Washington is cutting back on programs for its own poor. The U.S. is already a major contributor to international anti-malaria efforts, and in Myanmar, is promising $20 million per year in health assistance under its recently resumed bilateral aid program.

White said the problem was less one of lack of funds, than in countries having the will to take quick action to fight a disease that hits the rural poor, which have less of a political voice than urban populations.

He said infection rates have been dropping but the disease needs to be wiped out entirely or it could be distilled to the most resistant parasites and infection rates will rise again. “Once it reaches a higher level of resistance where the drugs don’t work, we are technically stuffed,” White said.

Food-Sourced Melatonin Provides Natural Way to Help Sleep.

Studies on melatonin have documented that the body’s own melatonin production helps us fall asleep, yet research on supplemental melatonin has been disappointing. What many have missed is that certain foods provide natural forms of melatonin, which have been shown to raise melatonin blood levels naturally and significantly aid sleep.

An abundance of research has linked higher melatonin levels with the ability to fall asleep. Yet this research has been done on the body’s own melatonin production. Melatonin production is stimulated by the pineal gland as the sun sets and the lights dim during the later evening. This helps us fall asleep, as melatonin helps slow down cellular metabolism.


As most of us age, and especially with higher stress levels, our body’s ability to produce melatonin wanes. This can produce a chronic issue of sleeplessness – which has the potential for producing greater risk of various disorders as we age – as lack of sleep quality has been linked with a myriad of chronic disorders, from chronic fatigue to dementia.

Does Supplement Melatonin Work and Is It Safe?

Yet synthetic melatonin – either produced in the lab or from cow urine – does not produce the same effects as the body’s own (endogenous) melatonin. Some studies have shown that synthetic melatonin can help ones sleep-phase cycles slightly – helping during jet lag or similar situations – when our sleep cycles get messed up.

But as a sleep inducer – synthetic melatonin has been disappointing at best. Some research – such as studies by Dement and Vaughan (1999) – has even found that synthetic melatonin can stunt growth among younger people along with producing a myriad of other side effects such as dizziness and headaches.

Furthermore, supplemental melatonin’s effectiveness as a sleep aid has been shown to be questionable. In an extensive review by researchers from the University of Alberta (Buscemi et al. 2004) prepared for the U.S. Department of Health and Human Services, 932 studies on melatonin since 1999 were analyzed—with 132 being qualified as offering clear results with good protocols. The study concluded that supplemental melatonin was:
• Not effective for treatment of most primary sleep disorders
• Not effective in treating most secondary sleep disorders
• Offered no evidence of effectiveness for jet lag and shift-worker disorders

Certain Natural Foods Provide a Safe Means of Melatonin

Yet little attention has been put on the fact that nature provides another means for increasing blood melatonin levels – by eating certain natural foods.

And recently, research from Thailand’s Khon Kaen University has found that the body’s levels of melatonin can be naturally raised through eating of some tropical fruits.

The researchers used a crossover study design with 30 healthy human subjects to see which fruits – tropical fruits selected for their melatonin content – would naturally raise the body’s melatonin levels.

The researchers tested six tropical fruits among the volunteers, giving them a diet heavy in that particular fruit for one week following a one-week washout. During these periods the researchers analyzed the subjects’ urine levels of 6-sulfatoxymelatonin – also referred to as aMT6s.

Higher levels of 6-sulfatoxymelatonin or aMT6s in the urine indicates higher levels of melatonin circulating within the bloodstream.

With each different fruit, the subjects’ aMT6s levels were tested. The 6-sulfatoxymelatonin (aMT6s) levels after eating some fruits – notably pineapples, bananas and oranges – increased significantly. Pineapples increased 6-sulfatoxymelatonin (aMT6s) levels by over two-and-a-half times (266%) while banana increased aMT6s levels by 180% – almost double. Meanwhile, oranges increased aMT6s levels by 47%.

The other fruits also moderately increased melatonin content among the patients.

Learn more about natural ways to boost melatonin levels and over 200 other natural remedies for getting to sleep.

Other Foods also Provide Melatonin Safely

Other research – as reported by Realnatural – has shown that natural melatonin from red tart Montmorency cherries (Prunus cerasus) can increase sleep efficiency and quality. A study from an international group of researchers found that drinking tart cherry juice for seven days increased sleep by an average of 34 minutes a night – by speeding up falling to sleep – and increased sleep efficiency by 5-6%.

