Selenium Against Viruses: More Exciting Research from Dr. Will Taylor
By Richard A. Passwater, Ph.D.
You are witnessing a scientific breakthrough develop from theory to public health practice. In November 1994, Dr. Will Taylor, Associate Professor in the Department of Medicinal Chemistry at the University of Georgia, explained his hypothesis that opened new inroads into possibly controlling many viruses including AIDS, Ebola and even several "more-routine" viruses. Last month, Dr. Marianna Baum of the University of Miami discussed her published results with selenium and HIV/AIDS. We didn't discuss her latest results because they had not yet been peer-reviewed for publication, but I can tell you that they are very exciting. Dr. Orville Levander of the USDA has published his latest findings with selenium and viruses. These three aspects of research with selenium and human viruses recently gained interest at an International Conference on the subject held in Germany in April.
As one who has conducted laboratory research with selenium and other antioxidants for more than 35 years, I can attest to the scientific and public health importance of this "new direction" in virus research. I don't believe that I have used that terminology to describe completely new concepts since my 1973 publication, "Cancer: New Directions," in which I reported my laboratory research showing that selenium and other antioxidants reduce the incidence of cancers. [American Laboratory 5(6) 10-22 (1973)] By the way, an upcoming chat with Dr. Larry Clark will discuss his clinical trial which found that selenium supplements can cut the cancer death rate in half.
Let's chat again with Dr. Taylor to see how his new theory has had an effect on AIDS and viral research. It is not necessary to understand the technical aspects of the theory, just that, as his analogy illustrates, that selenium can be a birth control pill to some deadly viruses. If you are interested in the details of his theory, please refer to our November 1994 discussion which describes it in detail.
Passwater: Dr. Taylor, it has only been two years since we discussed your exciting new theory about selenium and HIV, but thanks to your new concept, a lot of important and exciting related findings have resulted in that relatively brief time as research goes. Not only has selenium and AIDS research leaped ahead, but research with selenium on many viruses from the rare Ebola to the common flu has produced dramatic findings.
Are you pleased with the way in which some researchers are comprehending the significance of your research on the role of selenium in limiting the spread of at least some viruses? Or are you disappointed that more scientists have failed to look into this relationship?
Taylor: There certainly are a lot of exciting developments about selenium and viruses, some of which is new work and some of which is research that is only now gaining the attention it deserves, even though it was done a few years back. I am referring to the use of selenium to treat an Ebola-like hemorrhagic fever that broke out in China in the late 1980s. Hemorrhagic fevers can kill up to 90 percent of those infected, but this study showed that selenium supplementation can reduce that mortality rate dramatically. But let's talk about that later.
From my perspective, however, I'd honestly have to say that despite the accumulation of supporting evidence, it has been somewhat frustrating to me that few major virology groups have made any attempt, let alone a serious effort, to rigorously prove or disprove what I now call the "viral selenoprotein theory." In essence that hypothesis, first proposed in my 1994 paper, is the idea that certain viruses (initially HIV, other retroviruses, and also some strains of Coxsackievirus) may interact directly with selenium in host cells by incorporating selenium into viral proteins. This would mean that the role of selenium deficiency in some viral diseases might be far more complex than previously thought - and believe me, the potential roles of selenium and other antioxidants in the body's defenses against infectious disease are already very complicated, even without this possibility.
On the positive side, a number of studies have recently come out or are being prepared for publication (Allavena et al. 1995, Constans et al. 1995, Look et al. in press, Baum et al. in preparation), confirming that low serum or plasma selenium is a highly significant correlate of HIV disease progression, and a risk factor for mortality. While this does not prove anything about the MECHANISMS involved, there seems to be more going on here than a simple nutritional effect, and these observations are consistent with my 1994 prediction, based on theoretical genomic evidence, that dietary selenium might inhibit HIV replication and slow disease progression. Of course, based on his studies of the mouse mammary tumor virus (MMTV), a retrovirus relative of HIV, Dr. Gerhard Schrauzer had already predicted over ten years ago that selenium would have an anti-HIV effect. So he has had to be far more patient than I have so far, in waiting to see his idea rigorously tested.
