Georg Hoffmann

Lüneburger Strasse 9

D 27367 Sottrum






Oncogenes and HIV



Oncogenes are important for the classification of cutaneous lymphomas, leukaemia’s and other cancers. The pathologist Peyton Rous observed 1911 in ill chickens the transfer of cancer over the injection of tumour infected fluidics into the body of healthy chickens [1]. The oncogene src leads for healthy chickens to cancer (tumour sarcoma). This oncogene src is also infectious or contagious for human cancer that has been proven sufficiently. The HIV infection - over the blood is a mechanism of gene transfer from an ill body to a healthy body via oncogens (DNA or RNA). The src - oncogene is able, to produce an unlimited cell growth. The transfer of oncogens is not the same as a viral infection. HIV is not a virus but the gene transfer via blood of an  e.g. myc oncogene that initialize at first a pre stage of cancer as the cause of  HIV and HIV- PCR-, ELISA-test results.


The pathologist Peyton Rous [1] observed 1911 in chickens the transfer of cancer by body fluidics. The injection of the extract with chicken sarcoma led to the illness of healthy chicken. Healthy chicken developed within a view months or years a cancer of sarcoma. Rous thought that was a virus (RSV), which is the cause for this cancer. Rous 1966 received the Nobel Prize medicine for his discovery. Only a gene or oncogene v-src or RSV con trigger the cancer and requires no virus for the transfer. The DNA of the src yields of a restriction enzyme of the DNA from the bacteria phage. The replication of a v-src DNA is cloned by a bacteria phage. The DNA can cut in pieces and recombined with plasmids, which are increased in bacteria cells. Different DNA are cloned by the bacteria with a certain fragment of the Phage- DNA and carries also the DNA of the RSV (src) oncogene in it. The transfer of these RSV gene fragments in the DNA by cells transforms lead to a cell degeneration and tumour grow. A weight has marked. The oncogene src has a weight of 60kD or called p60-src The proto-oncogenes (c-src) is also in healthy cells, that converts to virale oncogenes (v-src) the origin for the tumour. Many oncogenes have been discovered:



Proto oncogene und cancer by animals


c-abl Abelson- mouse leukaemia

c-bcl B-cell lymphoma

c-erb Erythroblasts

c-fos  FBJ- mouse-osteo sarcoma

c-fps  Fujinami-PRCII-avian sarcoma

c-int   insertions activate onc of mouse mamma


c-jun  avian sarcoma-Virus 17-Gen (junana)

c-met  methyl-nitroso-guanidine treated human

           osteo sarcoma

c-mil   avian gel-Mill-Hill-2-Retrovirus

c-mos  Molony- Mouse sarcoma

c-myk Myelozytomatose

c-myb avian-myeloblastose

c-ras   Kirsten-Ratt sarcoma

c-rel    avian-retikuloendotheliose

c-src    Rous-sarcoma

c-sis     simian sarcoma



Proto oncogene of human cancers


c-abl    leukaemia

c-bcr   B-cell lymphoma

c-my   Burkitt lymphoma

c-bcl   follicular B-cell lymphoma



Cancer associated with oncogene


Virus      Genome          cancer


RSV        v-src              sarcoma

ALV                              B-cell- lymphoma

MC 29     v-myc            myeloid leukaemia

MLV                              T-cell-lymphoma

Abelson    v-abl             B-cell- lymphoma



HIV can better understand to know the history for the most important medician R.C. Gallo [6]. He has at first analysed leukaemias because his sister was died on this illness. He found the HLTV-I virus [6] that he has held for a virus with the cause of leukaemia although HLTV-I is found in the blood of 5% in all leukaemias. Cutaneous B-Cell and T- cell- lymphomas have also been investigated by Gallo [7]. The Kaposi sarcoma is a cutaneous B-cell lymphoma with a direct connection of HIV and AIDS. Today, Kaposi sarcoma and other tumours are the second stage of HIV and AIDS. HIV corresponds directly to the HLTV- III virus and is derived from the leukaemia virus HLTV-I.

