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Chapter 6
Gallo's Research Anthology -The AIDS
Buck and Virus Stops Here
EARLY the next morning, I made my way to Countway's Cumulated Index
Medicus to look up all of Gallo's early work. I started my search in
1965, figuring it would have taken him at least five years to
establish himself as an expert in the field of retrovirology by
1970. The 1965 and 1966 year-books cited nothing of Gallo's efforts,
but 1967 held two such references in what became a long list of
Gallo publications.
By days end, I held a stack of nearly
forty research reports published by Gallo and coworkers before 1975.
It took me about two weeks of reading, with frequent referencing of
medical texts for explanations to technical information that I found
difficult to understand. My earlier lessons in biochemistry, cell
physiology, genetics, and virology all needed refreshing. With my
head buried in scientific literature, I saw very little of my family
those weeks.
I began my review of Gallo's papers by
organizing them chronologically. I read each paper, highlighted
important details in yellow, then noted the purpose, conclusions,
and potential relevance to the development of AIDS-like viruses. In
the end, I held six pages of tables summarizing the data (see fig.
6.8).
Introduction to Retrovirology
A fundamental understanding of what HIV is and how it works is
required before discussing the development of AIDS-like viruses by
Gallo and his coworkers. The AIDS virus is an extremely unique germ.
Most astonishing is that it incorporates elements that cause normal
white blood cells (WBCs) to produce more viruses through a somewhat
unnatural and uniquely backward process. One of HIV's main
components is a single chain of genetic material.
This single strand is called RNA, short
for ribonucleic acid. It comprises sugars combined with chemical
(molecular) rings called purines and pyrimidines (see fig. 6.2).
After the virus gets into a T4lymphocyte or CD4 helper cell (a type
of WBC), its RNA genetic code directs the blood cell to produce a
similar nucleic acid chain called DNA, short for deoxyribonucleic
acid. DNA is the genetic blueprint all cells use to reproduce
normally. DNA directs the manufacture of all new proteins and other
cell parts, including RNA.
In the case of an RNA retrovirus
infection, however, this natural direction is commandeered to run in
reverse. In this case, the viral RNA directs the manufacture of
deadly foreign DNA, which then commands the cell's reproductive
machinery to produce more viruses rather than healthy new cells.
This switch in reproductive control is accomplished partly because
RNA and DNA are very much alike. The only difference between them is
the substitution of one sugar-linked molecule, called uracil in RNA,
for another one, called thymine, in the DNA (see figs. 6.1 and 6.2).
As shown in fig. 6.3, AIDS viruses have
a special attraction for T4 lymphocytes. These blood cells possess
special magnet-like CD4 receptors. These attachments normally serve
to detect and help destroy foreign invaders, called antigens, via a
complex immunological defense system. These CD4 receptors bind to a
portion of HIV's outer envelope known as the gp 120 antigen.
The CD4-gp 120 interaction allows the
AIDS virus to be transported across the lymphocyte's protective
outer membrane, and once inside the cell, the viral envelope opens
releasing the unique RNA and special enzymes into the human cell.
[1] Then, by means of the special reverse transcriptase enzyme-so
named because it prompts the "reverse" process of copying DNA to RNA
- the RNA code is copied to produce a new "proviral DNA" strand.
This enzyme is technically called RNA-dependent DNA polymerase.
It directs the cell to produce a DNA
gene sequence from the viral RNA template, the exact opposite of
what normally occurs in the non-infected cell. This DNA provirus
then enters the cell's nucleus where genetic materials are stored.
Here the provirus is inserted into the host's normal gene sequence
through the work of another unique enzyme known as viral
endonuclease. The endonuclease enzyme functions like a pair of
scissors. It cuts open the cell's normal DNA strand allowing the
newly formed provirus to be inserted.
Later, during normal cell operation, the provirus directs new viral
proteins to be produced, which eventually bud off the cell forming
new viruses. [1] This is the theory Gallo advanced first in 1972
during the "war on cancer" in order to explain retrovirus related
cancers such as lymphoma, leukaemia, and sarcoma.
Twelve years later, he advanced the same
theory to explain AIDS.
Fig 6.1
- The Molecule Structures
Comprising Nucleic Acids RNA and DNA - Life's Building Blocks:
PENDING
Source: Asimov I. The Intelligent Man's Guide To Science. Volume
II, The Biological Sciences. Basic Books, 1960. pp.526-527.