The most encouraging development on the clinical side is the long-overdue initiation of some rigorous clinical studies of selenium supplementation in HIV patients. These include a study by Dr. Marianna Baum in Miami, and a study in African AIDS patients that is being set up by Prof. Luc Montagnier of the Pasteur Institute, who recently told me that he thought the data on selenium and HIV are now sufficiently compelling as to justify such a study. I find that very gratifying, particularly since most AIDS patients in impoverished nations in Africa and elsewhere are unlikely to receive any of the expensive new antiviral drugs, like the HIV protease inhibitors. In those countries, all they can realistically hope for is inexpensive ways of slowing down the disease until a vaccine is found- and there is nothing I know of that can do this that is cheaper than selenium!
Passwater: Dr. Montagnier is the discoverer of HIV. Our readers may wish to review his research in the September 1995 issue. When I visited Dr. Montagnier in his Pasteur Institute Laboratory, I handed him our 1994 article and he became very interested in your theory. Also, I used that article to introduce your theory to Dr. Baum and she became very interested in your theory as she commented in last month's column.
Are clinical researchers better understanding the significance of the role of selenium acting directly on viruses themselves, as opposed to protecting the host via such mechanisms as stimulating the immune system?
Taylor: It has been my impression that there has been a lot of interest in my research among practitioners of holistic or alternative medicine, and M.D.s who appreciate the value of prevention and nutritional approaches to therapy, but that "mainstream" HIV clinicians are less likely to have heard of it, or indeed to place much hope in any type of nutritional supplementation approach. Thanks to a story in Dr. Jonathan Wright's excellent newsletter, "Nutrition and Healing", I have been invited to present these concepts to a large group of M.D.s at a meeting of the "American College for Advancement in Medicine" in Tampa, Fl, next spring.
There is no doubt that part of what is catching these people's attention is the idea that selenium may have a direct effect on some viruses, rather than merely a non-specific immune-boosting effect. However, it's the whole story - putting my findings in the context of the various Chinese selenium studies, the work of Drs. Levander and Beck, Dr. Schrauzer, and so on - that is so intriguing.
Passwater: There is no doubt that you will have an interested audience at the ACAM Conference. These medical practitioners are very familiar with selenium. In addition to the clinical studies that you mentioned, linking selenium status to HIV disease progression, what are some of the specific new developments that you can point to as support for your "viral selenoprotein theory"?
Taylor: There is not as much as I'd like, because in many ways the theory has hardly been tested. However, we can say with considerable confidence that there is now virtually no doubt that some viruses can make selenoproteins - it's more a matter of which viruses can do it. This statement is possible because Dr. Bernard Moss, a scientist at the National Institutes of Health (NIH), recently reported the complete DNA sequence of a common wart virus, the pox virus Molluscum contagiosum. This virus appears to encode a gene that is 80% identical to the known mammalian selenoprotein glutathione peroxidase (GPx). So far he's only done what I have for HIV: show the potential gene is there by theoretical analysis. But with such an unmistakable match to a known selenoprotein, there's no reason to doubt that this is a real GPx gene.
Similarly, we have now demonstrated GPx-like sequences in Coxsackie B virus, the viral cofactor for Keshan disease, and the subject of the now famous Levander and Beck studies. If our readers will bear with me for just a moment, I want to point out to our technical readers that other developments include a published experimental verification of an RNA "pseudoknot" that we predicted in HIV, in vitro experimental verification in my lab of a novel frameshift site in HIV associated with a conserved UGA codon, and most recently, from the lab of a collaborating virologist, immuno-histochemical evidence in patient samples for some novel HIV protein variants that I predicted. Finally, in the test tube, selenium has been shown to be a potent inhibitor of HIV reactivation from latently infected cells. In summary: still no absolute direct proof that a virus can make a selenoprotein, but an increasingly strong body of favorable circumstantial evidence.