And like the study from Thailand, the research found that drinking cherry juice increased 6-sulfatoxymelatonin levels naturally – without the need of exogenous or synthetic melatonin supplements.

Other foods that naturally increase melatonin levels include oats, sweet corn, rice, ginger, tomatoes, bananas, mangosteen and barley.

Source: Nature

5 Vital Prerequisites to Rocket Your Dream off the Ground.

What is more joyous in life than having a dream and knowing it’s possible?

The answer – going for it and making that dream your reality.

We’re going to share with you 5 vital prerequisites to support you to get your dream off the ground.


Do you have a dream? Do you know it’s possible to create/achieve it?

Most people get stopped right here – they don’t seriously entertain living their dream and/or they don’t believe it’s possible. So they pretty much kill their dream before it’s even had a chance to breathe.

1 – Allow yourself

Allow yourself to have a dream. Sounds simple right? And it is, but somehow in our modern society many of us have become constrained and suppressed, and focused primarily on working hard, toeing the line, doing what others expect of us, putting ourselves last after everything and everyone else, and making decisions based on fear – so much so that we’ve lost the ability to allow ourselves to follow what our hearts really want.

And here’s a HUGE truth that we’ve learnt first-hand… what your heart wants is  good for you in all respects. Your passions, what inspires you, what lights you up, what rocks your boat, what spins your wheels… those are the things that you need to pay most attention to. When you live from that passion and are driven by your dreams, you thrive, flourish, relax, laugh, smile and contribute. You become the best, most joyful and therefore healthy and happy version of yourself. That is the you that the world needs. That is the you that you need! You have to allow yourself to have what you most need.Self-denial has no place in our emerging world. If you’re going to have a happy and healthy life, and help others along the way, you need to help yourself first because when you thrive, everyone around you thrives.

Everyone has at least one dream, if not many dreams, for what their life can be like. The first step is to ALLOW yourself to release your dream, dig it out of wherever deep inside you it’s been buried. Commit now to being the Director of your own life. Take ownership for all areas of your life. No one else can stop you, only you can let others and circumstances block you from being who you are and doing what you love.

We had the dream to live on Waiheke Island and we did it. We dreamt of a journey through Thailand and we did it. We dreamt of a nomadic adventure to Hawaii and it happened. We dreamt of getting married in a tropical location and we did it. We dreamt of doing our first triathlon/duathlon and we did it. We dreamt of sharing our life changing adventures in books and publishing them onto the Amazon best seller list, and we did it. Those things all started with one defining moment, a moment of allowing. In a single moment of declaring a dream and acknowledging it’s possible, everything changes. If you give your dream air time and energy, it can grow.

You don’t need to know how it’s possible, you just have to believe it is. Every time we’ve created a big dream, we’ve literally never known exactly HOW that dream would be possible.  Like how the heck we’d go to Thailand to live for 3 months when we had jobs and commitments (dog, mortgage) in NZ, like how on earth we’d afford to go to Hawaii for 3 months with new businesses and a mortgage or like how we’d write and publish books when we had absolutely zero experience or knowledge to do so.

But you don’t need to know how, in order for the dream to take flight. You simply have to trust… which leads on to Prerequisite 2.

2 – Trust yourself

When you have a dream, there are always plenty of reasons to say no to yourself. You could come up with a million reasons why you shouldn’t, won’t or can’t follow your dream. But, if you trust yourself, you can make it happen. What do we mean by trust yourself?

Well, dreams aren’t random thoughts plucked from nowhere. They are unique to you. They are emotionally charged, heartfelt, passionate endeavours that come from somewhere within you. Which is the exact point of #2, you have to trust that feeling you get when your dream moves you and motivates you. Trust your gut instinct, intuition, your heart – no matter how radical your dream might seem.

All of us humans have become way too obsessed with our minds and we let our minds drive all our decisions. Our intuition is a very real 6th sense, equally if not more powerful than the mind. Our intuition tells us what direction is healthy and happiest for us to move in, and then we can use our minds as a brilliant tool to navigate in that direction. Over analysis causes paralysis and the mind has a great way of reasoning, rationalising, blocking and destroying dreams. Definitely use your mind, just don’t let your mind use you.