Fig 6.2
- A Model of the Nucleic-Acid
Molecule:
PENDING
The drawing at the left shows the double helix; in the center a
portion of it is shown in detail (omitting the hydrogen atoms);
at the right is a detail of the nucleotide combinations. Source:
Asimov I. The Intelligent Man's Guide To Science. Volume II, The
Biological Sciences. Basic Books, 1960. p.532. Reprinted with
permission.
Fig 6.3
- Replication of the AIDS Virus -
HIV/CD4 Cell Interaction:
PENDING
Source: Germain RN. Antigen processing and CD4+ T cell depletion
in AIDS. 'Cell' 1998;54:441-414
Gallo's Cancerous Creations
In 1971, the year following the $10 million DOD appropriation for
the development of AIDS-like viruses the NCI acquired the lion's
share of the Fort Detrick facilities, and the Cell Tumor Biology
Laboratory's output increased as measured by the publication of
eight scientific articles by Gallo and his coworkers compared to at
most four in previous years.
Among Gallo's earliest reports was the
discovery that by adding a synthetic RNA and cat leukaemia virus
"template" to "human type C" viruses - those associated with cancers
of the lymph nodes - the rate of DNA production (and subsequent
provirus and virus reproduction) increased as much as thirty times.
Gallo and company reported that such a virus may cause many cancers
besides leukaemias and lymphomas, including sarcomas. [10]
Regarding Gallo's widely accepted 1983
speculation that the AIDS virus arose from an African monkey virus
that naturally jumped species and then was carried by Portuguese
seamen to Japan (see fig. 6.4), in 1971 he and his team published a
seemingly conflicting statement.
"Only one virus [of 27 then known
RNA retroviruses] which contains reverse transcriptase," they wrote,
"does not seem to be oncogenic [cancer causing]" - the simian foamy
virus. [10]
At the time, simian foamy viruses were
known to be common, humanly benign, vaccine contaminants. Had the
simian virus simply jumped species then, I considered, it is
doubtful it would have gained the cancer-causing capabilities seen
in AIDS. Additional mutations would have been needed to make it so
carcinogenic.
Then, suddenly, there it was. "Mama
Mia!" I exclaimed. "I can't believe he published this."
Gallo and company, including frequent
coauthor Robert Ting from Litton Bionetics, reported modifying
simian monkey* viruses by
infusing them with cat leukaemia RNA to make them cause cancers as
seen in people with AIDS (see fig. 6.5). [9,10]
[* The
word "simian" before monkey, introduced by the mass media, is
actually redundant. Since most people now associate the two,
however, particularly in connection with the origin of the AIDS
virus, the phrase "simian monkey" will be used in this book to mean
just "monkey."]
Furthermore, Gallo and his coworker
Seitoku Fujioka concluded from studies conducted in late 1969 or
early 1970 that they would need to further "evaluate the functional
significance of tRNA changes in tumor cells." To do this, they
designed an experiment in which "specific tumor cell tRNAs" were
"added directly to normal cells."
They explained that one way of doing
this was to use viruses to deliver the foreign cancer producing tRNA
to the nonnal cells. The viruses that they used for this purpose,
were the simian monkey virus (SV 40) and the mouse parotid tumor (polyoma)
virus. [11] These experiments, I realized, could have easily
established the technology for the development of HIV-allegedly of
simian virus descent - which similarly delivers reverse
transcriptase and a foreign cat leukemia/sarcoma-like RNA to nonnal
human white blood cells.
Fig 6.4
Possible Origin of HTLV:
PENDING
This diagram was presented by Dr. Robert Gallo of the National
Cancer Institute during his introductory speech before a meeting
on "Human T-Cell Leukemia Viruses" at the Cold Spring Harbor
Laboratory in New York.
Source: Essex M and Gallo R. Human
T-Cell Leukemia Viruses: Abstracts of papers presented at the
Cold Spring Harbor Laboratory Meeting, Sept. 14-15, 1983. New
York: Cold Spring Harbor Laboratory, 1983, p. iv.
