Chesebro B, Wehrly K, Doig D, Nishio J
Proc Natl Acad Sci U S A. 1979 Nov;76(11):5784-8. doi: 10.1073/pnas.76.11.5784.
The Rfv-3 gene was found to influence the level of Friend leukemia virus production in spleens of leukemic mice later than 30 days after virus inoculation. Rfv-3r/s mice [(B10.A X A)F1 and (B10.A X A.BY)F1] had decreased spleen virus levels 30-90 days after virus inoculation compared to Rfv-3s/s mice [A.BY, A, BALB.B, and (BALB/c X A)F1)]. In (B10.A X A)F1 X A backcross mice the spleen virus titer segregated with the level of viremia. The Rfv-3 gene appeared to act by controlling anti-Friend virus antibody production. The interaction of antiviral antibody with infected cells led to a decrease in release of infectious virus by late leukemic spleen cells in Rfv-3r/s mice to 1/300th that in Rfv-3s/s mice. This decrease in virus release appeared to be due to interference with the virus budding process due to antibody-mediated modulation of virus-induced cell surface antigens.
研究发现,Rfv - 3基因对白血病小鼠脾脏中Friend白血病病毒产生水平的影响发生在病毒接种30天后。与Rfv - 3s/s小鼠(A.BY、A、BALB.B以及(BALB/c×A)F1)相比,Rfv - 3r/s小鼠((B10.A×A)F1和(B10.A×A.BY)F1)在病毒接种30 - 90天后脾脏病毒水平降低。在(B10.A×A)F1×A回交小鼠中,脾脏病毒滴度与病毒血症水平相关。Rfv - 3基因似乎通过控制抗Friend病毒抗体的产生发挥作用。抗病毒抗体与受感染细胞的相互作用导致Rfv - 3r/s小鼠晚期白血病脾脏细胞释放的感染性病毒减少至Rfv - 3s/s小鼠的1/300。病毒释放的这种减少似乎是由于抗体介导的病毒诱导细胞表面抗原调节干扰了病毒出芽过程。