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Bona Fide Progress on the Virus Front That Doesn’t Attract Much Notice

Doc Gumshoe looks at progress in antivirals

By Michael Jorrin, "Doc Gumshoe", July 14, 2016

[ed. note: Michael Jorrin, who I dubbed “Doc Gumshoe” years ago, writes for us a couple times a month on medicine and health issues. He is not a physician, but explains the science and the data well, and helps provide some background understanding and perspective that often benefits both investors and folks who are attentive to their own health. He chooses his own topics and doesn’t usually focus on investment ideas, but follows our trading rules when investments are featured in his articles. You can see his past articles and comments here.]

It’s always the scary news that hits prime time and social media news feeds and the front pages of even reputable papers like the Good Gray New York Times, as it used to be called before it got so trendy with giant color spreads on every page. A few days ago, the Times broke the news that in the United States 234 pregnant women had been infected with the Zika virus. A statement that, while not intended to instill panic, was by no means calm inducing. What, women infected with Zika in the United States? One had to read considerably further on in the article to learn that not one single one of those women had been infected in the United States. These unfortunate ladies were in the United States, but they had been infected outside the United States. Indeed, of the 755 confirmed cases of Zika in the US (according to the CDC), not one single one acquired the infection in the US.

It is thought, however, that during the summer months, there may be some Zika infections in Florida and along the Gulf coast, in areas where the Aedes aegypti mosquito is likely to breed. But this bug travels only a very short distance – maybe a quarter of a mile – from where it is hatched, and to transmit the infection, it first has to suck a little blood from an infected human, so there has to be an infected human near where the mosquito hatches, and since there are supposedly not many such in the whole US, the chances of transmission in the continental US, at least, may be small.

I do find the figures a mite dubious, however. If there are only 755 Zika-infected persons in the US, how can 234 of them be pregnant women? My suspicion is that it was mostly pregnant women who got tested, based on their rational fears for their unborn babies. There was no reason for symptom-free men and non-pregnant women to go and get tested, so that likely accounts for that huge disparity. But that would suggest that there are many Zika-infected people out there who have no symptoms, have not been tested, and are potential reservoirs for the virus.

But let’s turn our attention away from the headline-grabbing Zika virus and consider the enormous progress that has been made in the treatment of another virus, much more threatening to us, and take a look at a prospective treatment that promises to hugely to reduce the time it takes to achieve a cure. That virus is hepatitis C.

What is hepatitis C and why is it of particular concern?

Hepatitis C, by any measure, is a highly successful virus, by which I mean that it has all the characteristics that lead to widespread transmission. It is transmitted by blood (more about that later); in the early stages of infection it is almost always asymptomatic, meaning that infected persons have no notion that they have been infected and have no reason to seek treatment. But most patients, perhaps as many as 85%, go on to develop a chronic infection. Again, most of these chronic hep C patients have only mild symptoms such as fatigue. However, about 20% will eventually develop cirrhosis, and some of these will experience liver failure. Hep C is the most frequent indication for liver transplantation in the US, and was listed as the cause of death on 19,659 death certificates in 2014.

The factor that enormously contributes to the transmission of hep C is that it can take a very long time for the cirrhosis signs to appear, sometimes as long as 40 years, during which time the virus is present in the patient and can be transmitted to another person.

And it is estimated that there are almost four million persons with chronic hep C in the US at this time, many of whom have no idea that they are infected. Nonetheless, these individuals can pass the virus on to another person.

How does this happen?

How is hepatitis C transmitted?

Hep C is transmitted in blood. Until the mid 1990s, blood transfusions were the source of much hep C infection, but starting in 1992 it became standard practice for all donated blood and organs to be tested for hep C, and subsequently this source of transmission was essentially halted. Indeed, the incidence of hep C plummeted after blood used in transfusions began to be tested, from a peak of about 6,000 reported new cases per year before 1992, to about 2,000 reported new cases currently. However, there is an enormous disparity between reported cases and estimated actual cases. Since most infected persons do not demonstrate symptoms, most new cases are not reported. The CDC estimates that for every reported case, about 13 more cases go unreported.

Accidental needle sticks in medical facilities may account for a few cases, and it should be assumed that most of those cases are tested and reported, and that the individuals who acquire hep C by that route are not major reservoirs of infection.

