Saturday, August 29, 2015
Maria Mejia & Jason Wood
A Warrior’s Path
Photo by Sean Black
Maria Mejia’s story may be an uncomfortable read for some individuals, but it’s a must-read for many of us. It talks about sexual molestation, abuse, drug use, violence, and HIV/AIDS in such a way that I had to remind myself that it wasn’t fiction I was reading, but the real-life story of a flesh-and-blood woman. The woman is AIDS activist Maria Mejia. The story is her journey of spiritual, and physical transformation, told candidly in her new book, From a Warrior’s Passion and Pain.
Upon reading her story, words from a Whitney Houston cover came to mind: “I’m every woman.” That’s because Mejia’s life reflects every woman’s life, and every man’s for that matter. What is unique about her story is that it connects to people from all walks of life. It’s relatable. Mejia, a native of Colombia, has specific experiences, but everyone will understand her battles and her triumphs.
Reading the book, one may wonder why she waited so long to tell her story. Truth is, she has been offered the opportunity several times in the past, but each time she didn’t feel she was ready, especially when she wanted to talk about more than HIV/AIDS, about her upbringing, her family and life in a street gang. But when Jason Wood, publisher of Kantanoose Global, an independent publishing house specializing in “sharing compelling stories about the human spirit,” contacted her, Mejia felt that she could trust him with her story. And now, a year later, From a Warrior’s Passion and Pain saw print.
I caught up with both Maria Mejia and Jason Wood to find out more about their collaboration on the book. During our conference call, they would chat with ease, sometimes anticipating what the other was about to say…just as old friends would do.
Alina Oswald: So, how did you two meet?
Jason Wood: I was on Facebook, browsing around, and I saw her name. Her middle name had HIV in quotations, [Maria “HIV” Mejia.] I thought to myself, it can’t be real. Nobody is that bold. I went to her page and started looking around, and realized it’s real. I messaged her that I wanted to talk to her.
Maria Mejia: To tell you the truth, I was not shocked, because I get messages like that all the time, from men and women. When Jason [contacted] me, I explained that I was HIV-positive, and that I’m an activist. My mission is to prevent new infections.
What made you decide to collaborate?
JW: Many of us have an experience [that we never fully process]. Say, we were molested or raped or something happened to us. We get older, but we never grow up…and I can say that from my own life. But Maria reinvents herself. And you look at the finished product right now, and she’s an incredible woman! She didn’t let any one thing [from her past] define her.
MM: [The book tells] exactly what I’ve been through, and then some, because I’ve been through so much, but it was very important for me to share my story. [In terms of collaborating on the book,] I felt that Jason and I were meant to be. We have similar backgrounds. I trusted him with my story. I’m glad that I made the choice, because he really [wrote it] as if it was me writing it. We are a team!
Jason, could you explain the book writing process?
JW: It took over one year to finish it. We went at a pace that was comfortable for both of us. In my experience, you can’t rush somebody to go through the most intense parts of their life. [The book] is not just about HIV. It’s a very intimate look into her life. A lot of times we’d go back [and forth, until] we’d really narrow it down to her words, her feelings, and experiences.
For me, on day one, when I saw [the word “HIV” in her name, she was] my hero, but it has become more than that. By day 365 I have learned that this is a completely complex and diverse person. HIV is [only] one of a thousand things that she’s experienced. I don’t want to spoil the book, but between the foster home system, sexual abuse, having to live in different places, and adapting, adjusting, and surviving, I mean…she’s a warrior. She earned the title.
[What] I found very unique about the process [of writing Maria’s story, is that] there are other people she talks about [in the book], and she’s extremely protective of [their] privacy. No matter what has happened, she wanted to be fair and very cautious about other people’s feelings, even when those people did not [return] the [same] feelings. We were very careful to tell her story, and not go too far into the lives of other people [involved] in her story.
What do you want to accomplish with this book, Maria?
MM: I want to humanize the virus, and to prevent new infections. I want people to understand that no matter what struggles they go
through in their lives, it’s not the end. It is all about how [they] react to the situation, manage to pull through [and] continue to fight, because life is about that—good and bad moments. I’m a fighter by nature. I still continue to fight.
To me, it doesn’t matter where you come from or what you’ve done or what you’ve been through. The important thing is what you are today, what you do now. I don’t let my past define me, but I [use] my past and my present to teach people to have a more positive future.
In the book, you talk about the “misunderstood chimera that is HIV,” and speak to readers from all walks of life, in languages they each understand. Why is that important?
MM: The education of HIV has helped me in my activism, because I’m relatable to everybody, not only in the Latino community. I could speak to the biggest thugs in jail, which I have, and they would relate to me; to doctors, and scientists, people in Europe, young, old…. I can reach anyone. Anybody can relate to me.
[HIV education is important because] HIV is still here. Unfortunately the statistics show a rise in infections. We need to educate [everybody, and show them that they] can overcome any obstacle with dignity; that they should not be ashamed of their past. The forgiveness that I gave [those who hurt me] was a gift to myself, because I could not be chained to that hate. It’s within us to make that [kind of] change. By doing that we can change the world, one person at a time.
You also reverse HIV stereotypes, in particular when it comes to the topic of women and the disease.
MM: There’s still a lot of stigma, misinformation, and lack of education out there. [People who are not infected or affected by the virus, don’t think of HIV.] So it’s very important for me to talk about women and HIV because of that, and also to give hope to the hopeless, because there are a lot of women with HIV who feel worthless, [or not worth of anybody’s love.]
One can live and love while living with HIV. My wife, who is HIV-negative, and I have been together for almost seven years. HIV doesn’t define who I am. There is life after the diagnosis. It’s not an easy road, but it’s not the end.
Anything you may want to add, Jason?
JW: I think that, unlike other diseases and conditions, [when it comes to HIV/AIDS,] information itself can be a huge preventative medication. Not for people that have contracted [the virus] but for billions and billions of people that have not. You talk about women, but the problem is, it still isn’t cool for a guy to be reading a book or watching a program about HIV.…
There’s a chapter in the book [that talks about] a guy who’s hitting on Maria [and cannot believe she has HIV because she’s too pretty.] It sounds comical, but that’s typical, [even] in 2014. When you’re in the world of HIV/AIDS and medicine, it seems silly. But when you’re not in that world, it’s common….You need to realize that there’s no typical face of this virus.