AIDS antiviral medicaments such as Zitrovir AZT (originally a cytotoxic) decrease the number of leukocyte and diminish the powers of resistance of the body. The only once definition of AIDS is the reduction of the relationship CD4/CD8 between the T-helper- to T- cytotoxic cells CD4/CD8. The decreasing of leukocyte CD4 or T -helper cells has the cause in the antiviral therapy and the following immunodeficiency. The transfer of oncogenes into  another body can trigger a tumour that repeatedly was proved. In this sense is HIV the result of exchanged fluidics, particularly blood of two bodies. After an infection with an oncogene it appears often a cutaneous tumour such as Kaposi sarcoma in the second stage of AIDS in proximally 30-40% of all HIV–positive cases. The important knowledge of HIV is, that cancer can be initiated by an infection over the exchange of body fluidics such as blood.


Current experiences show, that no HIV - virus can be selected by Virchows law. The original methods after R.C. Gallo do not find a virus with scientific methods of the virology. If HIV is considered as a pre stage of cancer we can cancel the virus theory. The argumentation for HIV would be better for the clarification and is not as dangerous as a deathly illness. The time after incubation of a viral HIV infection is too long. The HIV test for AIDS shows more connectivity to cancer and leukaemia or cutaneous B-cell-lymphoma NHL and the Kaposi sarcoma.


The main protein of the HIV- infection is a gene segment with a weight of 24000 Dalton  (24 kD = p24) that we can also find in cutaneous B- cell- lymphomas [3] and  cutaneous T-cell lymphomas- and leukaemias. The HIV test is a genetic PCR analysis and was investigated by R.C. Gallo [1].


The solution of this problem could be the feature or ability of the v-abl oncogene to initialize leukaemia or B-cell lymphoma by the v-myc oncogene.  Oncogenes can infect a body by an infection over the blood, but it is not an infection of a real virus. A HIV-infection is than a transfer of an oncogene via the blood into another body and a pre stage of cancer. The T-cell-infection of CD4+ is a normal reaction of T-cells after an infection as the immune response of cancer but it s not an immunodeficiency.


The essential difference between a virus and a DNA- or RNA oncogene is that an oncogene leads to cell growth a virus replicates in a cell for a real infection. An oncogene can triggers a point mutation for cell growth (increased cell division). The diagnosis HIV positively can be examined as an initial pre stage of cancer with the p24, p41, gp120 protein.


CD4 and CD8 are markers of T-cells lymphomas- and leukaemias are important in the later stage of HIV.




















                         Fig. 1   v-src- and pre- c-src- oncogene [3]






The progress of cancer is often visible by a translocation or displacement of cncogenes in the chromosomes. Leukaemia. is an example for the translocation of oncogene abl from chromosome 9 to chromosome 22 and the translocation of oncogene sis from chromosome 22 to chromosome 9.




         Fig. 2 chromosome –translocation  by the oncogene  abl und sis [3]





The conclusion of the previous statements about HIV is, that is more a cancer or the initial pre stage of cancer, than a virus infection. The skin of HIV-patients shows in the later stage of  HIV a Kaposi sarcoma.  An example for HIV and Kaposi sarcoma are Ukraine immigrants, who had lived in the near of the nuclear accident of Tschernobyl (Fig. 4, 5, 6), they have a Kaposi sarcoma in connection with HIV. The cause of a Kaposi sarcoma could be the radioactive radiation. The same connection is given by the HLTV-I virus of leukaemia which was found in Japanese’s. It could be the same cause of radiation with HLTV-I virus and HIV is derived from HLTV-I  These Japanese’s have lived or were born in the near of the nuclear bomb of Hiroshima in 1945. Today, 64 years later the leukaemia is still in these Japanese’s  or in  its children.


