Medical Hypotheses (1992) 39, 22-29
Kaposi's Sarcoma and HIV
E. PAPADOPULOS-ELEOPULOS(1), V. F. TURNER(1), and J. M. PAPADIMITRIOU(2)
(1) Department of Medical Physics Emergency Department,
Royal Perth Hospital, (2) Department of Pathology University of Western
Abstract - Recently published informed debate affords strong indication
that in patients with the Acquired Immune Deficiency Syndrome, HIV cannot,
directly or indirectly, be the cause of Kaposi's sarcoma. This paper provides
reasons for disallowing a current alternative theory that Kaposi's sarcoma
is due to an unidentified sexually transmitted infectious agent and proposes
instead that Kaposi's sarcoma is the result of prolonged and repeated exposure
to nitrites and/or semen. If this alternative hypothesis is strengthened
by confirmation of its predictions then the relationship of HIV to Kaposi's
sarcoma, one of the principal AIDS-associated diseases, becomes somewhat
remote. This may facilitate a shift of emphasis and encourage the development
of alternative therapies.
A theory is a good theory if it satisfies two requirements:It
must accurately describe a large class of observations on the basis of
a model that contains only a few arbitrary elements,and it must make definite
predictions about the results of future observations.
In spite of the passage of more than a century since Kaposi's original
description, Kaposi's sarcoma (KS) remains enigmatic with its precise nature
in doubt. Recently even its classification as a malignant neoplasm has
been questioned and John Brooks, a pathologist from the University of Pennsylvania,
has argued that KS is a "benign potentially reversible hyperplasia
that may at times terminate in true malignancy" (1).
Summary of KS sub-types.
Kaposi's sarcoma is classified on the basis of pathological,clinical
and epidemiological descriptions (2). Epidemiologically Kaposi's sarcoma
occurs as "Sporadic", "Endemic","Iatrogenic"
and "Epidemic" disease with obvious major differences between
these sub-groups. The "Sporadic" type has a predeliction for
Italian and Ashkenazy Jewish males over the age of sixty years (although
in a series from the Armed Institute of Pathology published in 1959 22%
of the patients were black (3)). This sub-type of KS is associated with
a near normal life span. However,some cases exhibit the aggressive form
and there are cases occuring in younger patients under the age of 45 years
The "Endemic" group,which constitutes the highest caseload
in the world,occurs in eastern equatorial Africa. Here KS affects young
adults (25-45 years of age) and children between the ages of two and fifteen.
Any of the clinical patterns may occur in this group and there is an appreciable
incidence of the generalized variety in the young adults and children,most
of whom die within two years of diagnosis (5). Prior to the AIDS era "Iatrogenic"
KS accounted for approximately 15% of all cases enumerated in Europe and
North America (2). These were associated with immunosuppressive agents
administered to organ transplant recipients or to patients with other diseases.
The incidence of post transplant KS in the United States is 0. 18-0. 3%
of all transplant patients while interestingly the incidence in Saudi Arabia
is considerably higher at 5. 3% (2). Penn,who reported a series of 68 post
organ transplant cases from the USA, considered that 72% were "benign"(skin
and mucosa involved) and 28% malignant(gastrointestinal and respiratory
involvement) (2). The reason why KS and also lymphomas occur in these patients
while there is no increased incidence of the common epithelial neoplasms
is unclear. However,in a comprehensive review of this subject published
in 1982 Kinlen discounted failure of immune surveillance and argued the
case for a specific viral- related effect in the pathogenesis (6).