In the book Mejia mentions that “thirty years from now, we could have a new generation that barely remembers the old days of HIV. [Making sure that doesn’t happen is] up to us.” I asked her what her thoughts were on the progress we’ve made so far in finding new treatments, and possibly, a cure. “What I really want, because I’m really tired of having HIV, [is] a cure. [But] I don’t think it’s going to happen within at least ten to fifteen years, because the truth is that [AIDS is] a business,” she says, worrying that profits are ultimately trumping people’s lives but hopeful that researchers will prevail and deliver a cure or vaccine despite the drive for money. When she speaks to HIV-positive and negative teens, she reminds that, while HIV is not a death sentence, medications are no joke—they often come with another set of problems, such as toxicities and side effects, no matter what the benefits. “This is like getting chemotherapy for the rest of your life without a break,” she says, stressing that if a cure is not forthcoming then she wants improvements on medications to make them less toxic.
Mejia’s story is a story of human resilience that takes the readers on a journey of self-discovery, while experiencing the full spectrum of emotions. An important take-away from this story is Mejia’s ability to “take the shame out of the game,” as Wood refers to it. Once people are not ashamed or afraid anymore of their past, they can learn from their experiences, and open up the much-needed conversation about unpopular, yet vital topics, such as HIV, drug use, violence, or abuse.
After all, nobody is ashamed today of having breast cancer, or diabetes, anymore. The same has to happen with HIV/AIDS. And for that to be possible, the conversation about HIV/AIDS has to become a topic of discussion at the dinner table. Maria Mejia’s story helps jump-start this conversation around many dinner tables across the world, because her story is relatable to many people, and because we are not so different after all.
To find out how to purchase the book click here. Find out more about Jason Wood by visiting:www.kantanoose.com. Connect with Maria “HIV” Mejia via Youtube :
www.youtube.com/user/Mariasjournal; Twitter: @MariaHivMejia; and Facebook: www.facebook.com/mariahivmejia.
Alina Oswald is a writer, photographer, and the author of Journeys Through Darkness: A Biography of AIDS. Contact her at www.alinaoswald.com.
Thursday, August 27, 2015
You Want PrEP, but Your Doctor Disagrees
Summer 2015
If there are two things that we know about PrEP, the first is that it's super effective in reducing one's risk of contracting HIV. The second is that bringing it up at your next doctor's appointment can be particularly stigmatizing, especially for those who are trying to access the little blue pill in a traditional healthcare setting.
So what can you do to make sure that your voice is being heard?
"First things first," says Bryan Bautista-Gutiérrez, PrEP Coordinator for Howard Brown Health Center in Chicago. "You really have to do your research before you set foot into the doctor's office asking for PrEP," he emphasizes.
According to Bautista-Gutiérrez, this work can include:
Assessing your actual risk for transmission: "I see a lot of clients who come in asking for PrEP, who have boyfriends who are HIV-positive, but have an undetectable viral load, making transmission very difficult." So PrEP is an additional layer of protection that they may or may not want to consider.
Talking to your friends: It's interesting that we can talk to our friends about PrEP, but healthcare can still be a barrier. Start a conversation with your friends about whether they are on PrEP, or know of someone who is and who prescribes it to them.
Finding a local LGBT/HIV health clinic: We recognize that in too many areas in our country, such as the rural South, healthcare facilities that specialize in PrEP may seem like a pipe dream. But for those who do have one, opt for accessing their PrEP program in order to increase the odds that you are receiving culturally competent care, although even long-time sexual health providers and community clinics might not yet serve transgender people and people who currently or formerly injected drugs.
And once you get to the doctor's office, Bautista-Gutiérrez, stresses, "There isn't a lot of time in your appointment to beat around the bush, so use this time wisely and advocate for yourself."
Standing your ground: Communicate clearly and succinctly that you believe PrEP is an important prevention tool that you need. Don't be afraid to be assertive or ask questions about lab work processes, follow-ups, and prescriptions.
Being willing to listen: While homophobia and other forms of intolerance are real issues, PrEP is relatively new, especially to providers who may have little to no HIV/AIDS experience. What may seem like slut shaming may also be your doctor demonstrating their lack of knowledge about HIV and prevention. And if that seems to be the case, ask for a referral to a provider who has more experience with PrEP. Referrals are also a good option when providers are medically uncomfortable providing PrEP.
Speaking up and out: If you do feel that your doctor is judging you or making assumptions about you, drop them and find a new physician. Remember: You are entitled to respectful healthcare that is culturally competent and empowering.
Granted, when it comes to PrEP, not all of the responsibility should be placed on the patient. Therefore "doctors really do need to get over themselves when it comes to bias," says David Malebranche, M.D., M.P.H., a primary care physician at the University of Pennsylvania's Student Health Center in Philadelphia. "PrEP is not a hard drug to prescribe to patients, nor is the follow up."
But Malebranche stresses that in order to make PrEP a household word in healthcare settings, eradicating bias isn't enough. Doctors, nurses, and other healthcare staff are in dire need of support -- both structural support for the logistics of offering culturally competent sexual healthcare and to address barriers in the public health realm.
Kellee Terrell is an award-winning filmmaker and freelance writer who writes about race, gender, health, and pop culture. Her work has been featured in Essence, the Advocate, The Root, POZ, The Huffington Post, and TheBody.com.
3 Reasons Gay Teen Boys Don’t Get Tested for HIV
HIV rates are increasing among young men who have sex
with men (MSM), but only one in five gay male teenagers have been tested
for the virus, according to findings of a study by Northwestern
University and the Center for Innovative Public Health Research.
The study, published in the Journal of Adolescent Health, notes that the main challenges to these teenagers getting tested include not knowing where to get an HIV test and not wanting to be seen going into the testing site. To a lesser extent, another reason they didn’t get tested is related to the fact that younger people tend to think they’re invincible and simply will not contact the virus.
The study, published in the Journal of Adolescent Health, notes that the main challenges to these teenagers getting tested include not knowing where to get an HIV test and not wanting to be seen going into the testing site. To a lesser extent, another reason they didn’t get tested is related to the fact that younger people tend to think they’re invincible and simply will not contact the virus.
The barriers are important to understand so that they can be overcome, said the study’s first author, Gregory Phillips II, PhD, in a Northwestern press release.
