Two companies have an effective 100% cure for Hepatitis C without interferon or ribavirin. But this cure is literally being withheld from millions

Two companies have an effective 100% cure for Hepatitis C without interferon or ribavirin.  But this cure is literally being withheld from millions by pharmaceutical giant Gilead Sciences because they are more concerned about profits than human lives.
This cure is a combination Bristol-Myers Squibb’s drug daclatasvir and Gilead Science’s GS-7977 (sofosbuvir). When these two drugs were used together, 100 percent of Hepatitis C patients were cured.  These results are amazing for the approximately 170 million people in the world with Hepatitis C.  The problem is that Gilead Sciences is unwilling to work with Bristol-Myers. The cure exists while people continue to suffer and die.
 Dr. Douglas J. Manion, a senior vice president for Bristol-Myers, said his company was keen” on working with Gilead but that “thus far, they have been unwilling to engage in that collaboration.”
Quote from Dr. Paul Thuluvath – Wall Street Journal:
“We had never, ever imagined—even in our wildest dreams—we could treat” hepatitis C so quickly, effectively and without serious side effects, said Paul Thuluvath, a doctor at Mercy Medical Center in Baltimore who had six patients test the new treatment. “I think the pharmaceutical companies have a moral responsibility to work together and bring it to market instead of [following] their own vested interests.” 
Quote from Dr. Scott Friedman – New York Times:
“The only appropriate motivation should be what is the best and fastest way to get cures, not what is best for the shareholders,” said Dr. Scott Friedman, chief of liver diseases at the Mount Sinai School of Medicine in New York, who was not involved in the trial.” 
Quote from EASL Secretary General Mark Thursz:
EASL Secretary General Mark Thursz wants to see the two companies work together.
“The combination of daclatasvir and GS-7977 has shown positive results at Phase II. EASL is disappointed that development of this combination has been halted as daclatasvir and GS-7977 promised to deliver a highly effective oral regimen that we hoped would be available to HCV patients soon,” said Thursz.
Act NOW and sign the petition to insist Gilead Sciences work with Bristol-Myers on the Phase III drug trials necessary to get this cure to market.
More than 240,000 people have died since these results were released this past April and there is still no collaboration. How many more must die before Gilead Sciences starts putting human lives before profits?
Gilead Sciences
Gilead Sciences
Gilead Sciences
Bristol-Myers Squibb, Media
John C. Martin, Gilead Sciences, CEO 
Open Letter to Gilead Sciences, their Board of Directors and shareholders:

The recent data from the Boston AASLD meeting confirmed the amazing 100% cure rate with Gilead’s sofosbuvir and Bristol-Myers Squibb’s daclatasvir. Not only did this combination cure genotypes 1, 2 and 3, this cure was achieved without the toxic and debilitating side effects of ribavirin which is known to cause severe anemia and other life-threatening conditions. There are even some concerns that ribavirin may in fact be carcinogenic (see So millions of patients and their families were so very hopeful about the possibility of quick access to this safer and effective HCV drug combination without ribavirin.

But to our continued disbelief and monumental heartbreak, Gilead refuses to move forward in this collaboration with Bristol-Myers Squibb and the most significant discovery in the history of hepatitis C. The rationale for this appears to be nothing more than Gilead’s determination to corner the market with its own in-house NS5a inhibitor GS-5885, which is not effective in the three genotypes and most likely will require the addition of the dreadful ribavirin. Other companies, such as Abbott, are now seeking their own ribavirin-free cocktails and hopefully will prove successful… but it will take years. In the meantime, Gilead could be forging ahead with this combination of sofosbuvir and daclatasvir and bring it to market much sooner than any others in development and start recouping its $11 billion investment as well as saving millions of lives. This would be a win-win situation for everyone involved, i.e., Gilead Sciences, its shareholders, the people suffering and dying with this disease, as well as their families who love them just as much as you love your own families.

Although we may not have hundreds of thousands of signatures on our petition and we have not yet been able to capture the world’s attention about this urgent and dire situation, do not take that as any indication of our intent to quit in the pursuit of this cure. We have no other choice in this matter and we will continue on… day after day, week after week, month after month… until we no longer have any life left in our bodies, or until another company comes up with a cure as safe and effective as this is.