But the largest numbers of hep C infections are transmitted through intravenous drug use (IDU). Despite repeated warnings, despite programs to provide free hypodermics to reduce that risk, junkies routinely continue to share needles when they partake of their drug of choice in little social get-togethers. It’s hard to say whether they are aware of the risks they are taking. If some of their fellow-junkies are hep C infected, they may be symptom-free and thus unaware, or they may be in denial, of they may be infected with a disease even more serious than hep C, namely terminal fatalism – “It doesn’t matter – my life is a mess anyway.”

My non-medical response to this is, “Just because your life is a mess doesn’t give you the right to mess up somebody else’s life.”

An interesting and frequently overlooked route of hep C transmission is tattooing. I find no mention of tattooing as a risk factor for hep C in a lot of widely-available material, although the Mayo Clinic does mention tattooing as risk factor. Tattooing is done by injecting pigments into the dermal layer of the skin (beneath the epidermis) by means of a needle that punctures the skin at the rate of 90 to 150 times per second. If the tattooing needle is not sterilized between uses, or if the pigments used to create the tattoo are not sterile, tattooing might play the same role in transmitting infections as IDU.

Tattooing is especially prevalent among younger people, also in some socio-economic and ethnic groups, and especially in prison. In trying to determine the risk for hep C transmission presented by tattooing, it is crucial to exclude drug users and individuals who may have acquired hep C through other routes. One study, a meta-analysis of 83 studies in which the relationship between tattooing and hep C was a study variable, found a combined odd ratio of 2.24 for the link, meaning that tattooed individuals were more than twice as likely to have hep C as non-tattooed individuals, when other possible routes of transmission were excluded. In prison, that odds ratio increases to about 5. (Jafari S. Int J Infect Dis 2010;14:e928e940)

The study authors point out that tattooing has also been reported to be a strong risk factor for the transmission of several other diseases, including HIV, hepatitis B, leprosy, and methicillin resistant Staphylococcus aureus (MRSA). They also point to an association between the surface area covered by the tattoo and the risk of hep C infection. Larger tattoos, covering more than 20 cm2 (about 60 square inches) increase the odds ratio for hep C infection to more than 12.

In another study that found a strong association between tattooing and hep C, the finding was that individuals with hep C were 5.17 times more likely to have a tattoo than those without hep C. (Carney S. Hepatology 2013;57:2117-2123)

Those two analyses are not in disagreement, by the way. In the first analysis, they were comparing tattooed and non-tattooed individuals and found that those with tattoos were more than twice as likely to have hep C, while in the second analysis, they were looking at individuals with and without hep C and found that those with hep C were more than five times as likely to be tattooed.

I find it difficult to understand how a risk factor that is intuitively obvious, that affects a significant number of persons, and that results in major health-care costs – think of the cost of treating prisoners who get infected with hepatitis C – is not subjected to more prominent warnings. Is it viewed as a “life-style choice,” favored by some demographic cohorts, and therefore not subject to criticism?

But let us move on to some better news.

How is hepatitis C treated these days?

The Gumshoe citizenry surely have heard of Sovaldi and Harvoni, if for no other reason than the immense impact these two drugs have had on Gilead’s fortunes. Those two, along with another newcomer, Daklinza, have completely changed the hep C treatment landscape, and that is by no means an exaggeration.

Prior to the introduction of these agents, treatment for hep C was based on some form of interferon given with ribavirin. Interferons are cytokines, a protein that is an essential actor in the immune system and is part of the organism’s defense against viruses. The particular form of interferon that was most commonly used in patients with hep C was pegylated interferon alpha 2b, in which the interferon molecule is linked to polyethylene glycol to extend the activity of the interferon in the body and make it possible to give the interferon injections weekly rather than two or three times per week. (If polyethylene glycol sounds familiar to you, it’s because that’s what antifreeze is, and it’s also an ingredient in some cosmetics.)

Ribavirin is an antiviral drug which is also used for the treatment of respiratory syncytial virus. Used alone, it is entirely ineffective against hep C. The combination of ribarivin and interferon given by subcutaneous or intramuscular injection for 6 to 24 months was formerly the only even moderately effective option for the treatment of hepatitis C. Depending on which hep C genotype a patient was infected with, the cure rate varied. The most common hep C genotype in North America and Western Europe is genotype 1, and ribavirin-interferon treatment results in a cure rate of about 50% in that population. That treatment does a bit better with genotypes 2 and 3, perhaps achieving a 75% cure rate.

