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But he reasoned that if he could remove enough H.I.V. genes to make it safe, the modified virus could work.
The modified virus was injected into mice with brain cancer, and it did bring about remission.
Cancer cells then produce their own version of the blocked protein, filling in the deficit and allowing the modified virus to thrive within cancerous tissue.
As it turned out, the modified virus was so crippled that it could only slow tumor growth.
While the modified virus can get the genes into egg DNA, he said, the problem is that the genes are usually silenced and inactive, so that they do not direct cells to make proteins.
This allows the modified virus to circulate for longer in a patient's blood stream and thus have a better chance of getting to tumours disseminated around the body.
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When a droplet of blood from a patient is mixed with the modified viruses, any antibodies they have latch on to human virus proteins they recognise as invaders.
Pathogenicity tests indicated that all the modified viruses were highly attenuated in chickens.
The modified viruses grew like wild type TB4-wt even at the low MOI of 0.01.
In earlier constructions of Ad5 vectors with modified cellular tropism, we have observed that the deletion of the knob domain, compensated for by the insertion of a nonviral trimerisation motif, had deleterious effects on infectivity, growth rate and even viability of the modified viruses.
Cells infected with the parental vR26 virus were recognized by the two anti-E2 mAbs (WH211 and WH303) specific for the CSFV-E2 proteins, in contrast cells infected with the modified viruses vR26_TAV and vR26_E2gif, rescued from the recombined BACs, were not detected by these mAbs.
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