[Your name]
Here is the petition:

Groundbreaking Gene Therapy Study Gets The Go-Ahead By The FDA

Calimmune, a small biotechnology company, is  giving people a low dose chemo agent (as conditioning) and then infusing them with stem cells  that have been modified to inhibit the CCR5 receptor and to contain their own built-in HIV fusion inhibitor peptide, thereby blocking two sites that are essential for HIV infection.  

The study is enrolling only for HIV+ people who have an R5 virus and who are not taking HIV medications due to their own choice (side effects, etc) for at least 6 weeks. Over 500 CD4 cells required.  Very promising approach  by Calimmune!

An Adaptive Phase I/II Study of the Safety of CD4+ T Lymphocytes and CD34+ Hematopoietic Stem/Progenitor Cells Transduced With LVsh5/C46, a Dual Anti-HIV Gene Transfer Construct, With and Without Conditioning With Busulfan in HIV-1 Infected Adults Previously Exposed to ART

This is the Los Angeles investigator. San Francisco also has a site but it has been fully enrolled

Nelson, how did you manage to survive HIV ?

hello nelson, I have a curiosity about building body after HIV infection.I am guessing that I should have infected in august 1st by sexual intercourse although I used a condom.I am 38 year old and I want to live 30 more years being healthy and strong economically.Being a long term survivor you have some clue.Did you build your body after HIV infection? How long it took ? Can you share tips to live long ?
Response from Mr. Vergel

People who start HIV treatment early usually do not have unintentional weight loss due to the infection, and may have less weight gain after starting antiretrovirals. So, that is my first suggestion: start treatment early even if yourCD4 cells are above 500 cells/ml.
The key is to find a regimen that agrees with you. Some people are lucky to tolerate their first regimen (usually Atripla), but others develop side effects that lead them and their physicians to switch them to other regimens (like Complera, Isentress+ Truvada, Stribld or boosted Reyatazplus Truvada). Your physician will guide you through that process. But, as I said, most people do well on their first try.
I am a long term survivor that had to combat wasting and lipodystrophy syndromes through my HIV infection, so I have been able to learn a lot about therapies to gain lean body mass and lose visceral fat. Luckily for most, these two syndromes are not as common with newer HIV regimens. This is an old article describing my path back in the days of struggle:Nelson’s story
When it comes to nutrition and exercise, I have written two articles that I consider basic reading for all who want to stay in shape while living with HIV:
Outsmarting HIV with Healthy Eating
Exercise: The Best Therapy
I also suggest that people who are newly infected watch this short video that tells them all the steps to follow: Video
I hope this helps you with a starting program that you can follow. Please let me know if you have any more questions by writing it here:
Ask a question
In health,

Six Promising HIV Drugs in the Pipeline (2013-2014)