In the early 1980's the Centre for Disease Control (CDC) in Atlanta
USA observed a high frequency, 26 cases by July 1981, of KS occurring in
young homosexual men (4). Eight of these patients died within 24 months
of diagnosis. Thus was ushered in "Epidemic" KS,that associated
with the Acquired Immune Deficiency Syndrome (AIDS). In addition to KS
many of these original patients also had opportunistic infections and in
four a diagnosis of Pneumocystis carinii pneumonia (PCP) was made by open
lung biopsy. At this very early stage in the evolution of the syndrome,AIDS,for
all practical purposes,consisted entirely of KS and PCP. In 1982 Robert
Gallo,who had spent many years researching retroviruses and cancer at the
National Cancer Institute, proposed that the cause of AIDS was a retrovirus
(7). In 1983 Luc Montagnier and fellow researchers at the Pasteur Institute
detected a retrovirus,presently known as Human Immunodeficiency Virus Type
I (HIV-1),in the cultured T cells from a homosexual patient with lymphadenopathy
(8). With few exceptions (9,10), the hypothesis that the causative agent
of AIDS is HIV has been universally accepted. However,as early as 1984
it became apparent that HIV does not exist in the cells from the lesions
of KS and hence cannot cause KS directly (11). It was assumed then,that
in AIDS patients,HIV indirectly caused KS and opportunistic infections
by its detrimental effects on the immune system. Alterations in T lymphocyte
subsets (T4 and T8 cells) and a decrease in the T4/T8 ratio were believed
to be the hallmark of AIDS and the immune deficit that defined this condition
(7). However, in heterosexuals, evidence existed that many diverse causes
could be associated with the same (and additional) laboratory abnormalities
of immunodeficiency that were manifest in AIDS patients. These causes included
a number of infections (12),blood transfusion (13),the intake of many drugs
including antibiotics (14) and even solarium exposure (15). It is noteworthy
that in none of these reports was there a single case of associated KS.
Conversely, some researchers at the time were of the opinion that KS
could result from immunostimulation with angiogenesis-promoting factors
formed as a result of alterations in immunoregulation,a mechanism that
had been earlier suggested in patients receiving immunosuppressive therapy
(16). As recently as 1988 researchers from the Walter Reed Army Institute
of Research,disallowed KS from the definition of AIDS stating that,"in
our system the presence of opportunistic infection is a criterion for the
diagnosis of AIDS,but the presence of Kaposi's sarcoma is omitted because
the cancer is not caused by immune-suppression"(17). Most recently
data has been published confirming the fact that in some homosexuals KS
can occur in the complete absence of both immune deficiency and HIV (18).
Thus neither HIV nor immune deficiency is a prerequisite for the development
of this disease,at least in homosexuals.
Despite all this uncertainty,acceptance of HIV as the cause of Kaposi's
sarcoma prevailed for over six years until early 1990 (19). In January
of that year Valerie Beral and her colleagues from the CDC published a
paper (20),in which they concluded that "Kaposi's sarcoma in persons
with AIDS may be caused by an as yet unidentified infectious agent transmitted
by sexual contact". This argument was based on the epidemiological
spectrum of KS in different AIDS risk groups and the fact that in homosexuals
KS may appear in the absence of HIV. This conclusion, to which we cannot
accede, is based on the authors' assumptions that:-
(a) "The agent that causes Kaposi's sarcoma must be the same irrespective
of whether there is any associated HIV infection". Implying that KS
in all individuals, homosexual or heterosexual, African or European, black
or white, is caused by one and the same agent).
(b) The agent is infectious but is not HIV.
Before this theory becomes accepted and as a necessary overture to our
own hypothesis, we will present evidence that:-
(a) There is no need to assume that the same causative agent is responsible
in all cases of KS regardless of age, race or geographic region.
(b) The assertions upon which Beral and her colleagues base their infectious
theory are themselves only hypotheses which their various authors acknowledge
as being largely unproven and have even suggested alternative explanations.
(c ) There are plausible explanations for the apparent correlation between
sexual activity and KS in homosexuals other than sexual transmission of
an infectious agent.
It is inconsistent with current knowledge of other neoplasms to assume
that KS is exceptional by having a single cause in all individuals. At
present it is well recognised that many neoplasms have multiple aetiologies.
One may also argue that,since the precise cause of most if not all neoplasms
is unknown,it is impossible to state with any certainty that a particular
type has only one definite aetiology.
Beral derives support for an infectious origin of KS from the following
1. The massive increase in KS in AIDS patients-"at least 20,000
times more common in persons with AIDS than in the general population and
300 times more common than in other immunosuppressed groups".
2. The fact that "few known human carcinogens increase the risk
by more than 100 fold and,in the best documented example, hepatitis-B and
hepatoma,the cause of the cancer is an infection".