Obvious Link to NATO
That same year, Gallo and his coworkers presented research
describing the experimental entry of bacterial RNA into human WBCs
before a special symposium sponsored by the North Atlantic Treaty
Organization (NATO)? The paper published in the Proceedings of the
National Academy of Sciences discussed several possible mechanisms
prompting the "entry of foreign nucleic acids" into lymphocytes.
I flashed back to my knowledge of the
controversial symposium on the entry and control of foreign nucleic
acids, held on April 4 and 5, 1969, at Fort Detrick, and noted
Gallo's link to this work. Here was documented evidence that senior
investigator Robert Gallo presented the methods and materials used
to produce AIDS-like viruses before NATO military scientists at "the
NATO International Symposium on Uptake of Infonnative Molecules by
Living Cells" in Mol, Belgium, in 1970. [2]
I sat stunned while reading that Gallo
and his coworkers had also published studies identifying
-
the mechanisms responsible for
reduced amino acid and protein synthesis by T-lymphocytes
required for immune system failure [3]
-
the specific enzymes required to
produce such effects along with a "base pair switch mutation" in
the genes of WBCs to produce the small DNA changes needed to
create extreme immune system failure [4]
-
the methods by which human WBC "DNA
degradation" and immune system decay may be prompted by the
"pooling" of nucleic acids, purine bases, or the addition of
specific chemical reagents [5]
A subsequent study published in 1970 by
Gallo and his colleagues identified RNA-dependent DNA polymerase.
Gallo's team noted that this enzyme was responsible for gene
amplification and biochemical cyto-differentiation (the development
of unique WBC characteristics including cancer cell production) and
leukaemogenesis (the production of leukemia). [6]
Another of their studies identified L-Asparaginase
synthetase - an important enzyme that, if blocked, will cause
treatment- resistant leukemias and other cancers. [7] Just what the
DOD ordered, I recalled,
"[M]ake a new infective
microorganism... most important... that it might be
refractory to the immunological and therapeutic processes upon
which we depend to maintain our relative freedom from infectious
disease." [8]
Fig 6.5
- Development of AIDS-like Viruses
by Robert Gallo and Associates at the NCI and Litton Bionetics:
PENDING
Creating More AIDSLike Viruses
By 1972, Gallo and coworkers studied portions of simian monkey and
mouse salivary gland tumor viruses to determine differences in RNA
activity between infected versus uninfected cancer cells. [9]
They wrote:
"[B]y studying viral or cellular
mutants or cell segregants ... which have conditional
variations in virus-specific cellular alterations, it should be
possible to more precisely determine the biological significance
of the ... RNA variation reported here." [9]
The group was trying to determine the
importance of various viral genes on the development of human
cancers and immune system collapse. They reported their desire to
use this information to find a cure for cancer, but at this time
their activity was more focused on creating various cancers and
carcinogenic viruses that could infect humans. [9-11]
From this work, I also realized, Gallo
was actually cloning simian monkey viruses as early as 1970. So
allegations that he had cloned Montagnier's virus were buffeted by
the fact that he had over a decade of practice in the procedure.
Another example of Gallo's work in creating new viruses to cause
cancer in humans was published for the benefit of the NAS. Here
Gallo and company examined the activity of the special AIDS-linked
DNA polymerase enzyme in normal versus acute immature leukaemic
lymph cells, that is, lymphoblasts.
To do so, they evaluated the single
stranded "70S RNA retrovirus" found in chickens, which caused
prominent features of AIDS, including WBC dysfunction, sarcomas,
progressive wasting, and death (see fig. 6.5). [12] Gallo and his
team injected this chicken virus RNA into human WBCs to determine if
the cells were prompted to produce proteins and new viruses called
for by the viral RNA.13
Another Gallo team evaluated the human
cancer-causing effects of the single-stranded 70S RNA reverse
transcriptase enzyme-a genetic catalyst essentially identical to the
one found in HIV. They used cat leukemia viruses (FELV) and
Mason-Pfizer monkey viruses to deliver these carcinogens to normal
human lymphocytes. [14] I instantly realized that this work
foreshadowed the observation made ten years later by the CDC's chief
AIDS researcher, Don Francis, who noted the "laundry list" of feline
leukemia-like diseases associated with AIDS. [15]
Had Francis known about this early work?