By Warren Tong
December 5, 2012
What new HIV medications do we have to look forward to over the next few years? How will these newer drugs improve upon the older ones? To shed some light on these questions, Roy Gulick, M.D., provided an overview at ID Week 2012 of drugs in development.
Since the first HIV medication, zidovudine (AZT, Retrovir), was approved in 1987, 26 other antiretrovirals have been made available in the U.S. for treating HIV — a history that Gulick recapped in song during this conference. Our best regimens today are potent, convenient and relatively non-toxic.
However, according to Gulick, there is potential to make medications even better than those we have today. Newer drugs should build upon some of these aspects, he said:
  • Improve convenience (reduce dosage frequency, less than once a day).
  • Improve tolerability and reduce toxicity (even the best drugs today still have some of these issues).
  • Penetrate reservoirs more effectively (such as the genital tract and central nervous system).
  • Exploit new targets, thereby improving activity (particularly against drug-resistant viruses).
  • Improve formulation.
The list of drugs in the pipeline continues to be full of antiretroviral agents, whether they are in early development or undergoing clinical trials.
Gulick highlighted six of the most promising drugs.
GS-7340 (Also Known as Tenofovir Alafenamide, or TAF)
GS-7340 is an investigational nucleoside agent that is a prodrug of the approved formulation of tenofovir (TFV, Viread). A prodrug is a medication that, when metabolized in the blood, breaks down into the active form of the compound. The NRTI sold under the brand name Viread is actually tenofovir disoproxil fumarate (TDF), a prodrug that breaks down into tenofovir.
GS-7340’s antiretroviral activity was first presented in a study by Martin Markowitz, M.D., and others at CROI 2011. In a small, 14-day study, Markowitz and his team found that GS-7340 performed slightly better than the “old” TDF, with greater decreases in HIV RNA at lower dosages (GS-7340 at 50 or 150 mg vs. TDF at 300 mg).
These findings were further supported by study results from Peter Ruane, M.D., and others at CROI 2012. Ruane and his team compared GS-7340 (at dosages of 8, 25 and 40 mg) with TDF (at 300 mg) in 38 treatment-naive patients over 10 days of monotherapy. GS-7340 again performed better than TDF, showing 0.76, 0.94 and 1.08 log reductions in HIV RNA, respectively, while TDF only showed a 0.48 log reduction in HIV RNA. The findings were statistically significant for the 25-mg (P = .017) and 40-mg (P = .01) dosages.
Ruane and his group also found that the plasma concentrations of tenofovir, when the prodrugs were metabolized, were 10 to 100 times higher for TDF than for any of the three dosages of GS-7340. This finding suggests that, because GS-7340 delivers less compound to target tissues, it could reduce toxicity levels in the organs, Gulick said.
On the other hand, when comparing intracellular concentrations of tenofovir in peripheral mononuclear cells like lymphocytes (which is where we want the drugs to be), GS-7340 achieved up to 20 times higher levels than TDF, Gulick noted.
In both of these studies, GS-7340 was generally well tolerated and no serious adverse events were reported.
A third study of GS-7340 was presented at ICAAC 2012. It found that GS-7340 had high potency against 26 HIV-1 isolates representing 7 subtypes. The drug also showed high potency against three HIV-2 isolates. In addition, GS-7340 maintained its viral potency longer than TDF, showing its better stability.
Further GS-7340 studies are in progress. Particularly because of its low dosage and high potency, it can be readily co-formulated with other agents.
Gulick pointed out two studies exploring such coforumulations. The first study will compound GS-7340 with emtricitabine (FTC, Emtriva) plus elvitegravir (EVG) plus cobicistat, and compare that to elvitegravir/cobicistat/emtricitabine/tenofovir (Stribild). The second study will compound GS-7340 with emtricitabine, darunavir (Prezista) and cobistat (which would be the first one-pill, once-a-day protease inhibitor-based regimen), and compare that to tenofovir/emtricitabine (Truvada) plus darunavir plus cobicistat.
Dolutegravir (DTG)
Of the six highlighted compounds, Gulick stated that dolutegravir is the furthest along in development. Dolutegravir is an investigational integrase inhibitor, but it has distinguished itself from the two approved integrase inhibitors, raltegravir (Isentress) and elvitegravir.
Dolutegravir has a long half-life of 15 hours, indicating it can be taken once a day. Gulick emphasized that it does not require pharmacokinetic boosting. He noted that resistance does occur, but that dolutegravir showed activity against raltegravir- and elvitegraivr-resistant viral strains.
Its antiviral potency was shown in a phase-2a study by Sherene Min, M.D., and others. In 28 treatment-naive patients receiving either 2, 10 or 50 mg of dolutegravir, there was an average of a 1.51 to 2.46 log reduction in viral load after only 10 days of once-daily dosing. Seven of the 10 patients receiving 50 mg dosages achieved a viral load less than 50 copies/mL. Min and her team reported low pharmacokinetic variability and good short-term tolerability (the most common side effects were diarrhea, fatigue, and headache; adverse events were mild to moderate in severity).
According to Gulick, phase-3 results are complete and will be submitted to the U.S. Food and Drug Administration by the end of the year.
One of the phase-3 studies, known as SPRING 2, found dolutegravir to be non-inferior to raltegravir. The study followed 827 treatment-naive patients with a viral load above 1,000 copies/mL over 48 weeks. They were given either 50 mg of dolutegravir or 400 mg of raltegravir. Both groups were successful at achieving viral loads below 50 copies/mL (88% for dolutegravir and 85% for raltegravir). Both drugs were also very well tolerated, with only 2% in each group having to discontinue treatment because of adverse events.