Moreover, the adverse effects due to injected interferon are significant, and include fever, headaches, severe fatigue, joint and muscle aches, neutropenia, and some autoimmune effects such as hypo- and hyperthyroidism.

All this changed utterly with the approval by the FDA of sofosbuvir (Sovaldi) on December 6, 2013. Sofosbuvir is taken orally with ribavirin and is used without any form of interferon. Like some other antivirals, sofosbuvir is a nucleotide analog, which inhibits the RNA polymerase that the hep C virus requires for replication. However, unlike previous attempts to harness this mechanism, the cure rate for sofosbuvir with ribavirin after 12 weeks of treatment is about 95%; 24 weeks of treatment frequently attains a 100% cure rate. Sofosbuvir is used for the first-line treatment of all known hepatitis C genotypes, including genotype 1, which as mentioned above, is the most common genotype in North America and Europe. Treatment with sofosbuvir/ribavirin is also used in patients with HIV/hep C co-infections, a double whammy which had previously made treatment for hep C in those patients extremely complicated. Sofosbuvir may also be used in combination with a Bristol-Myers Squibb agent, daclatasvir (Daklinza), with or without ribavirin.

In contrast with the side effects profile of regimens that include interferon, the adverse effects associated with the sofosbuvir combinations are considerably less troubling. For example, fatigue and headache are nearly cut in half, influenza-like symptoms are reduced to 3–6% as compared to 16–18% with interferon, and neutropenia is almost absent.

Another major change in hep C treatment took place on October 10, 2014, when Harvoni, also from Gilead, was approved by the FDA for treatment of hepatitis C.

Harvoni is a combination of sofosbuvir and ledipasvir, also developed by Gilead. Ledipasvir is an inhibitor of a viral protein designated NS5a, which is crucial to viral replication. Harvoni, unlike Sovaldi/sofosbuvir, does not need to be taken with ribavirin, and thus avoids ribavirin’s most troublesome adverse effect, which is anemia. The cure rate for Harvoni is similar to that with sofosbuvir, around 95% after a treatment period of 12 weeks. Some patients who had not received any previous anti-viral therapy were able to achieve cures in 8 weeks. And in clinical trials in patients whose disease has already resulted in significant cirrhosis, 24 weeks of the Harvoni regimen resulted in a 100% cure rate.

Then, on December 19th, 2014, the FDA approved another combination therapy for genotype 1 hep C, this time not from Gilead, but from AbbVie. The combo package was called Viekira Pak, consisting of ombitasvir, paritaprevir, and ritonavir pills, combined with dasabuvir pills. It is sometimes used with ribavirin. It is taken for 12 to 24 weeks, and the cures rate is over 95% percent. And finally, on April 25th of this year, AbbVie received FDA approval for Viekira Pak in patients with hep C genotype 1b with compensated cirrhosis, this time without ribavirin. (Compensated cirrhosis means that the patient preserves adequate liver function and is not a candidate for liver transplantation.) The FDA’s approval was based on a clinical trial, TURQUOISE-III, in which 60 out of 60 patients were found to be free of the hepatitis C virus after 12 weeks. The 100% cure rate, the relatively short treatment period, the absence of ribavirin in the regimen, and the freedom from side effects add up to a highly effective drug to combat a pervasive and menacing viral antagonist.

The appearance of those three new treatment options within a time-span of less than three years, each of which have cure rates that are double the rates achieved by the best regimens available up to that time, and with much lower rates of adverse effects, is surely a testimony to the achievements of medical and pharmaceutical research and development. But rather than permitting Big Pharma to preen, it’s our mission to look for what more needs to be done. And, indeed, there are problems. One is that these treatments cost a lot of money. Another, related problem is that sometimes they take a really long time – as long as 24 weeks. Even 12 weeks is not nothing.

What about the cost?

There has been a great deal of sound and fury about the cost of these new hep C drugs and drug combos. Sovaldi’s list price is $1,000 per pill, which means that a 12 week treatment of once-daily pills costs $84,000. Harvoni costs a bit more – $1,125 per pill, or $94,500 for that 12 week treatment. The Viekira Pak sneaks in at just a bit less, $83,319 for 12 weeks. Gilead makes co-payment coupons available for some classes of patients, which reduces the total co-payment amounts by 25%, and what those co-payment amounts might be depends, of course, on the kind of health insurance one has.