Possible solutions to these barriers include using text messages and websites to help the young men find testing sites. Offering HIV testing in schools would also normalize the process and make it appear less stigmatizing, the authors write.
The study enrolled a “national sample of 302 gay, bisexual and queer males ages 14 to 18 years into a text messaging-based HIV prevention program (Guy2Guy),” according to the press release. The study included questions about HIV testing.
Wednesday, August 26, 2015
Scientists 'delete' HIV virus from human DNA for the first time
Scientists 'delete' HIV virus from human DNA for the first time
- Scientists used a DNA-snipping enzyme called Cas9 to cut out the virus
- The cell's gene repair machinery then takes over, soldering the loose ends of the genome back together – resulting in a virus-free cell
- Process could also be a cure for other latent infections, researchers say
- 'It's an exciting discovery, but not ready to go into the clinic,' said Dr Khalili
Once HIV conquers a human cell, it will stay there forever.
It
inserts its deadly genome permanently into its victims' DNA, forcing
them to require medical treatment for the rest of their life.
But
now, for the first time, researchers in Philadelphia have found a way
to completely delete HIV from human cells by ‘snipping’ them out.
Scroll Down For Video
For the first time, researchers in
Philadelphia have found a way to completely delete the HIV virus
(pictured) from human cells by ‘snipping’ them out. The process could
also provide a cure for other latent infections
The
team of Temple University School of Medicine said the breakthrough
marks the first successful attempt to eliminate latent HIV-1 virus from
human cells – and could be a cure for other latent infections.
‘This
is one important step on the path toward a permanent cure for AIDS,'
said Kamel Khalili, PhD, Professor and Chair of the Department of
Neuroscience at Temple.
'It's
an exciting discovery, but it's not yet ready to go into the clinic.
It's a proof of concept that we're moving in the right direction,' he
added,
In
a study published by the Proceedings of the National Academy of
Sciences, Dr Khalili and colleagues detail how they created molecular
tools to delete the HIV-1 proviral DNA.
When
deployed, a combination of a DNA-snipping enzyme called a nuclease and a
targeting strand of RNA called a guide RNA (gRNA) hunt down the viral
genome and remove the HIV-1 DNA.
From
there, the cell's gene repair machinery takes over, soldering the loose
ends of the genome back together – resulting in virus-free cells.
'Since
HIV-1 is never cleared by the immune system, removal of the virus is
required in order to cure the disease,' explained Dr Khalili.
These
molecular tools also hold promise as a therapeutic vaccine; cells armed
with the nuclease-RNA combination proved impervious to HIV infection.
Worldwide, more than 33 million people have HIV, including more than 1 million in the United States.
Every year, another 50,000 Americans contract the virus, according to the U.S. Centers for Disease Control and Prevention.
In the UK, around 100,000 people were living with HIV in the UK in 2013. That’s around one person in 665.
Although
highly active antiretroviral therapy (Haart) has controlled HIV-1 for
infected people in the developed world over the last 15 years, the virus
can rage again with any interruption in treatment.
Worldwide, more than 33 million people
have HIV, including more than 1 million in the United States. ‘This is
one important step on the path toward a permanent cure for AIDS,' said
Kamel Khalili, PhD, Professor and Chair of the Department of
Neuroscience at Temple
'The
low level replication of HIV-1 makes patients more likely to suffer
from diseases usually associated with ageing,' Dr Khalili said.
These include cardiomyopathy – a weakening of the heart muscle – bone disease, kidney disease, and neurocognitive disorders.
'These problems are often exacerbated by the toxic drugs that must be taken to control the virus,' Dr Khalili added.
Researchers
based the two-part HIV-1 editor on a system that evolved as a bacterial
defence mechanism to protect against infection.
Dr
Khalili's lab engineered a 20-nucleotide strand of gRNA to target the
HIV-1 DNA and paired it with a DNA-sniping enzyme called Cas9 and used
to edit the human genome.
'We are working on a number of strategies so we can take the construct into preclinical studies,' Dr Khalili said.
'We
want to eradicate every single copy of HIV-1 from the patient. That
will cure AIDS. I think this technology is the way we can do it.'
Friday, August 21, 2015
Thursday, August 20, 2015
THE HIV EQUAL SURVIVAL GUIDE: I JUST FOUND OUT I'M POSITIVE
By: Tyler Curry
November 5th, 2014
The moments after learning about your newly diagnosed HIV-positive status can seem like a virtual free fall. In a matter of seconds, you are sent into a tailspin of what-if scenarios and your vision is filled with horrific images from a bad movie montage. Your mind races, then stalls completely, working in frantic fits and spurts and grasping onto the nuggets of information you can remember about what it is to be HIV-positive today.
The nurse tells you that you are going to be just fine and that HIV is now a manageable disease. The doctor tells you that if you take care of yourself, you can expect to live the same amount of time as you would have if you were HIV-negative. But still, there is an inescapable fear of the unknown. What does it mean to live with HIV? What is going to have to change in your life and, more importantly, what can you expect to remain the same?
Luckily, you aren’t very special. There are so many others who have gone through the exact same thing and have already asked all the same burning questions that you need to know the answers to. Below are some short and sweet answers to those questions of yours.
What do I do now?
The first thing to do is to stop panicking. You are the same person that walked into the clinic before receiving your test results. Although it may seem like everything has changed, it hasn’t. But there are some things that you can do to ease your mind and find your way back to being okay.
Find a doctor who works for you, and that means a doctor who is highly knowledgeable about HIV. You might be surprised about howuneducated your average family doctor is about HIV and what it means to treat it. The last thing you need is to be treated by a doctor who has just as many questions as you have. There are many HIV specialists who know exactly how to treat you, and that includes how to ease your concerns. These doctors can also act as your general doctor, but with the added piece of mind that they will keep your HIV diagnosis in consideration when minor health issues arise along the way.
I found a doctor, now what?
During your first appointment, your doctor will do your initial lab work. This is to see what your CD4 count and viral load is. Your CD4 count is the amount of white blood cells you have in your body and your viral load is the amount of copies of the HIV virus that are in your system. Your doctor will also determine whether the virus you have is resistant to any medications; which is unlikely.
This sounds scary, but doesn’t have to be. No matter what your CD4 count may be, most people can bring their count up by simply taking a single-pill regimen. The same medication will also reduce your viral load to an undetectable level, making it highly improbable for you to transmit the virus to someone else. Most likely, this will be the extent of managing your virus, along with regular checkups with your doctor to make sure that your body is healthy and that your medication is working. As with any medication, the key to staying healthy and keeping an undetectable viral load is to never miss a dose.