Furthermore, a dolutegravir-based regimen consisting of abacavir/lamivudine (Epzicom, Kivexa) plus dolutegravir was actually found to be superior to tenofovir/emtricitabine plus efavirenz (Sustiva, Stocrin), according to the results of a companion phase-3 study by Sharon Walmsley, M.D., and others. In 822 treatment-naive patients studied over 48 weeks, 88% of the dolutegravir group achieved a viral load below 50 copies/mL, compared to 81% of the efavirenz group.
Gulick pointed out that the difference was because of tolerability: 10% of the efavirenz group discontinued treatment because of adverse events, compared to just 2% of the dolutegravir group. He commented that this would mark the first real challenger to efavirenz’s long-held dominance in treatment-naive studies with a 48-week primary endpoint.
In terms of renal safety, the study found dolutegravir did interfere with tubular secretion of creatinine. However, Gulick noted, the increase in creatinine was only about .1 to .15 mg/dL, and occurred only within the first two weeks after starting dolutegravir, then stabilized over the rest of the 48-week study. As the Walmsley study noted, dolutegravir does not affect actual glomerular filtration rate.
In terms of resistance, dolutegravir appears to have a higher barrier to resistance than the other integrase inhibitors. In the Walmsley study, among both the dolutegravir and efavirenz groups, only 4% experienced virologic failure (18 and 17 individuals, respectively). Of the nine in each group that had genotypic test results available, “You see no nucleoside and no integrase mutations in the dolutegravir group. And as you would expect in the efavirenz [regimen], there were some nucleoside and non-nucleoside mutations detected,” Gulick stated.
Because dolutegravir showed activity against elvitegraivr- and raltegravir-resistant viral strains, as shown in a study by Masanori Kobayashi and others, Joseph Eron, M.D., and others studied the use of dolutegravir for patients who had developed resistance to raltegravir. Their pilot study, known as VIKING, followed 51 patients with three or more class resistances, including demonstration of raltegravir mutations. The patients were given 50 mg of dolutegravir, either once or twice a day, for 10 days. A virologic response was defined as either a viral load below 400 copies/mL or a 0.7 log reduction. As Gulick explained, “The best responses were in the twice-a-day group. Whether you looked at all patients, those with the specific Q148 or other mutations, you can see response rates, over a short 10 days of therapy, exceeding 90%.”
The VIKING study went on to follow the patients over 24 weeks. After the initial two weeks, the patients added an optimized background regimen. These follow-up results were presented by Vincent Soriano, M.D., Ph.D., at the 2011 European AIDS Conference. Soriano and his team found that by the end of the 24-week period, 41% of the once-a-day group and 75% of the twice-a-day group were able to re-suppress their viral load below 50 copies/mL.
Further studies of dolutegravir in the setting of other integrase inhibitor resistance are ongoing.
S/GSK-1265744 (or simply “744”)
S/GSK-1265744 is an integrase inhibitor, similar to dolutegravir. Results from two studies presented at ICAAC 2012 found that 744 had high potency and an exceedingly long half-life. When given orally at once-daily doses of 30 mg, patients showed a median 2.6 log reduction in viral load.
More impressive, when using nanotechnology to formulate 744 to be injected subcutaneously or intramuscularly, a single dose showed a half-life between 21 and 50 days.
Remarkably, after a single dose, patients still had detectable levels of 744 up to 48 weeks after injection.
Similar to dolutegravir, 744 seems to have a high barrier to drug resistance. According to Gulick, using site-directed molecular clones (molecules created with specific mutations) associated with integrase inhibitor resistance, these mutations showed high levels of resistance to raltegravir and elvitegravir, but remained susceptible to 744 and dolutegravir.
In terms of safety, there were some injection site reactions and nodules associated with subcutaneous dosing. But conceivably, 744 could be taken as infrequently as every three months for treatment, or even as PrEP (pre-exposure prophylaxis). Research is ongoing.
HIV Entry Inhibitors
HIV entry inhibitors block HIV at the point at which they attach to CD4 cells. Many of the other classes of drugs, including protease inhibitors, NRTIs and NNRTIs, fight HIV after it has infected a CD4 cell.
Among the entry inhibitors, there are presently three sub-classes. We already have approved drugs in the first two sub-classes: CCR5 antagonists and fusion inhibitors. In the CCR5 antagonist sub-class, we already have maraviroc (Selzentry, Celsentri), and a new drug called cenicriviroc is being investigated. The fusion inhibitor class has long featured only enfuvirtide (Fuzeon), but a new drug called albuvirtide is being studied.
The third sub-class is an investigational one: CD4 attachment inhibitors. These new drugs are being developed to either bind at the location of HIV’s gp120 protein (such as BMS-663068) oron the CD4 receptor itself (such as ibalizumab, a once- or twice-a-day drug that’s still under investigation for both treatment and prevention).
Gulick offered a closer look at a few of these drugs in his overview.
Cenicriviroc (CVC)
Cenicriviroc is an investigational CCR5 antagonist. Not only does it antagonize CCR5 binding, it also antagonizes CCR2 binding. CCR2 is a receptor that sits on the surface of macrophages and may be involved in inflammation.
Cenicriviroc showed potent antiretroviral activity in a small study by Jacob Lalezari, M.D., and others. They followed treatment-experienced patients who had not been on treatment for at least six weeks, had a CD4+ cell count above 250 and a viral load above 5,000 copies/mL. They were randomized to receive either 25, 50, 75, 100 or 150 mg of once-daily cenicriviroc. At the highest doses, after 10 days, patients showed a 1.5 log reduction in viral load.