So, what do you instinctively feel is right for you? Trust and respect your inner knowing. Love yourself enough to take that feeling and hold onto it, protect it, let it guide you forward. Don’t disregard what drives you inside, don’t disregard who you know you really are and what you really want to do. That inner motivator for your dream is a very real part of the true you, it needs you to honour it and bring it into life. Don’t tell yourself you’re not good enough or you don’t deserve it or it’s not a priority. And most definitely do not tell yourself it’s not possible

Follow your inner compass!

If doubt is a killer for you, check out our Kick Doubt to the Curb workshop.

3 – Get clear on WHAT

What exactly is your dream? If you have undefined desires, how can those desires come to fruition? Getting clear on what your dream specifically is, is critical to creating it. That’s a no brainer!

Spend 10 minutes sitting quietly with yourself with pen and paper to write down anything that comes into your mind when you say:

  • “What do I dream of?”
  • “If I was being who I really am and doing what I really love, what would my life look like?”

Let me ask you:

  • What lifestyle inspires you?
  • What contribution do you want to make?
  • What hobbies, passions, job, business inspires you to express yourself?
  • Where do you want to live?
  • How do you want to live?
  • What environments do you thrive most in?
  • What do you want to create?

4 – Get clear on WHY

You have to have a big why. Your why is your motivator. In short, why do you want what you want? Why do you want that particular dream? Your “why” is what drives you, it will be what keeps you committed to taking action to create your dream, and it’s the energy that makes it happen. If your “why” is big enough you can create almost anything! Some people never quit, that’s because their “why” is really big and really juicy.


Write down why you want what you want. Never stop at the first answer that arises from your mind. Dig deeper to get the answer from your soul, from deep inside. It’s rarely about things, money, external circumstance. It’s usually always about the experience and the feeling you will get from having/living that experience. It’s the intangible inner state of happiness that really drives so many of us.

No external thing or place can ever make you happy. Happiness is an inner state that goes where you go, or not. You can thrive wherever you go in life, whatever you are doing – but not because of WHERE/WHAT but because of WHO you are being. Make choices about what you do and where you go that support you being who you really are, and naturally accentuate the true you.

For all our dreams, our “why” is always backed by our belief that if you’re not living a life you know you love, a dream you know you want, that you know is possible – then you’re robbing yourself of opportunity and you’re robbing the world of having you flying at your full potential and in your full happiness. The world needs all of us to be fully expressed – to be who we are and to do what we love.

If none of that sparks a why that is big enough for you, then check out what a nurse reported as the 5 most common regrets of people on their deathbeds, as reported by the Guardian in the UK. Take a moment to think seriously how this makes you feel…

  1. I wish I’d had the courage to live a life true to myself not what others expected of me
  2. I wish I hadn’t worked so hard
  3. I wish I’d had the courage to express my feelings
  4. I wish I’d stayed in touch with my friends more
  5. I wish I’d let myself be happier

Enough said, so on that note let’s move on to #5.

5 – Be aware of what stops you

If you’ve now stepped up and acknowledged your dream and you know it’s possible, you’ve allowed and trusted yourself, and defined your what and why, you may still fall victim to the biggest trap that keeps most people stuck.

You get stopped by your mind.

The human mind is incredibly capable of coming up with all the reasons why something can’t work, might not work, could go wrong, all the possible obstacles, all the cons, and this all happens with very little effort on your part. The human mind is also more than capable of coming up with all the exact opposite scenarios, pros, how and why something can and will work, but we’re just not conditioned togo into the possibility and positivity space without a little retraining and effort.

#5 is all about being aware of how your own mind might be stopping you. If you need to, you can actually write down all the negative stuff that your mind comes up with to stop you. Get it all out. Better out than in! None of what comes up will stop you, unless you choose to let it.

But at first you have to witness that it’s your own blocks that keep you stuck – your own reasoning, rationale, fears, worries, concerns, rehearsal for disaster, pessimism, and so on.

If you have a solid why that motivates you, your mind-made blocks won’t stand a chance. Your motivators and heartfelt passion will override those fears.

Simply be aware of your mind blocks, without having answers, without knowing how to resolve any of it.

Know it’s possible

We’ve applied this 5 step “allow, trust, what, why and awareness” process for getting goals and dreams off the ground in all areas of our life – from health and fitness to lifestyle, relationships, career and business. We’ve applied the same questions and tests each time. It works!