Passwater: When we discussed the mechanisms you elucidated and presented in your hypothesis, we also included a glossary for the non-virologists. Just so our non-virologists don't have to go back to that article or reach for their scientific dictionary, a codon is a three-letter code in DNA or RNA that directs insertion of an amino acid into proteins, a frameshift is a shift into a new protein coding region, a pseudoknot is an RNA structure that promotes frameshifts, and UGA not only stands for the University of Georgia but either a "stop" signal for protein synthesis or for selenocysteine insertion.
As I mentioned, I have had the pleasure of introducing your research to several clinical investigators, yet, I am still struggling to get the concept across to many nutritionists and clinical researchers who are not overly familiar with stop codons, frame shifts and pseudoknots. I have the advantage of getting help from my youngest son, Michael, when it comes to complex modern virology. You may recall that the fact that my oldest son, Richard, graduated from the University of Georgia that led me to your earlier research. Rich and I deal with antioxidants more than viruses. Now I find it ironical that what seems like just a few years ago that Mike asked, "Hey, Dad, what's DNA?" Now, I have to ask, "Hey Mike, why do RNA-based viruses mutate more than DNA-based viruses? Or "Why do the HIV family of viruses have the highest mutation rates among a family (retroviruses) of viruses with high mutation rates?"
Mike pointed out that the fleets of enzymes which check, double check, and transcribe DNA are at least as important as the DNA itself. RNA is not protected as well. Perhaps it would help clarify your findings if I lead you through the same line of questioning that Mike led me through when we first discussed your research. Could you briefly explain the significance of UGA codons in your findings on HIV, and how that may relate to the role of the known Selenium-containing antioxidant enzyme you mentioned earlier, glutathione peroxidase (GPx)?
Taylor: In essence, the UGA codon is the selenium link because it can direct the insertion of selenocysteine into proteins, an alternative to its more common role as a "stop" signal. We showed that in regions of HIV-1 that were presumed to be inactive or non-coding, UGA codons are "conserved," i.e. found in almost all isolates of HIV-1. Along with other structural features we identified, these observations suggested that the virus might encode selenoproteins in several such regions.
That was a radical suggestion because apparently no one had ever seriously considered the possibility that viruses might encode selenoproteins, which were believed to be very rare. Only about five mammalian selenoproteins were known at the time, although several more have already been found, and now some leading researchers in this field of research believe that many more probably exist. GPx is the prototypical selenoprotein, and is an essential antioxidant enzyme in living systems, used to break down harmful peroxides, to maintain cell membrane integrity, and to generally reduce the harmful effects of reactive oxygen species.
A deeper question is, what would a virus - say M. contagiosum or Coxsackievirus - gain by encoding a GPx? There could be many answers to that question. One is that it is now known that the immune system uses free radicals as part of the process of programmed cell death (apoptosis), which is also one of the mechanisms used to kill off cells infected with viruses. Thus, a viral GPx could serve a defensive function for the virus, by countering that process and at the same time keeping the host cell alive - again reminding us that viruses don't necessarily want their host cells to die.
Oxidative stress is also known to activate the replication of many viruses, especially HIV, so increasing the levels of either a host or a viral GPx could act to inhibit viral replication. Thus, a viral GPx could also serve as a repressor of viral replication, similar to what I proposed for one of the hypothetical selenoproteins in HIV, although that one is not a GPx.
Passwater: Regarding the potential role of selenium in viruses such as HIV, Ebola and Coxsackie, would a reduced level of selenium-containing enzymes countering the transcription and/or integration process contribute to the high mutation rate characteristic of these RNA viruses?
Taylor: There are several things going on here. First, as you mentioned, RNA viruses lack the "editing" or error correcting enzymes characteristic of the DNA based replication machinery of higher organisms. Furthermore, RNA is more chemically reactive and unstable than DNA. Thus, RNA viruses are inherently more mutation-prone even than DNA viruses, and far more than their DNA-based hosts. This can be advantageous for a virus because by mutating it can increase its ability to evade the host immune system.
