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:

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:

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:

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:

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

  1. the mechanisms responsible for reduced amino acid and protein synthesis by T-lymphocytes required for immune system failure [3]

  2. 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]

  3. 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:


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

Section on Cellular Control Mechanisms, Human Tumor Cell Biology Branch, National Cancer Institute.

National Institutes of Health, Bethesda, Maryland 20014


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:

  1. 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.

  2. 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.

  3. 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:



[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 Before A Subcommittee of the Committee 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, p. 689.

[21] Committee on Human Resources. United States Senate. Hearings before the Subcommittee on Health and Scientific Research. Biological Testing Involving Human Subjects by the Department of Defense. 1977: Examination of Serious Deficiencies in the Defense Departments Efforts to Protect the Human Subjects of Drug Research. Washington, D.C.: U.S. Government Printing Office, May 8 and May 23, 1977, pp. 80-100.

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