Can I only have sex with other people who are also HIV-positive?
Of course not! Today, there are multiple ways to have safe sex and, believe it or not, most men are knowledgeable enough to know that informed sex is the safest sex of all, regardless of status. Again, staying compliant with your meds and maintaining an undetectable viral load is the best way to ensure that you never transmit the virus. This method of prevention is for your protection just as much as it is for your partner.
How will I tell my friends and family?
First off, you don’t have to tell anyone except your future sexual partners. But talking about your status is the best way for you to feel like yourself again. Believe it or not, there are probably many people around you who are either HIV-positive or have been affected by HIV in one way or another. The first time you tell someone may be scary, but it gets easier every time. The first step is to just say the three little letters out loud. Start there.
What does it mean to manage my virus?
For most people who are diagnosed today, managing your virus simply means being compliant with a one-pill-a-day regimen. Once you find a doctor, start medication and achieve an undetectable viral load, you will just need to have your lab work done every four months or so to make sure that everything is all right.
I am afraid of dying.
Here’s the deal. A person diagnosed today has roughly the same life expectancy that a person who is HIV-negative. However, your virus does make you more susceptible to several health risks that you need to be aware of. Some of these risks include cardiovascular disease, kidney problems and bone density loss. But before you start to panic again, these issues can be prevented with the proper care. Being knowledgeable about what to look out for is the best way to ensure a long and healthy life.
Am I going to get AIDS?
The term AIDS does seem scarier than HIV, doesn’t it? The truth is, many people who are living with HIV will never be diagnosed with AIDS. HIV is a virus; AIDS is just a diagnosis that a person receives once the virus reaches a certain point. When your CD4 count dips below 200 and your immune system is low enough that common illnesses can be life threatening, it is classified as AIDS. As long as you stay on your medication and keep a healthy body and mind, you can keep your CD4 count in the healthy zone and far away from the level of AIDS. And if your CD4 count is already in the danger zone, the correct medication can bring you back up to healthy levels.
Your diagnosis is not the end of anything, but it may be the beginning of living a more informed and health-conscious life.
Illustrations by: Clarione Gutierrez
See more articles on HIV here: http://www.hivequal.org/
Wednesday, August 19, 2015
Weekly Injectable HIV Antibody Treatment Shows Promise
August 13, 2015
A weekly injection of an HIV antibody boasted a 98 percent success rate among participants in a small trial, Fox News reports. Researchers at the biotechnology company CytoDyn conducted a Phase IIb trial of the treatment, called PRO 140, as monotherapy among 40 HIV-positive participants.
PRO 140 works similarly to daily oral Selzentry (maraviroc), blocking HIV from connecting to the CCR5 coreceptor on the surface of CD4 cells. However, the weekly injectable is less toxic and has fewer side effects.
Ninety-eight percent of the participants maintained virologic control for four weeks. Fourteen of the participants continued in the study through the six-month point. All of them maintained control of HIV. Some of them successfully maintained viral control for eight months on the treatment.
CytoDyn is embarking on a Phase III trial of PRO 140 as a component of a combination regimen including daily antiretrovirals, and hopes to receive approval from the U.S. Food and Drug Administration (FDA) in 2017.
To read the Fox News report, click here.
To read a press release on the research, click here.
To find more articles like this click here.
Sunday, August 9, 2015
Why you should never miss your MEDS!!!!
Understanding Drug Resistance
What Is HIV Drug Resistance?
In simple terms, drug resistance refers to the ability of disease-causing germs—such as bacteria and viruses—to continue multiplying despite the presence of drugs that usually kill them.
With HIV, drug resistance is caused by changes (mutations) in the virus's genetic structure. These mutations can lead to changes in certain proteins, most commonly enzymes, that help HIV reproduce (replicate).
Mutations are very common in HIV. This is because HIV replicates at an extremely rapid rate and does not contain the proteins needed to correct the mistakes it makes during copying.
Mutations occur randomly, on a daily basis, but many are harmless. In fact, most mutations actually put HIV at a disadvantage—they reduce the virus's "fitness" and slow its ability to infect CD4 cells in the body. However, a number of mutations can actually give HIV a survival advantage when HIV medications are used, because these mutations can block drugs from working against the HIV enzymes they are designed to target. These are the mutations we are concerned about when we talk about drug resistance.
HIV relies on many enzymes to replicate inside a human cell. It also relies on proteins, including gp41, to latch on to CD4 cells and infect them. Mutations can occur in any of these parts of the virus and cause drug resistance:
- Reverse transcriptase: nucleoside reverse transcriptase inhibitors (NRTIs) and non-nucleoside reverse transcriptase inhibitors (NNRTIs) target this enzyme.
- Integrase: Integrase inhibitors target this enzyme.
- Protease: Protease inhibitors target this enzyme.
- gp41: Fusion inhibitors target this protein on HIV's outer wall.
For people infected with HIV, drug resistance can render drugs less effective or even completely ineffective, thus significantly reducing treatment options.
How Does It Occur?
HIV drug-resistance mutations can occur both before and during HIV treatment. Here's a look at how this happens:
- Transmission of drug-resistant HIV. Many HIV-positive people now take HIV drugs. If someone has developed resistance to one or more of these HIV drugs and has unprotected sex or shares needles with someone who is not infected with the virus, it is possible that they can infect their partner with a drug-resistant variant—a strain of HIV containing mutations that can cause resistance.
In the United States and other countries where HIV treatment is widely used, between 5 percent and 20 percent of new HIV cases involve strains of the virus that are resistant to at least one HIV medication.
- While using pre-exposure prophylaxis (PrEP). Truvada (tenofovir plus emtricitabine) was approved by the U.S. Food and Drug Administration in July 2012 for use by people who are HIV negative but at risk of becoming infected with the virus. There is a potential risk for people using Truvada as PrEP—if they becoming infected with the virus, aren't diagnosed quickly and continue using the drug, their newly acquired virus may develop resistance to one or both of the medications in Truvada. In clinical trials of Truvada as PrEP, this was a very rare occurrence. And provided that PrEP is used exactly as prescribed—daily, regardless of whether or not sexual activity is planned or occurs—experts believe the risk of resistance can be greatly minimized.