I considered it most conceivable that he would have. Other Gallo
publications detailed the steps involved in creating
immune-system-destroying-cancer-causing viruses by adapting monkey,
rat, and bird leukemia and tumor viruses for experimental use in a
human (NC-37) cell line. 16
One Gallo team discussed the synthesis
of new RNA tumor viruses induced by 5-iodo-2'-deoxyuridine (IdU), a
constituent of RNA in rodent cell cultures, and noted that chemical
treatment might be used to halt the reverse transcriptase-linked
viral reproduction cycle. [17] They were apparently looking for a
cure for AIDS-like symptoms as early as 1972. Then I read a Gallo
team discussion in 1973, which concerned the origin of the RD 114
cat-human virus. "It can always be argued," they wrote, that a virus
that jumped species would be expected to have foreign protein
markers, that is, antigens, that differ "from the antigen found on
the viruses of known" origin. [18]
So if Gallo and his coworkers had
synthesized HIV for military or medical purposes from various animal
virus components, I realized, it would be difficult if not
impossible to prove. Finally, in another report published in the
'Proceedings of the National Academy of Sciences,' Gallo and
associates proclaimed they had isolated a virus-like particle from
human acute, that is, quick-acting, leukemic WBCs.
This particle, they noted, has a
specific density of 1.16-1.17 g/ml, which allowed it to be
repeatedly recovered without being destroyed by physical handling.
Moreover, it was capable of producing the principal rapidly growing
cancers seen in AIDS, including leukemias, sarcomas, and carcinomas.
[19] In conclusion, I learned that Gallo and his group of
researchers created numerous AIDS-like viruses for more than a
decade before Luc Montagnier announced the discovery of LA V.
Links to the DOD
Throughout my review of Gallo's research, besides citing the NCI as
his chief source of support, the names Bionetics, Bionetics Research
Laboratories, and Litton Bionetics, Inc., repeatedly appeared (see
fig. 6.6). For days, I wondered who or what Bionetics was?
This mystery ended when I retraced Ted Strecker's steps through the Ninety-first Congress's House hearings
on DOD appropriations for 1970. The Congressional Record contained
several sections dealing with chemical and biological weapons
funding. One contained the list of major Army contractors shown in
fig. 6.7. Bionetics Research Laboratories, a subsidiary of Litton
Industries, Inc. was sixth on the list of acknowledged biological
weapons contractors. [20]
Later congressional records showed that
Bionetics's affiliate - Litton Systems, Inc., a subsidiary of Litton
Industries, Inc. - was among the most frequently contracted
companies involved in BW research and development between 1960 and
1970.20
Additional BW contractors with whom Dr.
Gallo or his coworkers associated during the late 1960s and early
1970s included the Universities of Chicago, Texas, Virginia,
California, Yale, and New York. [21]
Breaking the News
I emerged from my two weeks of laborious isolation noticeably pale.
My mind raced with questions about the risk of continuing the
investigation. I also wondered how I would break the whole truth
about my findings to Jackie. The pragmatist in our family, she would
immediately consider the sensitivity of the information and its
potential affect on our lives.
Following a brief summation of my
findings aided by the six pages of tables I had developed (see fig.
6.8), Jackie shattered a long and anxious silence.
"What are you going to do now?"
"I don't know. What do you think I
should do with this kind of information?"
"Bury it! Or else we'd better get
the hell out of this country. Do you know what the risk is in
getting this information out?"
"I don't even want to think about
it."
"Well you'd better think about it,"
she ordered. "Look what happened to Strecker's brother and that
congressman from Illinois. "And what about Strecker? Have you
been able to reach him?"
"No. Every time I call, the phone
just rings and rings. And that other doctor from Georgia who
wrote that article about Strecker, William Douglass, I've left a
half-dozen messages for him on his answering machine, but he's
never returned one."
"Well you better find out if
Strecker's still alive before you do anything else," Jackie
said. That night before bed, after her initial shock lessened, I
said, "You know, this thing is bigger than just us. This is
about the world. The kind of world we'll leave behind for our
children."
"I know it," Jackie replied. "That's
what scares me most."
Fig 6.6
- Sample Publication Documenting
Robert Gallo's Work With Investigators at Litton Bionetics:
NATURE VOL. 228. DECEM8ER 5, 1970
RNA Dependent DNA Polymerase
of Human Acute leukaemic Cells
by ROBERT C. GALLO
Section on Cellular Control Mechanisms, Human Tumor Cell Biology
Branch, National Cancer Institute.