3. In immunosuppressed subjects such neoplasms "may have an infectious
However a high incidence of a relatively rare disease in a confined
population does not necessarily indicate an infectious origin. Malignant
mesotheliomas are exceptionally rare in the general population,approximately
one case per million (21). However,in a study published in 1988 of a cohort
of individuals employed by the Australian Blue Asbestos Company that operated
in Wittenoom in Western Australia,there were 33 deaths from mesothelioma
recorded. Even though this study grossly underestimates the incidence of
mesothelioma,it still reveals a greater than 5000 fold risk of dying from
this disease in these individuals (22). Asbestos, a non-infectious agent,has
been accepted as the major causal factor in this condition. In another
study of 2271 deaths of insulation workers who came into regular contact
with asbestos the cause of death in 175 was mesothelioma,an incidence of
7706 in 100,000 (8%)(23). The risks quoted in these studies are considerably
higher (50 and 800 times) than that associated with hepatitis-B refered
to by Beral.
The data concerning hepatitis-B virus (HBV) and hepatoma were taken
by Beral et al from a paper by Beasley et al (24). This paper describes
a prospective study of 22,707 male civil servants from Taiwan where it
was found that"the incidence of primary hepatocellular carcinoma (PHC)
among carriers of hepatitis-B surface antigen (HBsAg) was much higher than
among non-carriers (1,158/100,000 vs 5/100,000)". These authors put
forward the hypothesis that hepatitis-B virus has a primary role in the
aetiology of PHC, an hypothesis that so far has not been conclusively proven.
The authors themselves state "alternative explanations of the very
high relative risk among HBsAg carriers are that HBV is a cofactor with
another aetiological agent or is simply a risk factor. Case control studies
have repeatedly shown that PHC does occur in HBsAg negative subjects. This
finding can be taken to mean either that HBV is not sufficient to cause
PHC or that there are several independent causes".
The authors also refer to the geographical correlation between the amount
of aflatoxin in food and the incidence of PHC that occurs in Africa. They
postulate that a similar relationship may exist in Taiwan but also point
out that,due to the eclectic nature of the Chinese diet,there are insurmountable
difficulties in studying this particular factor. In support of their argument
Beral et al also refer to a review paper published by Kinlen in 1982 (6).
This paper is cited as showing that the increase in KS in immunosuppressed
patients is caused by an infectious agent. However the substance of Kinlen's
review is to:
1. Acknowledge the appreciable increased incidence of non-Hodgkins lymphomas,primary
hepatocellular carcinoma,melanoma and KS in immunosuppressed individuals.
2. To refute the immune surveillance hypothesis of carcinogenesis by
pointing to the fact that these same individuals do not share an increased
incidence in the common epithelial neoplasms.
3. To argue,without any convincing proof,a role for ultraviolet light
in the skin cancers,HBV in hepatocellular carcinoma,Ebstein-Barr virus
(EBV) for lymphoma and cytomegalic inclusion virus (CMV) for Kaposi's sarcoma.
4. To speculate that antigenic stimulation or even the immunosuppressive
agents themselves may directly cause some of these neoplasms. Thus Beral
and her colleagues base their infectious theory of KS either on an unproven
hypothesis (HBV and hepatoma;lymphomas and EBV) or on an hypothesis (CMV
and KS) which they (and many others) consider to be incorrect.
Beral and her co-authors reported several interesting and relevant findings
concerning the incidence of KS in the various AIDS risk groups. Forty per
cent of homosexual and bisexual men in 1985 and approximately 21% in 1988
had KS compared with approximately 1% of haemophiliac AIDS patients. The
next highest incidence,6%,was from patients born in the Carribean and African
countries but living in the USA. There were 73 cases of KS in transfusion
recipients. KS was most unusual in patients less than 15 years old,occuring
in 1.6% of all children with AIDS,(13 cases). All but one of these US born
children with KS were children of Haitian women, the other child was born
in Central America and raised in the United States.
These data were interpreted as evidence that:-
(i) KS is "caused by an as yet unidentified sexually transmitted
(ii) The appearance of the agents in transfused patients older than
15 years "may be by routes other than blood".
(iii) The agent in children younger than 15 may be perinatally transmitted.
If the above conclusions are correct then because:-
(i) There is no cure for the disease;
(ii) In non AIDS patients the disease is chronic,that is median survival
is 8-13 years;
(iii) Prostitutes have a higher frequency of all the sexually transmitted
diseases especially in Africa where treatment is not readily available;
one would expect a high incidence of KS in families (mother-child,husband-wife)
However, in Africa where it was known as far back as 1962 (5) that "the
disease occurs not uncommonly in African children in the first decade of
life and is probably much underdiagnosed", the incidence of KS in
women (mothers) including prostitutes like elsewhere in the world is low,with
a male to female ratio of 17:1. Among the many theories put forward before
the AIDS era regarding aetiology of KS,the two most often mentioned were
infectious and genetic. In order to test these theories many investigators
searched for a familial incidence of KS. A very small number of cases with
a familial distribution of KS were reported before the AIDS era but in
none of these were sexual or mother-child relationships involved (25).