- During treatment. Even if someone is infected with HIV that doesn't contain drug-resistance mutations ("wild-type" virus), genetic changes still occur over time, even before treatment is started. This ends up creating a large mixture of virus in the body. Some of these variants contain the necessary mutations that can partially, or fully, resist an antiretroviral drug—which explains why one-drug treatment (monotherapy) should never be used to treat HIV.
Soon after combination HIV drug treatment is started, the amount of wild-type virus is dramatically reduced. However, if the amount of virus isn't pushed down and kept at very low levels, HIV variants can continue replicating, acquiring additional mutations. And once the virus has accumulated enough mutations, a high level of resistance to the drugs being used can occur, causing viral load to increase and CD4 cells to drop.
A major concern with these mutations is that they can result in cross-resistance. This means that HIV resistance to one drug can automatically become resistant to other drugs in the same class. For example, if you're on a drug regimen that contains the NNRTI Sustiva and your virus becomes resistant to it, chances are that your virus is also resistant to the NNRTIs Viramune and Rescriptor, even though you haven't taken these drugs.
What Factors Contribute to Resistance During Treatment?
If there's one "golden rule" of antiretroviral therapy, it is: the lower the viral load while on treatment, the less likely it is that the virus will continue reproducing and mutating. A powerful HIV regimen is the most effective way to keep the level of virus low—preferably "undetectable" (<50 copies/mL as measured by a sensitive viral load test)—and to delay additional mutations from occurring.
Unfortunately, there are a number of factors that can prevent an HIV drug regimen from being as powerful as it can be. These include:
- Poor treatment adherence: In order for HIV drugs to work correctly, they must be taken exactly as prescribed. Skipping doses or not taking your medication correctly can cause the amount of an HIV drug to decrease in the bloodstream. If the drug level becomes too low, HIV can reproduce more freely and accumulate additional mutations.
There are a number of reasons why someone might struggle with treatment adherence, including side effects, a hectic schedule or forgetfulness. If you've been having difficulty adhering to your drug regimen, it's nothing to be embarrassed about—be sure to tell your doctor so that you can up with solutions, which might including simplifying your treatment.
For a more complete understanding of the importance of adherence, click on the following lesson link:The Importance of Adhering to Your Treatment Regimen - Poor absorption: Not only must HIV drugs be taken on schedule, they also need to be absorbed effectively into the bloodstream. A drug, or combination of drugs, that is not absorbed properly can result in levels in the bloodstream that are too low and, ultimately, allow HIV reproduction and the accumulation of drug-resistance mutations. Certain drugs have dietary requirements, which can affect absorption. People with HIV can also experience diarrhea and vomiting, which can cause HIV drugs to be expelled from the gut too quickly and affect absorption.
- Varying pharmacokinetics: Pharmacokinetics is the scientific term used by researchers to mean how a drug is absorbed, distributed, broken down, and removed from the body. Interactions between drugs—including common HIV medications—can be a major problem in this regard. For example, if the NRTI Viread (tenofovir) is combined with the protease inhibitor Reyataz (atazanavir), blood levels of Reyataz can fall to dangerously low levels. This is why the protease inhibitor Norvir (ritonavir), which boosts Reyataz levels in the bloodstream, must be used if Viread is also prescribed.
There are many drug interactions like this. Be sure that your doctor knows all of the medications you are taking, including prescription drugs, over-the-counter remedies and nutritional supplements.
Do I Have Drug Resistance?
- Your viral load fails to go undetectable within the first several months of starting a new HIV drug regimen.
- Your viral load goes from being undetectable to detectable (note: A one-time "blip" in viral load is not usually a sign that a drug regimen is no longer working).
- Your detectable viral load continues increasing, even though you are still taking your prescribed HIV drug regimen.
When Should Drug-resistance Tests Be Used?
HIV treatment guidelines, including those produced by the U.S. Department of Health and Human Services (DHHS) and the International AIDS Society-USA (IAS-USA), recommend drug-resistance testing for all HIV-positive people. Here's a look at when these tests should be used:
- When HIV is first diagnosed. Knowing if you've been infected with a drug-resistant strain of HIV—and which drugs your virus is resistant to—can be very helpful. For the most accurate results, you should be tested for HIV drug resistance soon after you are diagnosed as HIV positive, even if you won't be starting treatment for several months or years (the information will be recorded in your medical file and help guide treatment when the time comes).
It is important to note, however, that drug-resistance testing does not always produce accurate results when used in this manner. Soon after a drug-resistant strain enters the body, it begins reproducing. Over time, a wild-type strain of HIV can emerge, forcing the drug-resistant strain(s) to go into hiding and escape detection using drug-resistance testing. In other words, testing may not produce reliable information if too much time has passed since infection occurred.
- If treatment doesn't appear to be working. If viral load fails to become undetectable after a new treatment regimen is started, or becomes detectable again after a period of being undetectable, drug-resistance testing may help determine the cause. For best results, the test should be conducted while you are on your regimen—provided that your viral load is detectable—or within four weeks of discontinuing treatment.
If no drug resistance is found, the problem might be poor adherence, absorption difficulties or drug–drug interactions. It is best to remedy these problems before resistance mutations develop. If drug resistance is found, these tests can help determine which medications have stopped working for you (people rarely develop resistance to all three or four drugs being taken) and also help figure out which medications to switch to.
- During pregnancy. If you are HIV positive and become pregnant, the most effective way to reduce the risk of transmitting the virus to your baby is to get your viral load undetectable and keep it there—at least until your baby is born. Drug-resistance testing before and during treatment can help achieve this important goal.
Which Tests Are Available?
Generally speaking, there are two types of drug-resistance tests available to HIV-positive patients: genotypic and phenotypic assays. Because genotypic testing provides results in one to two weeks—compared to the two-, three- or four-week turnaround associated with phenotypic testing—it is the preferred choice for patients who have yet to start treatment. For people whose HIV therapy has stopped working, DHHS Treatment guidelines recommend that resistance testing also be used to confirm treatment failure and to help select a new regimen. When a first or second regimen has failed, genotypic testing is preferred. Phenotypic testing, say the guidelines, should be used when a person has more extensive drug resistance.
