Virus Infections
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 (Unpublished by A-Viral).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.
This
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.