An update on the follow-up study was discussed by David Martin, M.D., at CROI 2012. In Martin et al’s phase-2b study, they randomized 150 treatment-naive patients into three groups to receive tenofovir/emtricitabine with either cenicriviroc (at 100 or 200 mg) or efavirenz. Cenicriviroc was administered using a new, 50-mg formulation. In preliminary data from 18 patients, cenicriviroc was found to be well-absorbed and within the expected therapeutic range of potency. Further study will assess the safety, efficacy and effect of CCR2 inhibition on inflammatory biomarkers.
The only approved fusion inhibitor, enfuvirtide, offers a lot of activity against HIV, but the obvious downside is that it requires twice-daily injections. Albuvirtide, on the other hand, is an investigational fusion inhibitor that when given intravenously has a long average half-life of 11 days, warranting weekly dosing.
Albuvirtide has a similar design to enfuvirtide. It is a peptide that is an analogue of gp41, one of the envelope proteins on HIV’s surface, and thereby blocks HIV through CD4 membrane fusion.
Two proof-of-concept studies by Dong Xie and others were presented at ICAAC 2012. In the first study, albuvirtide was given to 54 treatment-naive patients in a single dose; doses ranged from 20 to 640 mg. They found that albuvirtide’s half-life ranged between 10 and 13 days, and that the drug suppressed plasma viremia for between 6 and 10 days. Albuvirtide was generally well tolerated, with no injection-site reactions and no serious adverse events.
In the second study, albuvirtide was given to 12 treatment-naive patients in multiple doses of either 160 or 320 mg. Doses were given on days 1, 2, 3, 8 and 15. The participants averaged viral load decreases of 0.68 log copies/mL (at 160 mg) and 1.05 log copies/mL (at 320 mg). Similar to the first study, there were no injection-site reactions and no serious adverse events. No anti-albuvirtide antibodies were detected in patients for up to 42 days.
BMS-663068 (a.k.a. BMS-068)
BMS-068 is an HIV attachment inhibitor. It is an oral prodrug that breaks down into the active compound BMS-626529 (a.k.a. BMS-529). It inhibits CD4 binding by specifically binding to gp120, one of HIV’s envelope proteins that binds to CD4 cells. Gulick stated BMS-068 could be taken once or twice a day without boosting, but noted, “There is decreased baseline susceptibility in some patients due to envelope polymorphisms.”
BMS-068 taken over 8 days with or without ritonavir (Norvir) resulted in substantial declines in plasma HIV RNA levels and was generally well tolerated, according to a study by Richard Nettles, M.D., and others. The study followed 50 patients with a CD4+ cell count above 200 cells/mL and a viral load above 5,000 copies/mL. They were either treatment-naive or not taking any treatment. The median change in viral load ranged from a 1.21 to a 1.73 log reduction, demonstrating that CD4 attachment inhibition can be quite potent and effective.
In terms of resistance, a study presented by Neelanjana Ray, M.D., at CROI 2012, found little resistance after the eight days of monotherapy. Ray and his team analyzed the changes in phenotypic susceptibility and known attachment inhibitor resistance substitutions that may have occurred during the Nettles study. Of the 48 patients that completed the study, 42 had at least a 1 log drop in viral load, showing that BMS-068 was effective. However, the other six (about 12%) had no virologic response, even though their baseline IC50 (a measure of the effectiveness of a compound in inhibiting a biochemical function) levels were quite high.
“When they took a close look and they sequenced gp160, which is broken down into gp120, they showed that a mutation (M426L) was associated with resistance,” explained Gulick. “You can see that in patients with virologic response, very few (only 6%) have this mutation, whereas in those without virologic response, 5 of the 6 had this mutation. So it looks like this will be important in screening for activity of this compound as its development moves forward.”
New Fixed-Dose Combination and Antiretroviral Formulations
Gulick pointed out three one-pill, once-a-day formulations being developed:
  • GS-7340/FTC/elvitegravir/cobicistat.
  • GS-7340/FTC/darunavir/cobicistat.
  • Abacavir/lamivudine (3TC, Epivir)/dolutegravir.
In addition, three other in-development formulations that Gulick mentioned were:
  • Lopinavir/ritonavir/lamivudine.
  • Atazanavir (Reyataz)/cobicistat and darunavir/cobicistat (both in clinical trials).
  • Rilpivirine long-acting (RPV-LA).
Regarding the last drug in those lists, a small pilot study presented at CROI 2012 found that RPV-LA could potentially be given once a month in its long-acting nano-formation. It would likely need to be paired with other drugs, but research is ongoing for its use in treatment and prevention.
Warren Tong is the research editor for and
Copyright © 2012 Remedy Health Media, LLC. All rights reserved.
 This article missed the drug ibalizumab:
 TMB-355(Ibalizumab) is a humanized monoclonal antibody (mAb) and a member of an emerging class of HIV therapies known as viral-entry inhibitors. This drug candidate is distinct from other entry inhibitors in that it binds to the CD4 molecule, the primary receptor for HIV infection, thereby interfering with the penetration of the virus into the cell. It is the first entry-blocking humanized mAb to treat HIV/AIDS. TMB-355 caught the attention of the scientific community in February 2003, when results from the phase-1, single-dose clinical trial showed a transient but clinically significant reduction in the patients’ viral load. Moreover, it was well tolerated with no evidence of adverse effects on CD4 T-cells of treated subjects unlike the majority of approved drugs for HIV. The U.S. FDA granted TMB-355 fast track status in October 2003. The phase-2a clinical trial was successfully completed in 2006, with the results showing a clean safety profile and clear antiviral activity (10-fold reduction in viral load).  The Phase-2b clinical trial was also successfully completed in 2011. TaiMed Biologics is concurrently developing a subcutaneous injection dosage form and a phase 1 human pharmacokinetics bridging study is completed in 2012. Currently, TMB is developing a phase I/II study for HIV-negative and new HIV-positive subjects to begin by the end of 2012.