Among patients who have used multiple drugs in the past, interpreting the results of both tests together may be most useful. One company, Monogram Biosciences, will phenotype and genotype a blood sample and provide the results of both tests on the same lab report—called PhenoSense GT. In general, both tests work best when a person has a viral load of 500 or more, and preferably at least 1,000.
The next two sections review genotypic and phenotypic tests in detail.
What Is Genotypic Testing?
These tests examine the actual genetic structure—or genotype—of HIV taken from a patient (a standard blood sample is all that is required). The HIV is examined for the presence of specific genetic mutations that are known to cause resistance to certain drugs.
An example: Researchers know that the NRTIs Epivir and Emtriva are not effective against forms of HIV that contain the mutation "M184V" in its reverse transcriptase gene. If a genotypic resistance test discovers a mutation at position M184V, chances are that the person's HIV is resistant to Epivir and Emtriva and is not likely to respond to either of these drugs.
For many drugs, including the protease inhibitors and other NRTIs, complex patterns of mutations are required for resistance to occur. In this way, interpreting the results of genotypic testing can be tricky, given that different mutations—and different combinations of mutations, especially in patients with a lot of treatment experience—can mean different things. However, as knowledge of mutations and their different patterns has grown considerably over the past several years, laboratories are able to provide accurate and useful information to physicians.
Examples of available genotypic tests include: Bayer Health Diagnostics' HIV-1 TrueGene, Celera Diagnostics/Abbott Laboratories' ViroSeq, LabCorp's GenoSure (Plus) and Monogram Biosciences' GeneSeq.
What Is Phenotypic Resistance Testing?
Unlike genotypic testing, which looks for particular genetic mutations that cause drug resistance, phenotypic testing directly measures the behavior—or phenotype—of a patient's HIV in response to particular antiretrovirals. Because of the way phenotypic tests work and the results they provide, many experts believe that these tests are more comprehensive and trustworthy than genotypic tests, especially when testing samples from patients who have tried and failed a number of HIV drugs in the past.
Using the simplest terms, phenotypic testing is performed by placing samples of a patient's HIV in test tubes with each HIV drug to observe how the virus reacts. The ability of the virus to grow (or not grow) in the presence of each drug is evaluated. The virus is exposed to varying strengths, or concentrations, of each drug. The ability of the patient's virus to grow in the presence of the drugs is compared with some wild-type virus that is known to be 100 percent susceptible to all HIV drugs. The comparison between the patient's virus and the wild-type virus provides the phenotyping results.
These results tell doctors how much of a particular drug is needed to reduce HIV replication. In other words, the laboratory conducting a phenotypic test is trying to determine the amount, or concentration, of drug needed to stop HIV from reproducing.
For example, if four times as much of the NRTI Ziagen (abacavir) is needed to control HIV replication, the virus is said to have "fourfold resistance" to the drug. If seven times as much Ziagen is needed, the virus is sevenfold resistant to the drug.
When phenotypic tests first became available, interpreting these fold changes was difficult. It wasn't clear what a fold change meant in terms of the virus being fully sensitive, less sensitive, or not sensitive to a specific HIV drug. As a result, companies conducting phenotypic tests began working closely with researchers to better understand fold changes and what they really mean in terms of resistance to available medications. After several years of extensive research, these companies have developed "clinical cutoffs"—an important component of phenotypic testing that allows for much easier interpretation of fold changes as they relate to the sensitivity of HIV to many of the available medications.
Returning to the example of Ziagen, using Monogram Bioscience's PhenoSense HIV assay, the lower clinical cutoff is 4.5-fold resistance and the upper clinical cutoff is 6.5-fold resistance. In other words, HIV that is fourfold resistant to Ziagen is still technically sensitive to the drug, whereas HIV that is sevenfold resistant to Ziagen means that the virus is much less sensitive to the drug and, as a result, not a good treatment choice.
As for fold changes that fall between the lower and upper cutoffs, this means partial resistance (the higher the fold change, the less sensitive HIV is to the drug being used). While it is always best to use antiretrovirals that your virus is fully sensitive to, it is sometimes necessary to use (or reuse) medications your HIV is partially resistant to.
Each HIV drug has different clinical cutoffs, which can be confusing. To help make sense of these cutoffs and to make it easier for health care providers to interpret the results, laboratories conducting these tests provide detailed reports for every test conducted. Check out what a phenotypic resistance test report looks like by clicking on the following link:
Phenotypic Resistance Test: A Sample Report
There are two "conventional" phenotypic tests available: Monogram Bioscience's PhenoSense assay and Virco Lab's Antivirogram. Both tests evaluate the fold changes for all of the available NRTIs, Protease Inhibitors, and NNRTIs. Monogram Biosciences has a separate phenotypic assay, called PhenoSense Entry, which tests HIV's sensitivity to the entry inhibitorFuzeon.
Another test is Virco Lab's vircoTYPE HIV-1 assay. This is actually a "predictive" phenotypic test, using genotypic testing results to figure out what the virus's phenotype is, without actually performing a phenotypic test. To do this, labs use genotyping testing to determine if an HIV sample has mutations known to cause drug resistance. Once the genotype has been determined, the laboratory searches a database maintained by Virco containing the genotypes of several thousand HIV samples collected from other patients. It then retrieves the phenotypes—the fold changes—that correspond to these samples, averages the information together and predicts the drugs that the current sample will be more or less sensitive to.
How Can Drug Resistance Be Avoided?
There are a number of steps that HIV-positive people can take to prevent—or at least slow down—the development of resistance:
Among patients who have used multiple drugs in the past, interpreting the results of both tests together may be most useful. One company, Monogram Biosciences, will phenotype and genotype a blood sample and provide the results of both tests on the same lab report—called PhenoSense GT. In general, both tests work best when a person has a viral load of 500 or more, and preferably at least 1,000.
The next two sections review genotypic and phenotypic tests in detail.
What Is Genotypic Testing?
These tests examine the actual genetic structure—or genotype—of HIV taken from a patient (a standard blood sample is all that is required). The HIV is examined for the presence of specific genetic mutations that are known to cause resistance to certain drugs.
An example: Researchers know that the NRTIs Epivir and Emtriva are not effective against forms of HIV that contain the mutation "M184V" in its reverse transcriptase gene. If a genotypic resistance test discovers a mutation at position M184V, chances are that the person's HIV is resistant to Epivir and Emtriva and is not likely to respond to either of these drugs.