Now, we can understand that oncogenes can be transferred by exchanging blood of infected patients. This idea is surprising,  we must trust ourselves with an infection or transfection of oncogenes for HIV and cancer


A real picture of a HIV virus does not exist, because picture in Fig. 3 shows cells of blood. An oncogene has the feature of gene transfer via the blood from the infected- to the heath body. The transfer of an oncogene initializes the pre stage of a tumour that we can see in the p24- HIV-test. HIV transfer oncogenes by exchanging blood or fluidics between two bodies. The theory of a HIV virus or Retrovirus (RNA) must take leave, since a gene transfection is the cause of HIV. Rous take at first the idea of a virus by the transfer of oncogene src, but he did not have an electron microscope in the year 1911 to see a virus.  All pictures in Fig. 3 show cells of blood with but no typical virus structure. All pictures are the same as cells for leukaemia (HLTV-I)., lymphoma (HLTV-I) and HIV (HLTV-III).






                                  Fig. 3   HLTV  I, HLTV II, HLTV III (HIV) - virus [6]





Modern analytic used molecular biologic methods, the PCR- and ELISA test. Genetic investigation makes it possible to classify a gene via the length or weight in kilo Dalton. This can be done for the classification for an oncogene. The PCR analyse of a gene sequence is possible via the restrictions analysis of bacteria with cloning and setting of PCR primers for start and stop of the interesting gene sequence.


The reliability of a genetic test as PCR or ELISA is low with a slight percentage of probability. The PCR- HIV test is looking for a gene sequence with a weight of 24000 Dalton or 24 kD which is equivalent to p24. Genetic materials in the blood or in the cells, as the p24 have a very low concentration and must be cloning by the PCR for higher quantities.


HLTV I (leukaemia and cutaneous lymphoma) is the base for the HIV – virus, both have a connection with cancer. Oncogenes are exchanges by the blood as c-abl that can be found in leukaemia, c-bcr in B-cell lymphoma and c-myc in Burkett lymphoma and in HIV in the later stage.


Oncogenes are an explanation for a HIV infection via the blood or the translocalization of oncogenes in chromosomes. HIV is an initial stage of cancer. The immunodeficiency of HIV associated with the ratio CD4/CD8 of lymphocyte which is the result of a therapy of many years with cytotoxic antiviral medicines like as AZT or Zitrovir .





                                     Fig. 4  Western blood test (ELISA-PCR) of HLTV- III (HIV) antibodies

                                   and  molecular weights in Kilo Dalton from: A- sera of an AIDS patient,

                             B- cutaneous,  lymphoma- patient, C- positive and negative homo sexual patient [6]








The definition of HIV - after R.C. Gallo


The Adult T-cell leukaemia was indicated as the HLTV – I virus in Japan, Caribbean, South and Centrally - Africa and in the South east of the USA. The infection with HLTV-I appears primarily with Okt4+ (CD4+) cells and the destruction the T4 cells like at the T-Cell leukaemia ATLL. The HLTV–II humane T-cell-leukaemia virus was found in the Haar cell – leukaemia. The HLTV-III = HIV virus after R.C. Gallo is the cause of AIDS. These patients have the same cross reaction like the T4 - Cell destruction as HLTV –I.


HLTV-I, and a TCGF protein (tumour grow factor) was first found in the blood of black patients of the USA, the Caribbean and in cells of the aggressive cutaneous T- cell- lymphoma. HLTV-I attacks the bone and increases the amount the T8 - cytotoxic T- cells




                       Fig. 5  HLTV- I, HLTV – II and HLTV- III = HIV Genome with

                                  LTR, gag, pol, env und pX  cloning with  EColi bacteria






HLTV-III or HIV is defined by R.C. Gallo as infection with the HIV - virus and the destruction of T4 - helper cells. HIV appears accordingly at the risk group of homosexuals, consummates of drugs, haemophilia’s, Haitian and children of the risk groups. The surface molecule CD4 of the T4- leukocyte is infected, also CD8 of the T8 leukocyte


The HIV main protein p41 is found in the Genome of HLTV-III (HIV) of risk groups. HIV-AIDS patients are tested for the p24-protein. The ALV oncogene belongs after Gallo to the HTLV family. All HLTV-I, HLTV-II, HLTV-III (HIV) contain the p24 – protein as in leukaemia, lymphoma and HIV.




HTLV and HIV cellines


Cellines [7] are necessary for genetic investigations of cells and genetic tests such as PCR and ELISA that are important for HIV and cancer. HIV cellines are coming from the blood of a patient [13] with cutaneous T-cell lymphoma. The celline H9 and   HUT 78 are used for HIV tests.


