excellent find by forum member Impish on another thread that may relate to our thread. here is the other thread:
http://www.forums.aboutmecfs.org/sh...ng-for-MuLV-s-and-how-they-cured-them-in-mice...
and this is me summarizing Impish's notes from the above thread.
this paper looks helpful: "Search for oncogenic retroviruses in wild mice and man: Historical reflections"
http://www.cancer-therapy.org/CT6A/HTML/31._Gardner,_285-302.html
in this paper:
- they mentioned the spleen as a "virus factory" which suggests a place to look for MuLV in humans.
- They also mention using immunoglobulin as a suggested treatment (for mice)
- mentions that anti-retroviral's worked to protect mice from the CNS disease associated with MuLV's.
- MuLV's cause a CNS disease in mice suggest that they are on the right track with MuLV's = CFS.
- The fact that anti-retroviral's worked in mice again provides an animal model backing up what has been observed in humans taking them. Obviously it will be interesting to see what strains are affected.
- in the article that they found MuLV's in clusters (like CFS).
- They found that some mice don't get MuLV due to genetics.
- Since we know what gene's protect mice we should be able to look for similar gene's (or the lack thereof) in humans and relatives with CFS. That would provide absolute proof (IMHO) that MuLV's are causing CFS.
Quote from the paper: "Contrary to expectations based on the AKR mouse model, control of MuLV and prevention of lymphoma and paralytic disease in the high MuLV expressor LC mice was dramatically accomplished, as mentioned above, by foster nursing on virus-free NIH Swiss mothers (Gardner et al, 1979). Surgical removal of the spleen, the “virus factory” early in life, lowered the virus burden sufficiently to prevent the CNS disease completely and markedly reduced the incidence of lymphoma. Passive immunization of newborn LC mice with goat immunoglobulin, having a high neutralization titer to ecotropic virus and a low titer to amphotropic virus, completely prevented the paralytic diseases but only slightly lowered the incidence of lymphoma (Gardner et al, 1980b). Active immunization with inactivated LC MuLV had no effect, of course, in already infected immune tolerant LC mice, although they responded well to a heterologous MuLV vaccine and other foreign antigens (Klement, 1976). A decade later, the beneficial effect of transplacental anti-retroviral therapy with azidothymidine was shown in lab mice that were protected against the CNS disease after inoculation with LC ecotropic MuLV during mid-gestation or at birth (Sharpe et al, 1987). This is the first example of successful antiviral therapy for congenitally transmitted retrovirus. Finally, selective breeding could strongly suppress LC-MuLV. Because the MuLV of LC and other wild mice is N-tropic, i.e. grows preferentially in NIH Swiss mouse cells, and not in BALB-C mouse cells (B-tropic), introduction of the FV-1B virus resistance gene from C57 BL-10 inbred mice completely blocked LC MuLV expression in the F-1 hybrids (Gardner et al, 1976b)"
so that means that if we can get stem cells from someone with FV-1B virus resistant gene, we may be able to block some of the MuLV? would this be like blocking the CCR5 gene in HIV patients?
http://www.forums.aboutmecfs.org/sh...ng-for-MuLV-s-and-how-they-cured-them-in-mice...
and this is me summarizing Impish's notes from the above thread.
this paper looks helpful: "Search for oncogenic retroviruses in wild mice and man: Historical reflections"
http://www.cancer-therapy.org/CT6A/HTML/31._Gardner,_285-302.html
in this paper:
- they mentioned the spleen as a "virus factory" which suggests a place to look for MuLV in humans.
- They also mention using immunoglobulin as a suggested treatment (for mice)
- mentions that anti-retroviral's worked to protect mice from the CNS disease associated with MuLV's.
- MuLV's cause a CNS disease in mice suggest that they are on the right track with MuLV's = CFS.
- The fact that anti-retroviral's worked in mice again provides an animal model backing up what has been observed in humans taking them. Obviously it will be interesting to see what strains are affected.
- in the article that they found MuLV's in clusters (like CFS).
- They found that some mice don't get MuLV due to genetics.
- Since we know what gene's protect mice we should be able to look for similar gene's (or the lack thereof) in humans and relatives with CFS. That would provide absolute proof (IMHO) that MuLV's are causing CFS.
Quote from the paper: "Contrary to expectations based on the AKR mouse model, control of MuLV and prevention of lymphoma and paralytic disease in the high MuLV expressor LC mice was dramatically accomplished, as mentioned above, by foster nursing on virus-free NIH Swiss mothers (Gardner et al, 1979). Surgical removal of the spleen, the “virus factory” early in life, lowered the virus burden sufficiently to prevent the CNS disease completely and markedly reduced the incidence of lymphoma. Passive immunization of newborn LC mice with goat immunoglobulin, having a high neutralization titer to ecotropic virus and a low titer to amphotropic virus, completely prevented the paralytic diseases but only slightly lowered the incidence of lymphoma (Gardner et al, 1980b). Active immunization with inactivated LC MuLV had no effect, of course, in already infected immune tolerant LC mice, although they responded well to a heterologous MuLV vaccine and other foreign antigens (Klement, 1976). A decade later, the beneficial effect of transplacental anti-retroviral therapy with azidothymidine was shown in lab mice that were protected against the CNS disease after inoculation with LC ecotropic MuLV during mid-gestation or at birth (Sharpe et al, 1987). This is the first example of successful antiviral therapy for congenitally transmitted retrovirus. Finally, selective breeding could strongly suppress LC-MuLV. Because the MuLV of LC and other wild mice is N-tropic, i.e. grows preferentially in NIH Swiss mouse cells, and not in BALB-C mouse cells (B-tropic), introduction of the FV-1B virus resistance gene from C57 BL-10 inbred mice completely blocked LC MuLV expression in the F-1 hybrids (Gardner et al, 1976b)"
so that means that if we can get stem cells from someone with FV-1B virus resistant gene, we may be able to block some of the MuLV? would this be like blocking the CCR5 gene in HIV patients?
) to see where all that goes. Joey, your "eradication" thread has been interesting to read (at least from what my poor, burnt out brain has been able to glean from the posts in it.)