Thus, anything that slows down the replication rate of such viruses will reduce their ability to mutate, because mutants are just "sloppy copies": no copies, no mutants. That is why in the chemotherapy of AIDS, high drug levels are used, to reduce viral replication almost to zero: otherwise, resistant viral mutants will rapidly emerge and the drugs won't block them. As far as the potential role of selenoenzymes in this, we do know that selenium somehow boosts the immune system, and cellular immunity in particular, which should help keep viral replication in check. But in regard to how viral selenoproteins may act, this area is so new that we don't have any hard data; all we really have are some "educated guesses" like the repressor hypothesis I mentioned earlier.
Passwater: Wouldn't increasing the selenium concentration in a virally-infected cell cause an increase in host selenoenzymes as well as in viral selenoenzymes?
Taylor: Since the same pool of selenocysteine is involved, one would expect that levels of both host and viral selenoenzymes would increase if more selenium was available. This touches on an aspect of my findings that many people have had difficulty with from the beginning. Many people wonder: if the virus uses or "needs" selenium, then why would taking selenium slow viral activity - wouldn't that "feed" the virus?
The answer to this is, first of all, selenium is more essential for us than it is for the virus. So if selenium becomes depleted, we suffer far worse consequences than the virus. Secondly, it also depends on how the virus uses selenium in its selenoprotein. I explained above how a viral GPx could act to inhibit viral replication. Thus, I have proposed that in some cases a virus might use such a protein in a negative feedback loop, i.e. as a repressor. That would permit the virus to respond to conditions of low selenium in the cell - which could be a signal of impending cell death - by replicating at a higher rate, to "escape" from that cell.
For example, under appropriate conditions, HIV is known to remain in cells for long periods of time, either in a latent state or only replicating at a very low level. Selenium-based mechanisms could help regulate that state.
Passwater: You are right about many people asking why "feeding" the virus selenium is a good thing. They wonder if it would not be better to starve the virus. Nutritionists and clinicians tend to think of selenium in terms of nourishment, but in this case you are not talking about selenium for the nourishment of the virus. Even cancer researchers sometimes miss a similar point when they focus strictly on nutrients and tumor status instead of the more important question of nutrients and immune system status Your explanation will help more scientists that are non-virologists get the point!
In my lectures, I have used your comment about it's really not in the best interest of viruses to kill their hosts, because the viruses will also die. That is, unless they can jump ship (host) by spreading to their next victim. As you said, but I want to repeat it, the important point is that selenium is not really feeding the virus, but is used by the virus to determine the health of the host. If the infected cell (and thus the host) is well nourished and not in immediate danger of dying there is no urgent need for the virus to invade new cells.
Taylor: Perhaps it would help some of our lay readers if instead of thinking of selenium as nourishment or food for the virus, they would think of selenium as being part of a birth control pill for viruses. The viruses don't need selenium for survival so much as for growth regulation.I already explained how a viral GPx or other selenoprotein can inhibit viral replication by reducing oxidant tone in the cell: remember that oxidative stress activates HIV. So a very simple analogy would be that a viral selenoprotein could act as a viral birth control pill, inhibiting viral reproduction when selenium is abundant. Of course, at the same time selenium is boosting the immune system and having other beneficial effects in the host. But when selenium levels are too low, we not only have a weakened immune system, the viral birth control is reduced, and the virus replicates at higher levels. This obviously makes sense for the virus, because this is the best time for it to break out - when the i
mmune system is weakened by selenium deficiency. Thus, by strengthening the immune system with high selenium/antioxidant levels, the virus is forced to maintain a low profile. In essence, this analogy explains what a repressor mechanism is, using the "birth control" concept.
Passwater: Does increasing the selenium concentration in the HIV-infected stabilize the HIV genome?
Taylor: Slowing viral replication rate reduces the opportunity to mutate, which is what is meant by "stabilizing" the viral genome. Since oxidative stress is known to activate HIV transcription, selenium supplementation will reduce HIV replication activity, simply as a consequence of increased cellular GPx levels. That has been proved in cell culture studies (Sappey et al. 1994). Furthermore, by protecting against oxidative free radical damage to RNA and DNA, increased dietary Selenium would directly reduce mutation rate. But the possible contributions or roles of viral selenoproteins in these processes still need to be elucidated.