Gilead has also permitted the manufacture of generic versions of its drugs in India for sale in 91 low-income countries, but there has been extensive pushback around the question of precisely which countries are regarded as low income. Patient advocates point out that there are perhaps 180 million people with hepatitis C on planet Earth, and that the great majority of those will not conceivably be able to receive these curative treatments. That does not mean that these people will instead be treated with weekly or thrice-weekly interferon plus ribavirin. That form of treatment costs plenty of money too, especially because patients have to get their injections from a health-care provider, and in low-income countries, those health-care providers are stretched to the limit. Most of those infected persons will live with their disease, and some will die from it.

Health insurers in developed nations have been negotiating and bargaining with the drug manufacturers, as they do with doctors and hospitals. I have no idea what the out-of-pocket cost of a course of treatment with one of those new options would be for an insured patient. That would depend on the specific insurance plan.

A great concern, of course, is that hepatitis C preferentially affects individuals without any form of health insurance – intravenous drug users, prisoners, the lower economic strata, the socially disadvantaged. That means that treatment for those persons falls to the charge of the commonwealth. Will the taxpayers willingly shoulder that burden? That remains to be seen.

Reducing the cost of treatment by shrinking the time it takes to get to a cure?

There’s not much question that persons with hepatitis C can be cured, in the developed world, at least. But the cost of a course of treatment is certainly a problem. What if, instead of a minimum of 12 weeks, treatment only had to last 4 weeks? That would lop about 56 days, and about a grand a day, off the bill.

A very small biotech, Regulus Pharmaceutics, is working on a candidate that would do just that, and perhaps even more. Their drug, labeled RG-101 so far, has demonstrated results in a Phase I trial and preliminary results in a Phase II trial that can only be called highly impressive. In the completed Phase I trial, a single subcutaneous dose (either 2 or 4 mg/kg) of their drug as monotherapy resulted in significant and sustained viral load reductions in all treated hep C patients, including those with difficult-to-treat genotypes, liver fibrosis, and those who relapsed after treatment with a regimen that included interferon.

In an ongoing Phase II clinical study, interim data reported that two injections of RG-101 combined with just 4 weeks of commercially-available oral direct-acting antivirals achieved high virologic response rates. The study enrolled 79 treatment- naïve genotype 1 and 4 hep C patients treated with one of three drugs (Harvoni, simeprevir, or daclatasvir). Among the 38 patients with data through 8 weeks of follow up, 97% (37/38) had hep C viral load measurements below the limit of detection. For those patients through 12 weeks of follow-up, 100% remained below the limit of detection (14/14).

That Phase II trial flashes glints of hope that hep C might be able to be effectively cured with 4 weeks of treatment, consisting of just two subcutaneous injections plus oral therapy. That would likely result in a considerable reduction in the cost of a course of treatment, depending, of course, on the cost of RG-101. But two subQ injections of that new agent aren’t likely to eat up the cost savings of 8 fewer weeks of Harvoni.

However, that’s not all. Regulus is also investigating a joint treatment option with a new agent from Glaxo Smith-Kline dubbed GSK 2878175. Currently, there’s a Phase II trial evaluating the combination of a single subcutaneous injection of 4 mg/kg of RG-101 and daily oral administrations of 20 mg of GSK 2878175 for up to 12 weeks in treatment-naïve patients chronically infected with hep C genotypes 1 and 3. That doesn’t sound revolutionary. Are we back to 12 weeks of treatment? But no, there’s more.

As part of the collaboration agreement with Regulus, GSK is also working on a long-acting formulation of GSK 28781875 which would be given as a single intramuscular injection. That opens up the possibility of a treatment option for hep C that could result in the same cure rates in a single treatment as those currently attained by the best hep C drugs now on the market that require multiple weeks of treatment.

All this is highly speculative, of course. The Regulus candidate, RG-101, appears to be a reality, although probably a couple of years from getting the FDA imprimatur. The GSK candidate is farther away from the finish line. But the potential of a one-shot (okay, two-shot!) cure for hep C is so far from the poor outcomes and troubling side effects that patients had to accept in the interferon/ribavirin era that Doc Gumshoe is scrambling around for superlatives.