Thus before AIDS there was no evidence to suggest that:
1. KS, at least in heterosexuals, is sexually transmitted,
2. The cause of KS is an infectious agent.
Even today with the exception of CMV and HIV,which are still considered
by some as major aetiological factors,all the other factors considered
possibly pathogenic are non-infectious (2).
We hypothesize that in homosexual AIDS patients KS is caused by prolonged
and repeated exposure to semen,nitrites or both agents which,under normal
circumstances,in non-AIDS patients, are either absent or largely excluded
from contact with endothelial targets in the vascular or lymphatic system.
Both these agents are potent oxidising agents in biological systems (26,27)
and indeed oxidation is essential for many of their biological properties
and effects. For example,sperm maturation (and thus fertilisation) is a
process which requires the oxidation of sperm nuclear sulphydryl groups
to disulphides (28). All cells exhibit a thiol cycle and this cycle is
a principal determinant of many cellular functions including mitotic rate
(26). Thus nitrites and sperm, like all carcinogens and mitogens,by their
oxidative nature may induce perturbation of the thiol cycle,and this effect
may underlie the ample epidemiological evidence that semen and nitrites
are alone the two factors highly correlated with the appearance of KS in
Nitrites have as a major property a prominent effect on vasculature.
Although the use of nitrites (poppers) is highly correlated with the appearance
of KS in homosexuals, their causative role has been dismissed because of
the belief that it is impossible to disentangle their use from sexual practices
and also because they do not explain "the occurrence of KS in children
and elderly people with parenterally transmitted HIV and in one tenth of
AIDS patients in Africa where nitrites cannot account for the pattern of
occurence of KS" (20). The only reason for preferring the explanation
that an "undefined" infectious factor relating to sexual behaviour
appears to be the cause, and not the alternative,appears to be a predisposition
to favour a sexually transmitted infection. In fact in homosexuals evidence
exists that the variable most strongly associated with KS is the consumption
of more than four "hits" of nitrites per night of use (30). The
fact that the effects of nitrites and sexual practices are "difficult
to disentangle" does not negate the possibility that nitrites acting
alone or in combination with another highly correlated variable may have
a direct causal role. While it may be true that Africans do not use nitrites,it
is also true that in Africans KS has existed independently of AIDS, probably
for centuries and, although not disproven,an infectious origin of KS in
Africa has been discounted as far back as 1962 (5). The common diagnosis
of KS in African patients post 1983 as AIDS whilst "legal" (19)
is a semantic convenience with little, if any, scientific rationale,especially
in relation to a putative common pathogen.
KS in children
Beral states that,in the thirteen AIDS children with KS,the cases of
KS were "atypical" and admits that "diagnostic biases might
exist". Also,because all children were from Florida where nitrite
abuse is most prevalent and all but one were offspring of women born in
Haiti,the possibility cannot be excluded that:
1. Some of these children may not have developed KS.
2. Children of Haitian women,most of whom are descendents of African
slaves, may, like African children, have an appreciable incidence of KS
that has existed independently for many decades.
The mothers of these children may have used nitrites.
KS in recipients of blood transfusion.
A total of 73 cases of transfusion associated KS have been reported
by the CDC up to March 31st 1989. In these patients not one
of their sexual partners had KS. According to the CDC definition which
"accepts HIV as the cause of AIDS" KS occuring in anyone under
the age of 60 years, even when laboratory evidence regarding HIV infection
was either not obtained or was inconclusive, indicates AIDS. Individuals
with KS who are over the age of sixty and who have a positive antibody
test are also considered AIDS patients. KS which develops in persons who
received high doses or long term systemic corticosteroid or other immunosuppressive/cytotoxic
therapy but which were discontinued three months before the appearance
of the disease also indicates AIDS (19). In the United States,where approximately
3. 8 million people are transfused annually,approximately 20% receive blood
for treatment of malignant neoplasia (32).