Passwater: If the HIV genome is stabilized, does this give the immune system a more steady target that it can destroy with a "traditional" response?
Taylor: Certainly, if the ability of the virus to mutate is impaired or slowed, it will be easier for the immune system to neutralize it, because it will be less of a "moving target".
Passwater: Does increasing the selenium concentration in HIV-infected cells stimulate the immune system? In uninfected cells?
Taylor: As you know, there is a remarkably extensive body of literature showing that dietary selenium is critical for a healthy immune system, and that selenium potentiates various aspects of cellular immunity, such as T-cell proliferation responses, and the action of the cytokine interleukin 2. I think only a part of this can be explained by known human selenoproteins like GPx, and we really have a lot to learn about howselenium produces its immune-stimulating effects. This statement is supported by the fact that according to an early study by McConnell using radio-labeled selenium in immune cells, only about 20% of the total selenium content is contained in GPx. So selenium is probably doing important things in those cells that we still don't understand.
Passwater: I believe it was a 1959 study by McConnell in which he subcutaneously injected radioactive selenium (75Se) chloride in dogs and measured the amount of selenium incorporated into the leukocytes. This is the first reference to selenium being used in the immune system that I am aware of. I don't believe that anyone has published figures changing his finding that about 20 percent of the selenium became incorporated into the protein fraction of the leukocytes, which indeed may be essentially one or both of the glutathione peroxidases. That's a good point for me to check with Dr. Orville Levander. Sorry to interrupt, I hope it didn't make you lose your point.
Taylor: The point that I was getting to is that in HIV-infected individuals, I would expect this role of selenium in immunity to be at least as important as in the uninfected. In addition, since HIV targets the immune system, an important role for selenium in the normal immune response could also help explain why the virus might gain something by getting directly involved in selenium biochemistry, as I have proposed. Mimicry of host proteins and mechanisms is a common viral strategy.
Passwater: Does increasing the selenium level in HIV-infected cells increase glutathione or oxidized glutathione levels?
Taylor: Selenium increases GPx levels, and GPx uses glutathione (GSH) to reduce peroxides, forming GSSG (oxidized glutathione) in the process. So one might expect GSSG to increase when selenium is increased. But another enzyme, glutathione reductase, readily regenerates GSH from GSSG. So the total amount of both forms of glutathione is what is really important. Recently, French researchers showed that, counterintuitively, selenium supplementation actually increases free GSH levels significantly, which is good, because it is the reduced GSH form that is needed for many important detoxification reactions and free radical scavenging in the body. So some complex homeostatic mechanisms must be involved, that act to increase total glutathione levels when more selenium and GPx are available.
Passwater: It was recently noted that Keshan disease seems to have a viral component rather than being strictly a selenium-deficiency disease per se. Do you see your research as playing a role in understanding this development?
Taylor: Actually, this link was first noted by the Chinese in research published as far back as 1980. Coxsackie virus, a widespread relative of the common cold virus, was isolated from the hearts of Keshan disease victims, and was also shown to produce heart damage in selenium-deficient mice that was identical to that seen in human Keshan disease. I think this is extremely significant in terms of what I am saying about HIV, because Keshan disease is clearly a selenium deficiency disease, apparently with a viral cofactor. And I am saying: AIDS is a viral disease with selenium deficiency as a cofactor. And we now have compelling evidence for virally-encoded selenoproteins in both HIV and Coxsackie virus.
Passwater: Dr. Melinda Beck of University of North Carolina, Chapel Hill, made an interesting observation about how a fairly harmless strain of Coxsackie virus mutates within selenium-deficient mice (and presumably in people as well) to become a more harmful virus that can then spread and produce heart damage, even in others who are not selenium deficient. Was she aware of your research when she made her observation? How does her finding complement your research findings?