It’s easy to become lost in the notion that a dream is something that we aspire to but isn’t real. The very word ‘dream’ conjures up a sense of something out of reach. The truth is that dreams exist to be made manifest. Your dream needs you. It needs you in order to spark into life and become real. Don’t rob your dream of that opportunity. Don’t rob the world of your expression. All your dream needs is for you to know it’s possible and step outside of your questions, fears and concerns to give the dream a chance to sprout.



Antiretroviral PrEP for Injection-Drug Users?

In a randomized, controlled trial involving injection-drug users in Thailand, tenofovir reduced the risk for HIV infection.


Antiretroviral pre-exposure prophylaxis (PrEP) is effective in preventing sexually acquired HIV infection among men who have sex with men as well as heterosexual men and women. Might it also help to prevent HIV infection among injection-drug users? To find out, investigators from the CDC and the Thailand Ministry of Health conducted a study involving HIV-uninfected injection-drug users recruited at drug-treatment clinics in Bangkok.

A total of 2413 individuals were randomized to oral tenofovir or placebo, either administered daily via directly observed therapy (DOT) or provided at monthly visits. The decision to use DOT was up to the participants, who could switch at monthly visits. Each month during follow-up (mean duration, 4 years), participants received HIV testing and risk-reduction and adherence counseling. Drug levels were also measured at some of the clinics, and at the time of the first positive HIV test in all individuals who seroconverted.

The median age of participants was 31; 80% were men, and 48% had 

≤6 years of education. Twenty-two percent were enrolled in a methadone program. Baseline characteristics were similar between groups, except that sexual intercourse with casual partners and having sex with men during the 12 weeks preceding enrollment were more common in the placebo group.

HIV infection was confirmed in 50 participants — 17 in the tenofovir group and 33 in the placebo group — for an overall 48.9% reduction in HIV incidence with tenofovir in intent-to-treat analysis. Efficacy was higher — 73.5% — among individuals with detectable tenofovir levels in their plasma.

Comment: This study is the first to demonstrate the efficacy of tenofovir in preventing HIV infection among injection-drug users. Almost concomitantly, the CDC published interim guidance for pre-exposure prophylaxis in this population. Interestingly, the CDC recommended using tenofovir/FTC (not tenofovir alone, as studied in Thailand), arguing that tenofovir/FTC and not tenofovir alone is approved by the FDA for prophylaxis. The CDC also suggested that prevention services targeting injection and sexual risk behaviors be provided for injection-drug users.

I must emphasize that this study used directly observed therapy as one strategy, and that efficacy of antiretrovirals for prevention depends on adherence. Thus, any PrEP program should incorporate strong adherence counseling.


Source: Journal Watch HIV/AIDS Clinical Care

Antiretroviral prophylaxis for HIV infection in injecting drug users in Bangkok, Thailand (the Bangkok Tenofovir Study): a randomised, double-blind, placebo-controlled phase 3 trial.



Antiretroviral pre-exposure prophylaxis reduces sexual transmission of HIV. We assessed whether daily oral use of tenofovir disoproxil fumarate (tenofovir), an antiretroviral, can reduce HIV transmission in injecting drug users.


In this randomised, double-blind, placebo-controlled trial, we enrolled volunteers from 17 drug-treatment clinics in Bangkok, Thailand. Participants were eligible if they were aged 20—60 years, were HIV-negative, and reported injecting drugs during the previous year. We randomly assigned participants (1:1; blocks of four) to either tenofovir or placebo using a computer-generated randomisation sequence. Participants chose either daily directly observed treatment or monthly visits and could switch at monthly visits. Participants received monthly HIV testing and individualised risk-reduction and adherence counselling, blood safety assessments every 3 months, and were offered condoms and methadone treatment. The primary efficacy endpoint was HIV infection, analysed by modified intention-to-treat analysis. This trial is registered, number NCT00119106.


Between June 9, 2005, and July 22, 2010, we enrolled 2413 participants, assigning 1204 to tenofovir and 1209 to placebo. Two participants had HIV at enrolment and 50 became infected during follow-up: 17 in the tenofovir group (an incidence of 0·35 per 100 person-years) and 33 in the placebo group (0·68 per 100 person-years), indicating a 48·9% reduction in HIV incidence (95% CI 9·6—72·2; p=0·01). The occurrence of serious adverse events was much the same between the two groups (p=0·35). Nausea was more common in participants in the tenofovir group than in the placebo group (p=0·002).