Although exact data are unavailable it is certain that many of these
patients will have received varying combinations of immunosuppressive therapy,radiation
and chemotherapy,all agents known to be associated with the appearance
of KS (6). It is reasonable to question whether the occurence of 73 cases
of transfusion associated KS over a period of eight years, an average of
9 cases per year, represents a phenomenon peculiar either to the specific
practice of blood transfusion or to the AIDS era. In the United States
the annual incidence of KS in the general population pre-AIDS is unknown
but is estimated to be 0.2-0.6 cases per million (4). There are no data
available on the incidence of KS in transfusion recipients pre-AIDS but
these persons,50% of whom die within one year of transfusion, are likely
to have a higher incidence than the general population.
An incidence of nine cases in nearly four million transfused therefore
may not be significantly higher than expected since many of the post 1981
transfused group would be expected to be under the age of sixty years (and
therefore fulfill the CDC AIDS definition), and/or suffering from malignancy.
There has also been a well documented problem in establishing a definite
diagnosis of KS in AIDS patients, a factor which relates both to diagnostic
bias and histopathological interpretation (20,32). In the absence of data
to prove the contrary the low incidence of KS documented by Beral et al
may simply reflect the presence,in this population,of other causes of KS
which have previously operated and continue to operate independently of
AIDS related factors. Also in the United States there are 2.5 million exclusively
homosexual males, and perhaps another 2.5 to 7.5 million who may have the
occasional homosexual liaison (33). There are also at least 1.1 million
IV drug users,11% of whom use nitrites. Furthermore there are estimates
that 1% of American students between the ages of 12-17 years of age use
nitrites at least ten times per month (34). The CDC publically accepts
that this is likely to be an underestimate as not every person questioned
would feel comfortable admitting to drug abuse or homosexuality. We may
therefore argue that since KS even post AIDS is so rarely reported in the
non-homosexual non-drug abuser population that some, if not all, of the
blood transfusion-associated KS cases may be related to one of the above
mentioned mechanisms which include chemotherapeutic agents,radiation,semen
and nitrite exposure-that is,to a cause which is not a sexually transmitted
infectious agent. Even if it is true that not a single African,child or
transfusion recipient is exposed to nitrites there is still no compelling
evidence to exclude nitrites as a cause of KS in homosexuals since there
is no proof that KS in all these groups is caused by the one and the same
factor. However in the case of homosexuals with KS there is also other
evidence which suggests that nitrites may be aetiological agents:
1. One of the only two factors which changed in the lifestyle of homosexuals
in the late 1970's was increasing nitrite abuse (35).
2. In the early 1980's nitrite use became ubiquitous in California and
New York-the two areas where the vast majority of patients with KS were
3. The latency period for the appearance of KS in patients treated with
immunosuppressive drugs for organ transplantation is similar to that between
homosexual exposure to nitrite and the appearance of the disease (36).
4. The decrease in the incidence of KS in homosexual men coincided with
a decrease in nitrite abuse (37).
5. Nitrites and their metabolic products are mitogenic and carcinogenic
6. Nitrites have major pharmacological effects on blood vessels-the
site of the neoplasm-which is an unusual tissue for neoplastic transformation
A second factor directly relating to the development of KS is sexual
intercourse. While this may suggest that the disease at least in homosexuals
is caused by a sexually transmitted agent there are data available from
numerous large,well designed studies that strongly support the hypothesis
that semen itself has a direct causal role. All these studies have shown
that in homosexuals,the only sexual acts directly related to both the developement
of AIDS and Kaposi's sarcoma is passive anal intercourse (30,39,40). One
can surmise from these data that if a large group of homosexuals could
be studied where any individual could be guaranteed to practise exclusively
passive or active intercourse and not both,then one would observe that:-
(i) KS,like pregnancy,can only be acquired by the passive partner. (ii)
KS,like pregnancy,cannot be sexually transmitted. As far as the cause is
concerned at least two possibilities can be entertained:-
1. In the passive partner KS could be caused by an infectious agent
found in the ejaculate which is not bidirectionally sexually transmitted.
The active partner would have to acquire the agent by other means.
In the passive partner KS could be caused by a non-infectious agent
found in semen acting either alone or synergistically with nitrites. That
this is the case is strongly supported by the following data:-
1. Apart from nitrite abuse the second factor which changed in the lifestyle
of homosexuals in the mid 1970's was the high promiscuity rate (35). There
are also many examples from clinical practice of homosexual men who admit
to approximately one thousand partners per year. At 2-3 ml per ejaculate
this provides evidence that deposition of unusually large amounts of semen
into the rectum of an individual can occur,and that as a consequence,semen
may interact with and be absorbed by the intact or traumatised bowel.