Taylor: Dr. Beck's work is an extremely important breakthrough in establishing the selenium-virus link. She and her collaborator Dr. Orville Levander were working independently in this area before I was, developing their line of research based on the earlier Chinese observations linking Coxsackie virus to Keshan disease. When I discovered a potential HIV-selenium link in spring of 1994, based purely on genomic analysis of HIV, I was unaware of their selenium work because their first paper showing increased virulence of Coxsackie virus in selenium-deficient mice was not yet published, although I had seen an earlier paper they did showing a similar effect with vitamin E.
In a subsequent paper, they showed that when passed through selenium-deficient animals, the virus actually mutates into a more virulent strain, that retains its virulence in selenium-adequate animals. This has obvious implications in regard to "emerging" viral diseases. In their published work, Drs. Beck and Levander have focused on known mechanisms to explain their observations, along the lines we have already discussed: low selenium leads to weakened antioxidant defenses and reduced immune surveillance, higher viral replication rates, and thus to conditions favoring viral mutation. However, particularly now that my group has demonstrated unmistakable GPx-related sequences in the Coxsackie B virus strain that they studied, I think they are seriously considering the possibility of a direct virus-selenium link of the type I have proposed for HIV. Obviously, if Coxsackie virus encodes a selenoprotein, it would have to be involved in the mechanism underlying their observations.
Passwater: After publishing your selenium - HIV discovery, you proposed a possible relationship between selenium and the Ebola virus. What did you find and why did you think to look for this relationship?
Taylor: Coincidentally, I began to study Ebola less than a month before the 1995 outbreak in Kikwit, Zaire that brought this virus so drastically into the public consciousness. I did so because of a poster presentation I had seen that spring in Santa Fe, at a meeting of the International Society for Antiviral Research. A Russian group presented a world map showing the geographic areas where various hemorrhagic viral diseases tended to occur, and I was struck by the fact that the area shown for the filoviruses Ebola and Marburg matched a region in Africa that I suspected might be a low-selenium region. What we found was striking: several gene regions in Ebola contained large numbers of UGA codons, up to 17 in one segment. We later published a paper showing that it might be possible for Ebola to synthesize selenoproteins from these gene regions, and proposed a mechanism whereby this might induce artificial selenium deficiency and contribute to the blood clotting characteristic of Ebol
a pathology.During the revisions to the final draft of that paper, we learned of a 1993 paper in a Chinese journal that reported the use of selenium to treat an Ebola-like hemorrhagic fever, with remarkable results. Luckily, the English translation of the abstract was available. Using the very high oral dose of 2 mg selenium per day as sodium selenite, for only 9 days, the death rate fell from 100% (untreated) to 37% (treated) in the very severe cases, and from 22% to zero in the less severe cases. Apparently there were about 80 people involved in this outbreak. Dr. Hou of the Chinese Academy of Medical Sciences, the author of this study, has since told me that he thinks more lives could have been saved if he had been permitted to give the selenite by injection, because in many of the more severly affected there is so much organ damage due to internal bleeding that they may have been unable to fully absorb or retain the oral dose of selenium. All in all, this is the closest thing to
a curative result in the treatment of hemorrhagic fever that I have ever heard of.
Passwater: Dr. Hou used selenite because quick and dramatic action was required as the patients were dying in front of him. For normal, long-range protection, organic selenium supplements, such as selenium-rich yeast or selenomethionine, are preferred, as discussed by Dr. Gerhard Schrauzer in the December 1991 issue, and by others as will be discussed later in this series.
How do hemorrhagic fever viruses cause hemorrhaging? Would selenium's effect on blood clotting in the host play a role in such diseases, or is the effect strictly an interaction with the virus itself?
Taylor: The characteristic hemorrhaging produced by various "hemorrhagic fever" viruses involves the production of blood clots that ultimately block small capillary vessels, which rupture under pressure to produce internal and even external bleeding in severe cases. This is known as "disseminated intravascular coagulation", or DIC. Thus, paradoxically, the bleeding is produced by a pro-clotting mechanism, and anticoagulants (which usually promote bleeding) have been used to treat symptoms of the disease.