National Institutes of
Health, Bethesda, Maryland 20014
STRINGNER S. YANG, ROBERT C. TING
Bionetics Research
Laboratories, Bethesda, Maryland 20014
An RNA dependent DNA polymerase analogous to that of RNA
tumor
viruses has been found in lymphoblasts of leukaemic patients but
not of normal donors. The enzyme can use an RNA template from
mammalian cells to synthesize DNA.
RECENT reports by Temin and Baltimore that an RNA dependent DNA
polymerase activity is present in oncogenic ANA viruses, now
confirmed and extended in other laboratories provide a mechanism
by which an RNA virus may insert stable genetic information into
a host cell genome. The aetiology of human acute leukaemia is
not known, but a role for RNA oncogenic viruses in human
neoplasia has been proposed for several reasons.
Although RNA virus particles have
not been clearly associated with human leukaemia, we have
examined human leukaemic cells for the presence of an RNA
dependent DNA polymerase because:
-
It is possible that RNA
Virus particles are regularly present in human leukaemic
cells but cannot be detected by ordinary means. The presence
of a unique enzyme might be a more sensitive index.
-
The virus particles may
never be formed but the viral genome would be integrated and
undetected, yet functional in the host cell. The enzyme
could be required for subsequent formation of additional
viral DNA used in infection of other host cells.
-
Information flow from RNA to
DNA raises interesting questions regarding gene
amplification during biochemical cyto-differentiation. This
mechanism could have considerable implications for cell
growth and differentiation, and because human leukemia has
been considered a disorder of cell differentiation, it may
also have implications for leukaemogenesis"'.
Choice and Preparation of Cells
Several considerations influenced our choice of cells.
-
First, acute leukaemia was selected
rather than the chronic form because the characteristics of the
former cell type are more malignant and less often contaminated
with other types of leucocytes. In leukaemia of an acute "blastic"
type, a population of almost 100 per cent blasts can be obtined
directly from a patient.
-
Second, the lymphoblastic type was
chosen rather than the myeloblastic (granulocytic type) because
the latter are more likely to be associated with other more
differentiated cells of the myeloid (granulocytic) series. These
cells contain abundant lysosomes with high nuclease activities,
making any RNA analysis or polymerase assay extremely difficult.
-
Third, proliferative lymphoblasts
can also be obtained from normal human volunteers. This is
achieved by transformation of normal peripheral blood
lymphocytes to lymphoblast with a mitogenic agent.
-
Fourth, the polymerase activities of
tumor cells are generally higher than those of normal adult
organs. A much greater content of various polymerases would be
more likely to lead to a spurious interpretation of a unique
polymerase in such cell types. For this reason, we would expect
a better controlled comparison between normal and nooplastic
cells of comparable DNA and RNA polymerase activities.
The simple use of peripheral blood
leucocytes, which consist primarily of fully mature
non-proliferating granulocylcs and lymphocylcs, cannot be considered
as controls for leukaemic blast cells, particularly in view of the
fact that these cells have minimal or no detectable DNA dependent
DNA polemerase activity.
On the other hand, after 72 h of
stimulation of normal human lymphocytes with phytohaemagglutinin (PHA),
DNA synthesis is maximal. In addition, Loeb 'et al' have reported a
30 to 100-fold induction of DNA polymerase at this time, so that
activities reach levels comparable with neoplastic cells, and Hausen
'et al' have reported an induction of RNA polymerase in lymphocytes
stimulated with PHA.
We have confirmed both these finding
(unpublished results).
-
Fifth, human cells obtained directly from
peripheral blood instead of human tissue culture cell lines were
chosen for these initial investigations because they obviously are a
more true reflexion of the disease. Furthermore, there is much less
chance of contamination with microorganisms or of developing
mutations not relevant to leukaemogenesis.
The leukaemic cells utilized in this
study, therefore were peripheral blood lymphoblasts obtained from
three patients with acute lymphoblastic leukaemia (ALL). In each,
the number of lymphoblasts was more than 100,000/mm of blood. Two
patients were untreated and the third received hydroxyurea for one
day. Normal lymphocyctes were obtained from the peripheral blood
lymphocytes of forty-eight normal donors.
