Impish
Senior Member
- Messages
- 101
- Location
- Victoria, BC
So far in the distant past it seems like someone did for looking for MuLV's in humans...
http://www.cancer-therapy.org/CT6A/HTML/31._Gardner,_285-302.html
Too bad they didn't find them then.
They did find how to cure them in mice:
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)
http://www.cancer-therapy.org/CT6A/HTML/31._Gardner,_285-302.html
Too bad they didn't find them then.
They did find how to cure them in mice:
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)