For many drugs, including the protease inhibitors and other NRTIs, complex patterns of mutations are required for resistance to occur. In this way, interpreting the results of genotypic testing can be tricky, given that different mutations—and different combinations of mutations, especially in patients with a lot of treatment experience—can mean different things. However, as knowledge of mutations and their different patterns has grown considerably over the past several years, laboratories are able to provide accurate and useful information to physicians.
Examples of available genotypic tests include: Bayer Health Diagnostics' HIV-1 TrueGene, Celera Diagnostics/Abbott Laboratories' ViroSeq, LabCorp's GenoSure (Plus) and Monogram Biosciences' GeneSeq.
To learn more about the specific mutations and genotyping, we recommend Stanford University's HIV Drug Resistance Database web site. They maintain detailed lists of the various mutations associated with resistance to each of the approved antiretrovirals, along with an interactive tool that you and your doctor can use to double-check your genotypic testing results.
Unlike genotypic testing, which looks for particular genetic mutations that cause drug resistance, phenotypic testing directly measures the behavior—or phenotype—of a patient's HIV in response to particular antiretrovirals. Because of the way phenotypic tests work and the results they provide, many experts believe that these tests are more comprehensive and trustworthy than genotypic tests, especially when testing samples from patients who have tried and failed a number of HIV drugs in the past.
Using the simplest terms, phenotypic testing is performed by placing samples of a patient's HIV in test tubes with each HIV drug to observe how the virus reacts. The ability of the virus to grow (or not grow) in the presence of each drug is evaluated. The virus is exposed to varying strengths, or concentrations, of each drug. The ability of the patient's virus to grow in the presence of the drugs is compared with some wild-type virus that is known to be 100 percent susceptible to all HIV drugs. The comparison between the patient's virus and the wild-type virus provides the phenotyping results.
These results tell doctors how much of a particular drug is needed to reduce HIV replication. In other words, the laboratory conducting a phenotypic test is trying to determine the amount, or concentration, of drug needed to stop HIV from reproducing.
For example, if four times as much of the NRTI Ziagen (abacavir) is needed to control HIV replication, the virus is said to have "fourfold resistance" to the drug. If seven times as much Ziagen is needed, the virus is sevenfold resistant to the drug.
When phenotypic tests first became available, interpreting these fold changes was difficult. It wasn't clear what a fold change meant in terms of the virus being fully sensitive, less sensitive, or not sensitive to a specific HIV drug. As a result, companies conducting phenotypic tests began working closely with researchers to better understand fold changes and what they really mean in terms of resistance to available medications. After several years of extensive research, these companies have developed "clinical cutoffs"—an important component of phenotypic testing that allows for much easier interpretation of fold changes as they relate to the sensitivity of HIV to many of the available medications.
| The PhenoSense lab report also includes information on an HIV sample's replication capacity (RC). RC measures how well a patient's virus is able to replicate compared to a wild-type reference virus. Generally speaking, wild-type virus replicates the best inside the human body. When the virus accumulates drug-resistance mutations, it allows the virus to continue replicating in the presence of HIV treatment. However, these mutations can affect HIV's fitness—its ability to cause damage to the immune system at the same rate as wild-type HIV. Knowing HIV's RC may help to determine when to delay, start, switch or interrupt therapy. For example, in highly treatment-experienced patients with multi-drug resistance, viruses with low RC values may be associated with stable or increasing CD4 counts, which reduces the need for changing a regimen. However, more information from clinical trials is needed to better understand how best to use RC in making such treatment decisions. |
As for fold changes that fall between the lower and upper cutoffs, this means partial resistance (the higher the fold change, the less sensitive HIV is to the drug being used). While it is always best to use antiretrovirals that your virus is fully sensitive to, it is sometimes necessary to use (or reuse) medications your HIV is partially resistant to.
Each HIV drug has different clinical cutoffs, which can be confusing. To help make sense of these cutoffs and to make it easier for health care providers to interpret the results, laboratories conducting these tests provide detailed reports for every test conducted. Check out what a phenotypic resistance test report looks like by clicking on the following link:
Phenotypic Resistance Test: A Sample ReportThere are two "conventional" phenotypic tests available: Monogram Bioscience's PhenoSense assay and Virco Lab's Antivirogram. Both tests evaluate the fold changes for all of the available NRTIs, Protease Inhibitors, and NNRTIs. Monogram Biosciences has a separate phenotypic assay, called PhenoSense Entry, which tests HIV's sensitivity to the entry inhibitorFuzeon.
Another test is Virco Lab's vircoTYPE HIV-1 assay. This is actually a "predictive" phenotypic test, using genotypic testing results to figure out what the virus's phenotype is, without actually performing a phenotypic test. To do this, labs use genotyping testing to determine if an HIV sample has mutations known to cause drug resistance. Once the genotype has been determined, the laboratory searches a database maintained by Virco containing the genotypes of several thousand HIV samples collected from other patients. It then retrieves the phenotypes—the fold changes—that correspond to these samples, averages the information together and predicts the drugs that the current sample will be more or less sensitive to.
It is important to note that Monogram Biosciences and Virco calculate their cutoffs differently. As a result, the cutoffs determined for one company's test (e.g., PhenoSense) do not apply to the cutoffs determined for the other company's test (e.g., vircoTYPE).
There are a number of steps that HIV-positive people can take to prevent—or at least slow down—the development of resistance:
- Learn all you can about HIV treatment and the available options. The more you know, the easier it will be to make treatment choices that help you avoid drug resistance. Reading the information on this web site about HIV medicine is a good first step.
- Start treatment with a powerful HIV regimen. Your first shot at HIV treatment is probably your best chance at fully suppressing the virus and preventing the development of drug resistance. For an overview of when to start treatment and some guidelines on which drugs to start first, click on the following lesson link:
When Should I Start Treatment, and What Should I Take First? - When switching treatments, pick the most potent new regimen. Whenever possible, it is best to switch to a regimen that has three drugs that resistance tests predict will work. If necessary, two active drugs are better than one. For an overview of when to switching treatment and some guidelines on the best strategies for doing so, click on the following lesson link:
When Should I Change My Treatments, and Which Drugs Should I Switch To?
- Be sure to follow instructions. It is very important that HIV-positive people take their HIV medications exactly as prescribed. Missing doses and not taking the right number of pills can cause viral load to increase and cause drug-resistance mutations to develop (see our lesson on adherence).