The lymphocytes were separated from
other blood cells, as previously described, except that an
additional nylon column chromatographic step was carried out to
obtain more pure cell populations (more than 98 per cent
lymphocytes). These cells were incubated with the mitogenic agent
and harvested after 72 h as previously described. In our conditions,
at 72 h the number of cells transformed to lymphoblasts and the rate
of DXA synthesis are maximum.
After terminating the incubation, the
cells were extensively washed with 0.15 NaC1 and used for polymerase
assays.
RNA dependent DNA Polymerase Activity
Nucleic acid from preparations were made by gentle manual
homogenization (Ten.Broeck) of purified lymphoblast pellets in 3
volumes of 25 mM Tris-sulphate buffer, pH 8.3; 1mM MgSo; 6 mM NaCl;
4 mM dithiothrecitol; and 0.1 mM EDTA. The samples were centrifuged
at 15,000 r.p.m., and the supernatants and pellets seperated. The
pellets of membranes and nuclei were washed with the same buffer
with gentle homogenization.
After centrifugation the wash (second
supernatants) was combined with the forst supernatants and the
nuclei-membrane pellets removed. Nucleic acids were removed from the
supernatant fractions by successive precipitations with MnCl2 and...
[One of dozens of publications authored by
Robert C. Gallo and
colleagues affiliated with Bionetics Research Laboratories,
Bionetics, or Litton Bionetics. These subsidiaries of
Litton
Industries, Inc. were listed among most frequently contracted
companies involved in biological weapons research and development
during the 1960s and 1970s. [20,21]
Source: Gallo RC, Yang SS and
Ting RC. RNA Dependent DNA Polymerase of Human Acute Leukaemic
Cells. Nature 1970; 228:927.]
Fig 6.7
- Major United States Army
Biological Weapons Contractors for Fiscal year 1969: Mr. Mahon.
List for the record the major contractors and the sums allocated
to them in this program in fiscal year 1969.
(The information follows:)
The following list contains the
major contractors and amounts of each contract.
Contractor Fiscal year 1969
Miami, University of Coral Gables Fla $645,000
Herner and Co., Bethesda. Md
$518,000
Missouri, University of,
Columbia, Mo $250,000
Chicago, University, of Chicago,
Ill $216,000
Aerojet-General Corp,.
Sacramento, Calif $210,000
Bionetics Research Laboratories,
Inc., Falls Church, Va $180,000
West Virginia University.
Morgantown, W. Va $177,000
Maryland. University of, College
Park. Md $170,000
Dow Chemical Co., Midland, Mich
$158,000
Hazelton Laboritories, Inc.,
Falls Church, Reston. Va $145,000
New York University Medical Center, New York, NY $142,000
Midwest Research Institute.
Kansas Clty, MO $134.000
Stanford University, Palo Alto,
Califf $125,000
Stanford Research Institute,
Menio Park, Califf $124,000
Pfizer and Co., Inc., New York,
NY $120.000
Aldrich Chemical Co., Inc.,
Milwaukee, Wis $117,000
Computer Usahe Development
Corp., Washington, D.C. $110,000
New England Nuclear Corp.,
Boston, Mass $104,000
Source: Department of Defense
Appropriations For 1970: Hearings Before A Subcommittee of the
Committee on Appropriations House of Representatives,
Ninety-first Congress, First Session, H.B. 15090, Part 5,
Research, Development, Test and Evaluation of Biological
Weapons, Dept. of the Army. U.S. Government Printing Office,
Washington, D.C., 1969, p689.
Fig 6.8
- The Early Research of Cr. Robert
Gallo at the National Cancer Institute and it's Implications in
relation to the Theory of synthetic HIV Development:
PENDING
NOTES
[1] Germain RN. Antigen processing
and CD4+ T cell depletion in AIDS. Cell 1988; 54:441-414.
[2] Herrera F. Adamson RH and Gallo RC. Uptake of transfer
ribonucleic acid by nonnal and leukemic cells. Proc Nat Acad Sci
1970;67;4: 1943-1950. This paper was presented before the
"International Symposium on Uptake of Informative Molecules by
Living Cells, Mol, Belgium, 1970," the year in which $10 million
in funds were appropriated by the Department of Defense for the
development of AIDS-like viruses.