Late-breaking bulletin: an ongoing Phase I trial of RG-101 has been suspended when a patient developed jaundice 117 days after having received one dose of the drug. Regulus has stated that it is unlikely that the jaundice was related to the drug. In addition to hepatitis C, the patient has type 2 diabetes, end-stage renal disease, coronary artery disease, elevated cholesterol and hypertension, and is on about a dozen medications. This is the second patient to have developed jaundice after having been dosed with RG-101. A patient in a Phase II trial with RG-101 in combination with daclatasvir also developed jaundice. Three other Phase I trials in RG-101 are not affected, nor is the Phase II trial of RG-101 in combination with GSK2878175 discussed above. This might be a bump in the road, or it might be the edge of a cliff. Similar events have taken place in the development of lots of drugs that went on to great success.

What we’ve been going on about in this piece is the search for effective treatment options for one single virus, the hepatitis C virus, albeit a virus with at least six genotypes. That’s the way it seems to be with viruses – they need to be targeted singly and specifically, with an antiviral agent that takes dead aim at the individual virus, usually the mechanism that permits the virus to replicate.

Fortunately, that’s not the case with antibiotics, which attack bacteria and some other classes of microbes. Some antibiotics attack the cell wall of many different bacteria. Others attack DNA gyrase, which twists the single DNA strands into the familiar double helix. Yet others target protein synthesis. These are all broad-spectrum antibiotics.

At this moment, broad-spectrum antivirals have yet to come into existence. But researchers are working on the problem.

Progress in developing broad-spectrum antivirals?

Attacking viruses is much more difficult than attacking bacteria, largely because once viruses enter our bodies they quickly take up residence inside our cells, where they kidnap host cell resources for their own reproductive purposes. Bacteria and other related microbes are many orders of magnitude larger. The harmful ones meander around in our systems, destroying tissue, emitting toxins, and causing large-scale problems. The search-and-destroy mission on which we dispatch antimicrobials is a good deal simpler, because the enemy is easier to find.

Nonetheless, there has been progress on the broad-spectrum antiviral front. Let’s first look at the broad-spectrum potential of an existing antimicrobial, nitazoxanide. This drug is primarily used in the treatment of two very common intestinal diseases caused by pathogens that are present in polluted water. One is giardiasis, caused by Giardia lamblia, and the other is infection caused by Cryptosporidium parvum. Nitazoxanide was developed by Romark Laboratories, and Lupin Pharmaceuticals manufactures it. It is sold under the brand names Adonid, Alinia, Allpar, Annita, Colufase, Daxon, Dexidex, Kidonax, Mitafar, Netazox, Niazid, Nitamax, Nitax, Nitaxide, Nitaz, Nizonide, NT-TOX, Pacovanton, Paramix, Toza, and Zox. It is closely related to a large class of drugs called thiazolides that have been synthesized and tested against parasites and bacteria, but also against viruses.

This, by the way, is an intuitively obvious course in drug development. A drug is found to have activity against one pathogen, or one class of pathogens, so let’s by all means see if has activity against other pathogens. In the case of nitazoxanide, it initially has been found to be effective in vitro against many types of influenza, including H1N1, H3N2, H3N8, H5N9, H7N1, influenza B, as well as respiratory syncytial virus, parainfluenza, corona virus, picorna virus, rotavirus, hepatitis B and C, dengue, yellow fever, and HIV. Specifically, the drug appears to block the maturation of a glycoprotein (hemaglutinin) which is essential to viral replication. However, those findings are mostly so far only in the laboratory, and not in human beings.

At this point, a large global Phase III trial is under way in about 2000 patients with active influenza. The trial will compare nitazoxamide alone with placebo, with oseltamvir (Tamiflu), and with a combination of nitazoxamide and oseltamvir; no results are available so far. And even if this trial demonstrates positive results, that won’t be a huge deal. The really huge deal will be if the positive in vitro results can be replicated for several of those other non-flu-related viruses, and it will be a while before those start trickling in. Romark is far from being a wealthy outfit, and the way forward will require scratching around for funds.

But there’s no denying that the possibility that a single agent, whether nitazoxamide or one of the related thiazolides, will turn out to be a genuine broad-spectrum antiviral is big news. Most of the information about nitazoxamide, by the way, came from a paper by Jean-François Rossignol (Antiviral Res 2014;110:94-103), who was the original nitazoxamide developer, and is now the Chairman of the Board of Romark.