In this study, daily oral tenofovir reduced the risk of HIV infection in people who inject drugs. Pre-exposure prophylaxis with tenofovir can now be considered for use as part of an HIV prevention package for people who inject drugs.


Once-daily oral tenofovir decreased the risk of HIV infection by 48·9% in injecting drug users when provided with other HIV prevention services at drug-treatment clinics in Bangkok. Findings from other pre-exposure prophylaxis trials showed that adherence had an important effect on efficacy.1112 In this study, efficacy increased from 46% to 56% in the per-protocol analysis based on observed adherence and to 74% when limited to participants with detectable tenofovir concentrations. Although the trial was not powered to assess efficacy in subgroups, we saw higher efficacy in women (79%) and in participants aged 40 years or older (89%)—two subgroups with high levels of adherence. The modified intention-to-treat efficacy result did not rule out tenofovir efficacy at less than 10% as specified in the protocol.

We do not know why HIV incidence in the two groups did not differ consistently until after 36 months (figure 2). Low levels of adherence or low risk behaviour during the first 36 months could have masked the effect of tenofovir, but adherence did not change by time on study and risk behaviour decreased during follow-up. The low HIV incidence and slow accrual of infections might be why no between-group difference was seen before 36 months. At 36 months, there were 27 infections and, assuming 49% efficacy, the distribution should have been nine with tenofovir and 18 with placebo. However, there were 13 with tenofovir and 14 with placebo, a difference of only four events.

As has been reported in other trials,1112 participants in the tenofovir group reported more nausea and vomiting in the first couple of months of follow-up than did those in the placebo group. When used for treatment of HIV, tenofovir is associated with small decreases in renal function.2627 We did not find higher rates of increased creatinine or renal disease in participants randomly allocated to tenofovir.

Other pre-exposure prophylaxis trials have described antiretroviral-resistance mutations in HIV-positive participants, especially in those with unrecognised HIV infection at enrolment.11—13 We did not detect tenofovir resistance in HIV-positive participants in this study. The two participants with unrecognised HIV infection at enrolment were randomly allocated to placebo, limiting the possibility that acquired resistance would occur.

Participant reports of injecting drugs and sharing needles decreased during follow-up, consistent with previous trials in people who inject drugs in Bangkok.2829 The HIV incidence in placebo recipients in our study was 0·68 per 100 person-years. This incidence compares with an incidence of 5·8 per 100 person-years in a preparatory trial done in the same clinics in 1995—99 and of 3·4 per 100 person-years during the 1999—2003 AIDSVAX B/E HIV vaccine trial.2228 This decrease over time is probably due to many factors, including monthly HIV risk-reduction counselling, decreased needle sharing, and monthly HIV testing speeding up the diagnosis of HIV and limiting the number of people with unrecognised acute HIV infection able to transmit HIV to others.

Our study had several limitations. Participants could have under-reported stigmatised and illegal behaviours such as injecting drugs.30 However, the illegality and stigma attached to these activities did not change during the trial, meaning that rates of under-reporting should have remained constant. The study aimed to establish whether tenofovir would reduce parenteral HIV transmission, but participants might have become infected sexually. Previous studies in people who inject drugs in the same clinics in Bangkok have shown strong associations between injecting drugs and HIV infection, but no association between sexual activity and HIV infection.2829 In this study, although reports of injecting drug use decreased, 1018 (45%) participants reported injecting drugs during follow-up, including 35 (70%) of those who contracted HIV during the course of the study. Furthermore, similar to the previous studies in the drug-treatment clinics, drug overdose, traffic accidents, and sepsis were the most common causes of death, and participants were frequently incarcerated. Together these data suggest that participants were actively injecting drugs and that parenteral HIV transmission, not sex, was the primary route of HIV infection. Additional risk behaviour analyses are underway. The study was done in drug-treatment clinics offering a package of HIV prevention interventions and DOT; tenofovir effectiveness might differ in other settings.

Findings from three randomised, placebo-controlled trials have shown that a daily dose of tenofovir or tenofovir-emtricitabine can reduce sexual HIV transmission.11—13 Findings from two other studies showed that tenofovir and tenofovir-emtricitabine did not reduce sexual HIV transmission.3132 Adherence seems to be the key factor determining efficacy.33These trials draw attention to the need for methods to help people using pre-exposure prophylaxis achieve effective levels of adherence.