HTLV-I has the TCGF = T-Cell-growth factor, the ELISA test with these cellines H9 or HUT 78 indicates p19 and p24 proteins and the antigen CD4+


The celline HTLVCR was established from a 28- years old black man with a cutaneous T-cell lymphoma (mycosis fungoides).


The celline HUT 102 was established from the lymph nodes- und CTCL-3 and peripheral blood of the 28- years old black man with cutaneous T-cell lymphoma (mycosis fungoides).


The celline HUT 78 was established from a patient with a cutaneous T-cell lymphoma (Sezary lymphoma), the PM1 celline is derived from HUT 78. The ELISA test shows p24 und gp120. The T- cells of PM1 shows the CD marker CD3, CD4+, CD8-, CD26 und HLA-DR+.


The celline H9 is cloned from HUT 78 and is used for the isolation and production of HIV proteins  The celline PM1 is also a HUT78 T-cell line CD4+ clone with the genetic framework HXB2 and gp120 and gp41 [18]. CD4+ is in infected T-cells of a cutaneous T-cell lymphoma (HUT78)


HTLV-III (HIV) has no TCGF, the HIV- ELISA- test shows p24, p41 and the antigen CD4+





HIV and Oncogenes


Between HIV and oncogenes is a connection for specific cancers. Such proteins which are important for the cell nuclides were investigated in [13]. They are in connection with nuclide-protein- complex. Based on amino acids sequences by known nuclides or targets, peptide was tested with nuclear target potential on it, whether they can trigger an infection through the transfer in the cell. The control of an infection can be ascertained by reporter - genes PK.


The sequences of the c-myb target potential p53 and c-erb-A oncogene build a hybrid in the cell - nuclides, which can be identified by reporter -genes PK.


The HIV-tat protein fuses with the target nuclides of the cell. The blood of HIV- infected patients have following oncogenes: SV-40, tumour suppressor gene p53, c-erb-A, c-myb, c-myc, p53, myc-tat.


T-Cell-Receptor TCR and the CD-marker CD28 are necessary for the activation of primary CD4-T-cells that was investigated. The expression of the c-myc protein that be initialized by the stimulation of CD4–T-helper-cells was investigated in [14]. Cyclosporine hind   the nuclear import of the HIV-1 -DNA but also the expression of the c-myc proteins. It would be tested further whether the oncogene c-myc is necessary for the nuclide import of HIV-1- DNA. It  would  be tested  the function of  the HIV-1 -DNA over the activation of primary CD4-T-cells und des T-cell- receptor TCR und CD 28 and  understand the expression of the  c-myc protein as the stimulation of CD4–T- cells. Obviously the c-myc is an essential part of the total HIV- genome for an infection of the HIV- DNA.


