Virus infections with Herpes or HIV are inhibited significantly by Invasivol in cell culture. But in AIDS, the compound does not reduce the number of free HIV in the body. (Unpublished by A-Viral).
The HIV infection, however, is special since during many years T-cells infected with defective HIV are piling up. The inaccuracy of the enzyme reverse transcriptase is the reason since some HIV becomes defective and can’t kill the host cell. After some years the accumulation causes increased production of active HIV as the effect of the assumed natural clone inhibitors are increasingly depressed by the accumulated cells with defective virus.
This can’t be detected in HIV-infected cell cultures since the accumulation of cells with defective virus takes several years before sufficient quantities of such cells are created for transforming infection into AIDS. No cell cultures can be followed that long.
If this mechanism of the increase of the production of intact HIV is true, it should be possible to affect the infection favorably by Invasivol before the piling up of these cells with defective virus. Then it is possible that Invasivol will inhibit the production of active HIV so strongly that production of HIV stops and the infection may burn out. This would be sensational, however, for as I know this has not happened before.
Also a reduction of the number of these accumulated cells may possibly induce a positive effect with or without Invasivol. A simple reduction of the number of these cells containing inactive HIV may put the disease back to a stage before AIDS was developed. The greater reduction of these cells, the grater the shift will be of the stage of the disease.
A reduced production of HIV in T-cells seems to last for a few years after the infection. But then the production of active HIV gradually tends to increase. The final phase of the AIDS disease starts when the structure of the lymph nodes breaks down and leads to total immune deficiency. What then fails are probably the follicular dendritic cells, the skeleton of the lymph nodes. The failure may be caused by the increased production of HIV. That changes the identity of the majority of the follicular dendritic cells by either absorbing HIV or infecting the follicular dendritic cells. Then the assumed specific clone inhibitors will eventually inhibit the normal cells more than the virus-infected ones. This may induce an accelerating destruction of the lymphatic structure in the last stage of AIDS.
At a possible HIV infection, the size of the infection is probably of importance since surgeons who were hurt by an infected needle often escape being infected. This may be analogous to the results of transplantation of a malignant tumor in animals. Transplantation of a too low tumor cell number will not catch on either. These observations may both indicate that there is a natural factor in the body that specifically inhibits the metabolism and growth of sparsely distributed clones of tumor cells or virus infected cells. As mentioned before, this compound is less effective than Invasivol.
Recently infected persons need special attention since they probably have no cells containing defective HIV that may interfere with the effect of Invasivol. Therefore, HIV particle counts in blood from these patients would be particularly interesting during combined treatment with conventional anti-HIV drugs and Invasivol.
If it becomes difficult to get rid of the accumulation of immune cells infected with inactive HIV in individuals with AIDS, it may be possible if the marrow is destructed together with the peripheral immune system and new bone marrow is transplanted. Since it is hardly possible to get rid of the infection by this procedure, the same marrow could be transplanted back.
process, however, may be dangerous, especially if there are other active
infections. But after a successful bone marrow transplant, the HIV infection
would probably start again from scratch.
If the goal is eradication of HIV, one can hope that treatment that includes Invasivol may remove the last remnants. But it will not be achieved if cells containing defective HIV remain in collocations big enough to protect the replication of active HIV in the same area. However, such a failure will not become complete since the infection may need years before reaching the stage of AIDS again.
A significant reduction of the number of piled up cells with defective HIV, may increase the time period needed for the development of AIDS. If Invasivol is included in the treatment, the possibility of developing drug resistant HIV clones is expected to be significantly reduced.
In Herpes infection of the lip, Invasivol in Vaseline applied onto the eruption in a preliminary study, reduced the number of attacks from 3-4 in a year to only one eruption in about three years.
Also in oncology Invasivol is expected to significantly reducing the possibility of getting resistant tumor cell clones when administered together with cytotoxic drugs.
Invasivol was tried on patients with AIDS in Manila in the Philippines, but did not reduce viral production in the body in these patients. The result was unexpected and incomprehensible at that time since Invasivol was effective in cell culture.
Later after having tried Invasivol against transplanted cancer in mice and against Herpes the real mechanism was probably found.
Anti-HIV medication, e.g. HAART, usually helps patients. Resistance, however, may occur. When stopping the treatment the production of HIV increases immediately. Therefore, HAART seems to mask the stage that the disease really is in. It is possible that the described reduction in cells containing defective HIV and adding Invasivol to the treatment will change this.
New HIV infection or new exposure to HIV infection, probably need Invasivol combined with conventional drug combinations. That is expected to give a higher threshold before the exposure to HIV leads to infection or may be; termination of a recently established infection.