To our knowledge, this study is the first to show that daily oral pre-exposure prophylaxis with tenofovir, when used in combination with other HIV prevention strategies, reduces the risk of HIV infection among people who inject drugs (panel). The US Food and Drug Administration has approved the use of tenofovir-emtricitabine to prevent sexual acquisition of HIV in high-risk individuals.34 On the basis of the results of this study, regulatory and public health authorities can now consider whether pre-exposure prophylaxis with tenofovir should be part of an HIV prevention package to reduce the risk of HIV infection in people who inject drugs.


Research in context

Systematic review

We searched PubMed for phase 1, 2, and 3 randomised clinical trials in human beings assessing tenofovir for the treatment of HIV infection and animal trials using tenofovir to prevent HIV infection. We used the search terms “HIV”, “tenofovir”, “treatment”, “prevention”, and “clinical trials”, restricting our search to studies published in English through December, 2004. The study was launched in 2005 and, at the time, no phase 3 clinical trials using tenofovir in human beings for HIV pre-exposure prophylaxis had published results.


To our knowledge, this is the first study to show that daily oral pre-exposure prophylaxis with tenofovir, when used in combination with other HIV prevention strategies, reduces the risk of HIV infection in people who inject drugs. Much like findings from other pre-exposure prophylaxis trials, our findings showed that adherence had an important effect on efficacy. On the basis of these findings regulatory and public health authorities can now consider whether pre-exposure prophylaxis with tenofovir should be part of an HIV prevention package to reduce the risk of HIV infection in people who inject drugs.


Effect of double dose oseltamivir on clinical and virological outcomes in children and adults admitted to hospital with severe influenza: double blind randomised controlled trial.


Objective To investigate the validity of recommendations in treatment guidelines to use higher than approved doses of oseltamivir in patients with severe influenza.

Design Double blind randomised trial.

Setting Thirteen hospitals in Indonesia, Singapore, Thailand, and Vietnam.

Participants Patients aged ≥1 year admitted to hospital with confirmed severe influenza.

Interventions Oral oseltamivir at double dose (150 mg twice a day/paediatric equivalent) versus standard dose (75 mg twice a day/paediatric equivalent).

Main outcome measure Viral status according to reverse transcriptase polymerase chain reaction (RT-PCR) for influenza RNA in nasal and throat swabs on day five.

Results Of 326 patients (including 246 (75.5%) children aged <15), 165 and 161 were randomised to double or standard dose oseltamivir, respectively. Of these, 260 (79.8%) were infected with influenza virus A (133 (40.8%) with A/H3N2, 72 (22.1%) with A/H1N1-pdm09, 38 (11.7%) with seasonal A/H1N1, 17 (5.2%) with A/H5N1) and 53 (16.2%) with influenza virus B. A further 3.9% (13) were false positive by rapid antigen test (negative by RT-PCR and no rise in convalescent haemagglutination inhibition titers). Similar proportions of patients were negative for RT-PCR on day five of treatment: 115/159 (72.3%, 95% confidence interval 64.9% to 78.7%) double dose recipients versus 105/154 (68.2%, 60.5% to 75.0%) standard dose recipients; difference 4.2% (−5.9 to 14.2); P=0.42. No differences were found in clearance of virus in subgroup analyses by virus type/subtype, age, and duration of illness before randomisation. Mortality was similar: 12/165 (7.3%, 4.2% to 12.3%) in double dose recipients versus 9/161 (5.6%, 3.0% to 10.3%) in standard dose recipients. No differences were found between double and standard dose arms in median days on supplemental oxygen (3 (interquartile range 2-5) v 3.5 (2-7)), in intensive care (4.5 (3-6) v 5 (2-11), and on mechanical ventilation (2.5 (1-16) v 8 (1-16)), respectively. No important differences in tolerability were found.

Conclusions There were no virological or clinical advantages with double dose oseltamivir compared with standard dose in patients with severe influenza admitted to hospital.