[3] Gallo RC, Perry S and Breitman RT. The enzymatic mechanisms
for deoxythymidine synthesis in human leukocytes. Journal of
Biological Chemistry 1967;242;21:5059-5068.
[4] Gallo RC and Perry S. Enzymatic abnormality in human
leukaemia. Nature 1968;218:465-466.
[5] Gallo RC and Breitman TR. The enzymatic mechanisms for
deoxythymidine synthesis in human leukocytes: Inhibition of
deoxythymidine phosphorylase by purines. Journal of Biological
Chemistry 1968;243;19:4943-4951.
[6] Gallo RC, Yang SS and Ting RC. RNA dependent DNA Polymerase
of human acute leukaemic cells. Nature 1970;228:927-929.
[7] Gallo RC and Longmore JL. Asparaginyl-tRNA and resistance of
murine leukaemias to L-asparaginase. Nature 1970;227:1134-1136.
[8] Department of Defense Appropriations For 1970: Hearings
Before A Subcommittee of the Comminee on Appropriations House of
Representatives. Ninety-first Contress. First Session.
H.B. 15090. Part 5. Research. Development. Test and Evaluation.
Dept. of the Army. U.S. Government Printing Office, Washington,
D.C., 1969.
[9] Gallaher RE, Ting RC and Gallo RC. A common change
aspartyl-tRNA in polyoma and SV transformed cells. Biochimica Et
Biophysica Acta 1972;272:568-582.
[10] Gallo RC, Sarin PS, Allen PT, Newton WA Priori ES, Bowen JM
and Dmochowski L. Reverse transcriptase in type C virus
particles of human origin. Nature New Biology 1971 ;232:
140-142; see also Gallo RC. Transfer RNA and transfer RNA
methylation in growing and "resting" adult and embyonic tissues
and in various oncogenic systems. Cancer Research 1971
;31:621-29.
[11] Fujioka S and Gallo RC. Aminoacyl transfer RNA profiles in
human myeloma cells. Blood 1971;38;2:246-252.
[12] Smith RG and Gallo RC. DNA-dependent DNA polymerases I and
II from normal human-blood lymphocytes. Proceedings of the
National Academy of Sciences 1972;69; 10:2879-2884.
[13] Bobrow SN, Smith RG, Reitz MS and Gallo RC. Stimulated
normal human lymphocytes contain a ribonuclease-sensitive DNA
polymerase distinct from viral RNA-directed DNA polymerase.
Proceedings National Academy of Sciences 1972;69; 11 :3228-3232.
[14] Robert MS, Smith RG, Gallo RC, Sarin PS and Abrell JW.
Viral and cellular DNA polymerase: Comparison of activities with
synthetic and natural RNA templates. Science 1972; 176:798-800.
[15] Gallo RC, Abrell JW, Robert MS, Yang SS and Smith RG.
Reverse transcriptase from Mason-Pfizer monkey tumor virus,
avian myeloblastosis virus, and Rauscher leukemia virus and its
response to rifamycin derivatives. Journal of the National
Cancer Institute 1972;48;4:1185-1189.
[16] NCI staff. The Special Virus Cancer Program: Progress
Report #8. Office of the Associate Scientific Director for Viral
Oncology (OASDVO). J. B. Moloney, Ed., Washington, DC.:
U.S. Government Printing Office, 1971, p. 22.
[17] Wu AM, Ting RC, Paran M and Gallo RC. Cordycepin inhibits
induction of murine leukovirus production by
5-iodo-2'deoxyuridine. Proceedings of the National Academy of
Sciences 1972;69;12:3820-3824.
[18] Gillespie D, Gillespie S, Gallo RC, East J and Dmochowski
L. Genetic origin of RD114 and other RNA tumor viruses assayed
by molecular hybridization. Nature New Biology 1973;224:52-54.
[19] Gallo RC, Miller NR, Saxinger WC and Gillespie D. Primate
RNA Tumor Virus-Like DNA Synthesized Endogenously by
RNA-Dependent DNA Polymerase in Virus-like Particles from Fresh
Human Acute Leukemic Blood Cells. Proceedings National Academy
of Sciences 1973;70; 11 :3219-3224.
[20] Department of Defense Appropriations For 1970: Hearings
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[21] Committee on Human Resources. United States Senate.
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of Drug Research. Washington, D.C.: U.S. Government Printing
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