WORLD AIDS DAY: Time to Help Victims of HIV Drug Studies and Resistance

We have repeatedly heard the following statements about multi-drug resistant HIV (MDR-HIV) patients in a host of meetings on treatment access and HIV research: “These patients no longer exist – they’re either dead or have responded to the latest ARVs”; “Only patients who do not adhere to their HIV regimens have MDR-HIV”; and “Our clinic cannot provide expanded access programs (EAPs) due to cost and staff restraints.” However, after surveying physicians around the country, we have found that although these patients are in a minority, they do exist and are anxiously waiting for access to viable regimens that could save their lives.

No one can deny that many patients can now suppress their HIV with effective regimens that cause fewer side effects. However, a vulnerable and often forgotten minority of people are still struggling with MDR-HIV while they anxiously await for access to life-saving regimens that would finally control their virus replication. Although some of these patients may have developed resistant HIV due to lack of adherence or other issues, many of them have been strictly following their doctor’s orders for years.

They’re often veterans of drug development research who have accumulated HIV resistance as they repeatedly joined antiretroviral (ARV) studies or traditional EAPs of a single new drug out of desperation to control their HIV viral load. As they signed up for studies that helped companies get their drugs approved by the FDA, many of these patients were exposed to suboptimal HIV regimens (namely, functional monotherapy or the addition of a single new active ARV to a failing HIV regimen). It is time to create a new paradigm to break the vicious cycle of single drug access that has failed these patients.