In this large randomised controlled trial of antiviral treatment in patients with severe influenza we found that double dose oseltamivir was well tolerated but did not confer additional virological or clinical benefits over standard dose treatment in patients in South East Asia. There were no differences between the treatment arms in detection of viral RNA or infectious virus on day five, and there were also no differences in clinical failure rates, mortality in hospital, or rates of adverse events between the dose regimens on day five. We enrolled a heterogeneous population that included mostly children and also those infected with avian H5N1 or H1N1-pdm09 viruses. While subgroup analyses based on age cohorts, virus type and subtype, and time to treatment did not suggest additional virological efficacy of double dose oseltamivir in any subgroup, these results should be interpreted with caution as the study was not powered for these analyses.

Our patients presented relatively late after the onset of illness, a median of five days overall (seven days for H5N1). Despite administration of oseltamivir, about 30% of those enrolled remained positive for viral RNA (the primary endpoint) after five days of treatment. Timing of oseltamivir treatment is important as several studies have shown that early treatment confers greater virological and clinical benefits.4 5 6 32 33 34 In particular, later viral clearance has been noted with delayed treatment with oseltamivir compared with treatment within two to three days after onset of symptoms in observational reports from patients with H1N1-pdm09, especially those with severe illness.35 36 37 38 39 40 In the current trial, 73 (22.4%) patients presented within three days of illness, but even in this subpopulation, double dose oseltamivir was not associated with more rapid viral RNA clearance. Over a quarter of patients received neuraminidase inhibitors before enrolment, which could have influenced the effect size and contributed to the low proportion of patients shedding virus at day five in both treatment groups.

Although viral RNA detection in samples from the upper respiratory tract might not accurately reflect viral replication in the lower respiratory tract, especially in those with severe illness,39 prolonged viral RNA detection in upper respiratory tract samples has been shown to correlate with inpatient morbidity and prolonged hospital stay. In our study viral detection on day five was observed at about twofold the frequency in those meeting the criteria for clinical failure, although lack of clinical failure was not a surrogate for cessation of viral detection. Thus in our study the delays in starting treatment with oseltamivir also probably contributed to the substantial rates of admission to intensive care (18%), use of supplemental oxygen (30%), mechanical ventilation (12%), and mortality in hospital of 6.4%. Although our study was not placebo controlled for ethical reasons, other studies indicate that early oseltamivir treatment in people with severe influenza is associated with both clinical benefits and more rapid viral clearance from upper respiratory tract samples.4 8 14 36 37 38 39 40 41

Possible reasons for findings

It is unclear why double dose oseltamivir does not seem to offer benefit over standard dose in patients with severe influenza. Blood trough concentrations of oseltamivir carboxylate from 75 mg or 150 mg twice daily in influenza exceed the IC50 (inhibitory concentration) of influenza viruses.42 43 Inhibition of viral neuraminidase by oseltamivir might be a saturable process, and maximal inhibition might be achieved with a standard dose; exceeding these concentrations might not produce an additional clinical or virological effect. In this regard, a randomised oseltamivir controlled study of intravenous peramivir (BioCryst Pharmaceuticals, Durham, NC), which reaches over 20-fold higher peak blood concentrations of active metabolite than oseltamivir carboxylate, found similar viral reductions in patients with influenza A virus admitted to hospital.44 Further studies of peramivir and other intravenous neuraminidase inhibitors currently in progress should provide additional evidence regarding this hypothesis.

Infection with avian H5N1 virus, higher baseline viral load, and severity of disease were independently associated with longer viral RNA detection. The association between avian H5N1, severe illness, and prolonged shedding has been well described.14 The clearance kinetics of influenza viruses, both without antiviral treatment and with oseltamivir treatment,32 41 could explain longer viral RNA detection with higher baseline viral loads. It is unclear whether the independent association with disease severity might be related to impaired mechanisms of viral clearance or higher intrinsic rates of viral replication or both in these patients. Severe chronic comorbidities are seen commonly in industrialised countries and are related to prolonged viral shedding but most of our patients lacked these comorbidities.40 41