1. Targeting Proteins Class A [13]


p126   K-K-K-R.K-V-E         SV40 large T 2

p279   P-K-K-A-R-E.V          Polynoma large T 2

A1-P   T-K-R-K-G-S              SV40 VP1 26

p3l6    N-K-K-K-R.K-L         SV40 VP2 21

p120   A-A-K-R-V-K-L-D     Human c-Myc 5



2.  Protein sequences sub cellular distribution of PK (Pyruvate Kinase fusions) [13]


c-Erb-A    A. G22-K-R-K-R-K-S NT 32

                 B. S127-K-R-V-A-K-R-K-L Nuclear and

                  C. S251-H-W-K-Q-K-R-K-F NT (10-3076)

c-myb        p521     L-L-K-K-1-K-Q Nuclear and

c-myc        p387 -Q-K-K-I-K-S Nuclear (>95%) 34

p53            p416  Q - P - K - K - K - P Nuclear

HIV- tat   G46-R-K-K-R-R-Q-R-R-R-A-P                 

Myc-tat     P-A-A-K-R-V-K-L-D-Q-R-R-R-A-P







ALV     =    Avian Leucosis  Virus

RSV      =   Rous Sarcoma Virus

HIV      =   Human Immunodeficiency Virus

HTLV  =   Humane T-Cell Leucosis  Virus

MLV    =   Mouse Leucosis Virus

PCR     =   Polymere Chain Réaction

PK        =   Ppyruvate Kinase fusions

kD        =   Kilo Dalton – molecularly









[1]   Rous, P, Transmission of a malignant new growth by

        means of a cell-free filtrate, J. Am. Med. Assoc.,

        1911, 56, 198-201


[2]   Molekularbiologische und   biochemische   

        Charakterisierung  der reversen Transkriptase

        von Rous Sarcoma  Virus, Dissertation, Universität

        Bochum, Max-Planck-Institut für Molekulare

        Physiologie Dortmund


[3]  Vamus  H. Weinberg R. A.

       Gene und Krebs

       Spektrum 1992


 [4]  Passarge E.

       Taschenatlas der Genetik

       Thieme Stuttgart 1994


[5]   Keller R.

        Immunologie Immunpathologie

       Thieme Stuttgart 1994


[6]  Gallo R.C. et. al. The Human T-cell Leukemia-Virus 

       Family, Adult T-cell Leukaemia, and AIDS,  USA

       Hämatol. Blutransf. Vol 29  Science 1984;

       224(46-48) 500-503


[7]  Gallo R.C. et. al.. Human T-cell leukaemia-

       lymphoma virus (HTLV) is in T but not in B

       lymphocytes from a patient with  cutaneous T-cell

       lymphoma, Proc. Natl. Acad Sci USA, Medical

       Science, Vol. 79, pp. 5680-5683, September 1982


[9]  Gallo R.C. et. al.  NATURAL ANTIBODIES TO



       LYMPHOMAS   J: Exp. Med. The Rockefeller

       University Press  Volume 154 August 1981 333-346


[10]  Gallo R.C. et. al.  IN VITRO CELLULAR    


        VIRUS HUMAN HERPESVIRUS    J: Exp. Med.   

        The Rockefeller University Press, Volume 167 May

        1988 1659-1670


[11] Diepgen, T., Yihune, G. et al

        Dermatology Online Atlas


[12]  HIV Molecular Immunology 2006/2007

         Theoretical Biology and Biophysics Group T-10,     

         Mail Stop K710

         Los Alamos National Laboratory, Los Alamos,

         New  Mexico 87545 U.S.A.


[13]  Gallo R.C. et. al. Detection and isolation of type C

         retrovirus particles from fresh and cultured

         lymphocytes of a patient with cutaneous T-cell



[14]  Gallo R.C. et. al. Detection,  isolation and

         continuous production of cytopathic retroviruses

         (HTLV-III) from patients with AIDS and Pre-AIDS

         Science, VOL. 224, April 1984


[15] Gallo R.C. et. al. Serological Analysis of a

        Subgroup of Human T-Lymphotropic Retroviruses

        (HTLV-III) Associated with AIDS

        Science, VOL. 224, April 1984


[16] Fenyö E.M., Äsjö B. Growth of  the  (HTLV-III)

        Strain of the Human Immunodeficiency Virus in

        Different Cell Types

        Haematology and Blood Transfusion Vol. 31


[17] Gallo R.C. et. al. Expression of cellular

        homologues of retroviral onc genes in human 

        haematopoietic cells

        Proc. Natl. Acad Sci USA, Medical Science,

        Vol.79, pp. 2490-2494, April 1982


[18] Gallo R.C. et. al. Growth of Macrophage-Tropic  

        and Primary Human Immunodeficiency Virus

        Type 1 (HIV-1) Isolates in a Unique CD4+ T-cell  

        Clone (PM1): Failure To Downregulate CD4 and

        To Interfere with CD4-Line-Tropic HIV1

         Journal of Virology, June 1995, p. 3712-3720








                       HIV B-Cell-Kaposi sarcoma





                                              Fig. 6  HIV- B-Cell Kaposi sarcoma [11]





                         Fig. 7  HIV- B-Cell -Kaposi sarcoma [111





                      Fig.8  HIV- B-Cell- Kaposi sarcoma [11]









                                                                     Fig. 9   HIV Virus Genom





                                                       Fig. 10  HIV- Epitope – mass spectra [12]