2. Unlike all the other sexually transmitted diseases,where the possibility
of infection is directly related to the number of sexual partners,in homosexuals
the number of sexual partners is only a risk in relation to the number
of episodes of passive anal intercourse (40).
3. Homosexuals have a relatively high incidence of gastrointestinal
cancers other then KS and several researchers have implicated semen in
the developement of these neoplasms (41,42).
4. Reid and Coppelson described the relative high incidence of cervical
cancers in promiscuous Australian women. Amongst other factors,this was
attributed to semen (43).
5. Spermatozoal penetration into the submucosa of the rat uterine epithelium
can induce pre-cancerous changes in the cervix (44).
6. In humans spermatozoa fulfil a well known mitogenic role in embryogenesis.
There is also in vitro evidence that spermatozoa can penetrate somatic
mammalian cells and that sperm DNA is incorporated into recipient nuclei
Permanent transformation occurs within a few days and this is associated
with abnormalities in morphology and growth of recipient cells including
the appearance of bi- and multi-nucleated cells (45,46).
7. Extracts of pooled human semen are potent promoters of skin tumour
production in the skin of mice previously treated with topical carcinogen
8. Injection of sperm suspensions directly into the anterior prostate
of experimental rats can produce carcinoma of the prostate with metastases
9. Intratesticular injection of autologous spermatozoa in the rat can
produce malignant testicular neoplasms (49).
10. Seminal plasma is especially rich in polyamines, a group of positively
charged substances which have a significant role in cellular proliferation
(50,51). Moreover in human semen the polyamine spermine is present in higher
concentrations than in any other tissue or body fluid and it, like other
seminal polyamines, is oxidized by enzymes derived from seminal vesicle
secretion. The presence of polyamines in higher than normal concentration
in malignant tissue has prompted their assay as a diagnostic aid in cancer
patients and serial measurement has been suggested as a treatment marker
during chemotherapy. (Interestingly it appears that polyamines are essential
for optimal growth of most microorganisms and inhibitors of their biosynthesis
have been successfully employed for the treatment of protozoal diseases
including Pneumocystis carinii pneumonia (52)).
Thus a mitogenic and carcinogenic effect of nitrites and semen (or their
derivatives) may better account for the presently available epidemiological
data on KS in homosexuals than a currently unspecified,unknown new,sexually
transmitted infectious agent.
Conclusions and Predictions
We present evidence that the oxidative effects of semen and/or nitrites
play a pivotal role in the development of KS in homosexual AIDS patients.
If anally deposited semen causes KS, we predict that case-controlled studies
should show that:-
1. In a group of exclusively passive homosexuals who also use nitrites,cessation
of exposure to semen by the use of condoms should lead to a reduction in
the frequency of KS.
2. Women who do not use drugs including nitrites but who practise anal
intercourse should have a higher incidence of KS than those who do not.
If nitrites play an aetiological role in the development of KS then future
observation will show that:-
1. In groups of people who inhale nitrites and who have a high incidence
of KS the frequency should diminish when all other factors are kept the
same but nitrite inhalation is stopped.
2. In case control studies where the test population is identical in
all aspects to the control population apart from inhaling high concentrations
of nitrites,a high frequency of KS should be seen in the test cases but
not in the controls.
If anally deposited semen by itself cannot cause KS,but is an exacerbating
factor when nitrites are used, then case-controlled studies should show
an excess of KS in homosexuals who in addition to inhaling nitrites, practise
exclusive passive anal intercourse.
Most importantly, this theory predicts that reducing agents may prevent
or even ameliorate KS in homosexual AIDS patients. In this regard, the
recent discovery of significant reductions in cellular reduced glutathione
in AIDS patients lends strong support for contemplating such a therapeutic
We wish to thank all our colleagues and especially Bruce
Hedland-Thomas, David Causer, Richard Fox, John Peacock, Rod Minchin, David
Prentice, Ronald Hirsch, Patricia Shalala, Keith Jones, Alun Dufty, June
Rider Jones, Coronary Barrow, Dorothy Davis Julian Smith and Wallace Turner
for their continued support and assistance.
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