The heterogeneous population characteristics, geographical differences in recruitment (most patients were from Vietnam but there were no significant differences between Vietnam and other sites), and the variety of infecting viruses in our trial reflect the clinical circumstances in South East Asia during our study but might be viewed as a limitation. Most of these patients were children and had low or normal BMI, and for all patients only about a fifth reported a chronic underlying medical condition. Thus, our findings are applicable primarily to the region where the study was conducted and other settings with similar characteristics of influenza epidemiology. We did not have many adults in our study and results were inconclusive but indicate no difference in efficacy between the two oseltamivir regimens. We would caution the extension of our results to, for example, morbidly obese adults with severe influenza and those who could have underlying chronic illnesses. We conducted several statistical comparisons and inevitably subgroup analyses involved small numbers; thus power was limited and some significant results could have resulted by chance. Additionally, as all patients were randomised to an active treatment, our study was not designed to evaluate the efficacy of oseltamivir in severe influenza nor in H5N1 infections. This large randomised trial did, however, examine an important clinical and public health question and showed a lack of a clinical or virological benefit of double dose compared with standard dose oseltamivir in patients admitted to hospital with severe influenza. Our results and other observational reports from avian H5N110 and H1N1-pdm0911 36 infections do not support routine use of double dose oseltamivir to treat severe influenza. These findings have implications for both clinical management and pandemic preparedness including during the current H7N9 epidemic.16 17 18

What is already known on this topic

  • Clinical trials in patients with uncomplicated influenza have shown that treatment with oseltamivir has clinical and virological benefit when administered within 48 hours of onset of symptoms
  • Observational studies in severe influenza have shown that oseltamivir treatment, if given early, is associated with reduced mortality and shorter length of hospital stay. Reduced mortality has also been reported for patients with H5N1 influenza treated with oseltamivir
  • Several authorities have suggested the use of double dose oseltamivir for severe influenza, although there is no clinical evidence to support this
  • In the largest randomised trial on the treatment of severe influenza, no clinical or virological benefit of double dose oseltamivir over standard dose was found
  • These findings have implications for both clinical management of severe influenza and for pandemic preparedness of emerging influenza viruses including the current H7N9 epidemic

What this study adds


Source: BMJ


HIV vaccine ‘still a decade away’, say researchers.

An effective HIV vaccine may not be ready for another decade despite ongoing efforts by scientists around the world, AIDS Vaccine 2012 conference heard this week (9–12 September).

In 2009 a trial in Thailand, called RV144 and involving 16,000 volunteers demonstrated, for the first time, that a vaccine can protect against HIV infection in humans. The vaccine trial represented a milestone for HIV vaccine research: “until this point there was no proof of concept”, Bill Snow, director of the Global HIV Vaccine Enterprise, told the conference held in Boston, United States.

Further evidence of the vaccine’s effectiveness against HIV infection was published in Nature this week (10 September). Researchers examined the genetic sequences of HIV viruses in people who received the vaccine and those who received a placebo, and found the vaccine was most effective against HIV viruses with two specific genetic footprints.

“This was an independent confirmation of the efficacy of the vaccine,” Morgane Rolland, who led the research and is based at the US Military HIV Research Program, told SciDev.Net.

But despite the vaccine’s success, researchers are struggling to overcome research and manufacturing challenges, and say that the process of making it ready for roll-out is taking longer than expected.

Speaking at the Boston conference, Jerome Kim, who led the study in Thailand and is based at the US Military HIV Research Program, said: “We underestimated issues related to manufacturing [the vaccine product to be used in trials]”. Changes were made to increase the scale of the trial and guarantee the safety of the volunteers, prolonging the process.

In addition, researchers were not prepared for going to the next phase. The company that produced the component of the vaccine booster was small, and initially lacked capacity for producing the vaccine on a larger scale.

“The main reason for the delays in [further stage] RV144 trials is that they were not well prepared for success; nobody was ready for doing a follow-up study,” Snow told SciDev.Net.

Another reason for the delay was the decision to move later stage trials to South Africa, where the epidemic is severe. South Africa has more people living with HIV, estimated at 5.6 million, than any other country in the world, according to the Joint UN Programme on HIV/AIDS.

The trial in South Africa is expected to start next year, but scientists will need to adapt the vaccine for the particular HIV viruses circulating in the region.

“We have to be realistic on where the timeline will leave us; after three years of experience, we are less optimistic to have short-term results,” said Kim. “There is so much diversity [of the HIV virus], that it will never be possible to have a universal vaccine.”

Kim highlighted that a vaccine is unlikely to be ready before the next decade.

But Bruce Walker, a researcher at the Harvard University Center for AIDS Research and co-chair of the Boston conference, said “the HIV vaccine is a solvable problem, it is only an issue of human and funding resources”.