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results because they had not yet been peer-reviewed for publication, but I can tell you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.