This may be very significant in regard to selenium involvement, because the biochemical basis for an anti-clotting effect of selenium is very well established. Severe selenium deficiency, usually artificially induced in animals, is known to produce hemorrhagic symptoms. Thus, the idea that hemorrhagic fever viruses might produce a severe selenium depletion would be consistent with the established pro-clotting mechanism of DIC. So there may be an interaction here, where viral activity is having a direct impact on host selenium status over the period of one or two weeks, sufficient to cause serious pathology.
Alternatively, the results obtained in the Chinese study could have been simply due to the anti-clotting effect of selenium, or other mechanisms. Dr. Hou apparently decided to try the selenium treatment because of his own theories about the involvement of selenium in complement activation, another feature of hemorrhagic disease. So additional studies are badly needed, to determine what the predominant mechanism of protection by selenium really is.
Passwater: Then do you see multiple roles for selenium against other viruses?
Taylor: At this point, I've very optimistic about the potential of dietary selenium as a broad-spectrum chemoprotectant against various viral diseases. A lot of that may be entirely due to the immune-stimulating and antioxidant benefits of selenium, but I think that in a number of viral diseases, some degree of direct interaction between the virus and selenium is likely to be involved. We already have quite a few viral diseases where a clinical correlation or definite selenium benefit has been established: hepatitis B/liver disease, HIV/AIDS, Coxsackie virus/Keshan disease, hemorrhagic fever, MMTV/cancer, and a number of other animal viral diseases where selenium has been used in veterinary practice. I also strongly suspect that various herpes viruses will prove responsive to selenium therapy, and the strongest case of a selenoprotein in a virus to date is in a pox virus. So the potential scope of this chemoprotection approach is very exciting.
Passwater: Your research is getting dramatic scientific support at least by some researchers, what are you looking into now?
Taylor: After spending much of my efforts over the last two years in trying to extend the scope of our HIV findings in terms of other viruses, and trying to establish some collaborations in order to have the implications experimentally verified, I am now focusing on building up the capabilities in my own laboratory to do some of the necessary experimental research. It's been slow getting started, because we have been hampered by lack of financial resources, and only now is the hard evidence coming in that will enable us to convince Federal funding agencies that this research merits support. Along with a few other labs, we have already obtained evidence that some of the molecular features we predicted in HIV are real. Our objective is to clone several of the novel genes that we have found by genomic analysis, including several from HIV and the GPx homologue from Coxsackie virus, so the meantime we are trying to work with clinical researchers like Dr. Marianna Baum to promote the seri
ous assessment of the potential benefits of selenium as a complementary therapy in HIV disease.
Finally, I've also become very interested in the biochemical roles of selenium in health as well as in cancer and rheumatoid diseases, etc. My group is now engaged in a search for new selenoprotein genes in the human genome, and we are finding some rather intriguing things. All that I can say at this point is that I strongly suspect that selenium is playing a role in cell signaling and attachment - very important in the immune system - and that selenium is more than just indirectly involved in gene regulation. So I'm sure I'll be keeping busy well into the next millennium trying to find out if that hunch is really true! Hopefully our readers will be able to say they read it here first.
Passwater: Well, we will all be looking forward to the selenium millenium! Hopefully our readers will remember they read it here first.
The information that you have deduced by examining genes to see what they can make is a great help and gives great directions for the biochemists to check out. Without this help we are more or less left to "stumble around" trying to figure out biochemically how selenium does all those things that our laboratory studies show it does.
I am sure that the funding agencies will soon understand the importance of your research. They need time to fully understand its consequences. You have been on the program of the International Conferences on selenium and human viruses. Now let's see if we can get you on the programs of some of the NIH virus researchers. Remember NIH also stands for Not Invented Here -- and if not invented here (at National Institutes of Health) it takes longer to get the attention of the establishment funders. Thanks for helping us keep up-to-date on your exciting research.