- Communicate with your doctor. Knowing how to take your medicine properly and reporting any problems to your doctor are important for avoiding drug resistance.
- Monitor the effects of your treatment. This means keeping an eye on your viral load and other lab tests after you begin treatment and for as long as you remain on therapy. Every three months is a standard recommendation. Often an increasing viral load—or a viral load that fails to go undetectable—is the first sign that drug resistance is developing. Monitoring viral load is a good way to guard against drug resistance. For more information about understanding your viral load test results, click on the following lesson link:
Understanding Your Viral Load Test
Find more articles like this here: http://www.aidsmeds.com/
Tuesday, August 4, 2015
Flow Chart for Accessing PrEP for HIV Prevention
August 3, 2015
Project Inform has created a new flow chart for both consumers and health navigators to use for accessing services and covering costs related to PrEP.
The front side lays out the process as an infographic to give consumers the range of possible issues that may be involved when finding a doctor and getting a prescription for PrEP. The back side may be more useful for health navigators to use when assisting clients and other individuals with accessing various assistance programs for covering the cost of PrEP.
The flow chart is easily downloaded from Project Inform's website. It's laid out as a legal-sized sheet of paper ... easily printed on desktop printers!
Director of Education Alan McCord remarked, "We developed this tool in response to seeing the various problems around the country that some individuals have had in accessing PrEP. Providers also want to help as much as possible, so we hope this tool can assist on both the consumer and provider levels."
The PrEP Flow Chart will be updated as needed and always available atwww.projectinform.org/pdf/PrEP_Flow_Chart.pdf. If you have any corrections or additions to suggest, please email Alan McCord.
Get more information like this here: www.thebody.com
The front side lays out the process as an infographic to give consumers the range of possible issues that may be involved when finding a doctor and getting a prescription for PrEP. The back side may be more useful for health navigators to use when assisting clients and other individuals with accessing various assistance programs for covering the cost of PrEP.
 |
The flow chart is easily downloaded from Project Inform's website. It's laid out as a legal-sized sheet of paper ... easily printed on desktop printers!
Director of Education Alan McCord remarked, "We developed this tool in response to seeing the various problems around the country that some individuals have had in accessing PrEP. Providers also want to help as much as possible, so we hope this tool can assist on both the consumer and provider levels."
The PrEP Flow Chart will be updated as needed and always available atwww.projectinform.org/pdf/PrEP_Flow_Chart.pdf. If you have any corrections or additions to suggest, please email Alan McCord.
Get more information like this here: www.thebody.com
Saturday, August 1, 2015
Could HIV Prevention Pills Actually Increase Infection Risk by Cutting Condom Use?
July 30, 2015
It's been hailed as a major breakthrough and one of the much-needed tools to "end HIV". But there are also concerns about pre-exposure prophylaxis (PrEP), the use of antiretroviral drugs by HIV-negative people to prevent them from becoming infected with the virus. Will people taking PrEP stop using condoms and could this actually lead to an increase in HIV and sexually transmitted infections (STIs)?
PrEP appears to be a highly effective method of reducing risk of HIV transmission. Adding to growing international evidence, the Proud trialtested the use of PrEP with gay and bisexual men in England and found a reduction in HIV transmission of 86% amongst men who took PrEP every day. Truvada, the drug used in the Proud trial, is not currently licensed for use as PrEP in the UK. However, as a result of the findings, there has been a concerted effort by HIV policymakers and community activists to make Truvada available as PrEP on the NHS as soon as possible.
Evidence to date has shown mixed results when it comes to continued condom use with PrEP. The Proud trial, which recruited participants reporting some but not exclusive use of condoms, found the number of people not using condoms remained the same throughout the study. STI rates across both trial arms -- the group that received PrEP immediately and the group that had to wait 12 months -- also remained similar. Evidence from three locations from the iPrEX study in the US suggests that, although some younger participants reduced condom use, in most cases PrEP did not reduce condom use but did reduce stress, fear, and guilt.
We need to consider who might be willing to use PrEP. A number of surveys with gay and bisexual men in the UK have shown that men reporting lower levels of condom use and who are at higher risk of HIV are interested in PrEP. Introducing PrEP to this group might not necessarily reduce condom use, but could protect against HIV infections where condoms are not already being used. In this way, PrEP could fill a gap in HIV prevention for those individuals who find it difficult, or are unable, to use condoms as their main means of preventing HIV.
Our PrEP research in Scotland with gay and bisexual men, and men and women from migrant African communities, found that concerns about PrEP went beyond condom use. Participants in our qualitative study highlighted anxieties around the immediate and long-term side-effects of PrEP, a lack of trust that PrEP would work, and a belief that they were not at high-enough risk to merit taking a daily pill to prevent HIV. In addition, given that PrEP is not 100% effective, skills amongst participants in calculating risk reduction in relation to PrEP appeared to be mixed and will be an important factor in the effective "real-world" use of PrEP.
But our study also highlighted the fear that others would stop using condoms as a result of PrEP. One man compared the impact of PrEP to "women burning their bras" because he was concerned that other men would stop using condoms and threaten a 30-year history of HIV-prevention based on condom use. This suggests that many people still see condoms as the main HIV-prevention tool and demonstrates the need to engage with these fears and identify how PrEP might fit into, rather than disrupt, existing HIV prevention strategies.
Given the likely introduction of PrEP in the UK in the not-too-distant future, we need to draw on existing evidence to encourage its equitable introduction into health services and access by those most at risk of HIV. There needs to be clear guidance and support for using PrEP in combination with existing HIV-prevention strategies, including condoms. We need to find acceptable, effective and clear ways of explaining PrEP to potential users and work to improve understandings and skills in assessing and reducing risk.
Finally, we need to address existing -- and sometimes conflicting -- community concerns about PrEP . We need to find ways of talking openly about what a range of HIV prevention options might look like, without moralising or judging individual practices. Good sexual health needs to recognise the dynamic lives of people affected by HIV. No matter how well PrEP might work, it alone will not be the magic bullet to end HIV.
Lisa McDaid is Programme leader, MRC/CSO Social and Public Health Sciences Unit at University of Glasgow.
Ingrid Young is Research fellow, MRC/CSO Social and Public Health Sciences Unit at University of Glasgow.
This article was originally published on The Conversation. Read the original article.
Find more articles like this one at: http://www.thebody.com/