And a couple of others

One has been given the acronym “DRACO,” for Double-stranded RNA Activated Caspase Oligomerizer. The putative mechanism for DRACO drugs – actually a group of drugs – is that they are able to distinguish between virus-infected and healthy cells, based on differences in the length and type of RNA transcription helices within the cells. Viruses produce long double-stranded RNA helices during transcription and replication, while uninfected mammalian cells produce double-stranded RNA helices not longer than 24 base pairs. DRACO drugs are being studied at MIT, and in the laboratory they have been reported to have broad-spectrum activity against many viruses including dengue, arenaviruses, Guama bunyavirus, at least one strain of flu virus, and rhinovirus. The effect of these agents is to promote early cell death in infected cells, while leaving uninfected cells unharmed. Development of broad-spectrum antivirals along this line is now being pursued by Draper Laboratories, which is actively seeking funding for further research.

Another line of research focuses on cellular proteins present in all human cells that function as pathogen recognition receptors. These are encoded by a gene, labeled retinoic acid inducible gene (RIG); one specific variant, RIG-1, is a pattern recognition receptor that detects viruses based on RNA structure and can trigger the innate immune response to attack the virus. Early research suggests that a RIG-1-based drug may be able control viruses including West Nile, dengue, hepatitis C, influenza A, respiratory syncytial virus, Nipah, Lassah, and Ebola. Research along this line is being carried out by Kineta, Inc., a small Seattle biotech.

What do those three stories tell us?

Romark, Draper, and Kineta are not familiar names, at least not to me. Big Pharma is probably waiting to pounce, which is its normal posture, but it’s a bit strange that the outfits doing that research aren’t even the smaller biotechs that we hear about. What might account for this? Is it perhaps that a broad-spectrum antiviral is not such an attractive goal from the standpoint of an established pharmaceutical company? Are the bigger players skittish about spending a lot of money and then having their drug crippled by emerging resistance, or by piracy?

Currently, there’s a widespread perception that the pharmaceutical industry isn’t doing anywhere nearly enough to develop new antibiotics. We have discussed that before in these pieces – the disincentives are many. One is that the pharma outfit spends a couple of billion, brings a drug to market that works really well on a range of resistant pathogens, and then finds that the medical establishment’s recommendation is that their new drug be held in reserve for those really tough cases where nothing else will work. Or, if it gets used too much, that resistance will emerge and render it useless. Or that there is huge international pressure to permit generics to be manufactured, and that those generics invade the markets where the originators of the drug hoped to at least recover their investment.

Is it possible that some of the same concerns trouble the sleep of potential developers of broad-spectrum antivirals?

My guess is that the research will continue, not at warp speed, but I hope not ploddingly. Broad-spectrum antivirals would be very valuable indeed, especially because a lot of viral illnesses are diagnosed empirically and perhaps imprecisely. It would be good not to have to wait until severe symptoms emerge to start a course of treatment. It would be good to be able to give Timmy a tiny pill for his cold, and to billions of others for whatever ails them. But we’ll have to wait for that.

* * * * * * *
And if all that wasn’t enough to chew on, here’s one more: just before the Glorious Fourth Weekend, Gilead got yet another FDA approval for a hep C drug, this one for a combination agent they’re call Epclusa, a combo of sofosbuvir and their new agent velpatasvir, which is a NS5A inhibitor, like ledipasvir, discussed above. The duet cured 98% of hep C genotypes 1 through 6 in 12 weeks. Gilead is saying that it will be a bit less expensive than Sovaldi or Harvoni. In any case, I would venture to say that, money being no object, hep C is on the run.



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6 years ago

Lets not forget profit… You mention Retinoic Acid acid above. I and many others take it to cure URI’s in about 3 days. It will never be an approved treatment (FDA defined “Drug”), because you cannot patent a natural vitamin. It costs 1 billion + to get a new drug approved, so foods (especially synergistic combinations, taken in specific ways) or fractions of foods (read: “Chemicals” [which is what foods are]) can not be profitable under the current regime. Lastly, “Cures” are only profitable in the short run (at $1,000 per pill), and do not create a “future stream of income” like a treatment which must be refilled every month for life. Temporary “cures” (till Re-currence) of life-threatening conditions can be very profitable. Alas I am to optimistic (hopeful) to invest in never ending treatment of never ending disease…

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