Buesa-Gomez J, Teng M N, Oldstone C E, Oldstone M B, de la Torre J C
Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 92037, USA.
J Virol. 1996 Dec;70(12):8988-92. doi: 10.1128/JVI.70.12.8988-8992.1996.
Persistent infection of C3H/St mice with lymphocytic choriomeningitis virus (LCMV) strain Armstrong leads to disordered growth and hypoglycemia. Both host and viral determinants contribute to this growth hormone (GH) deficiency syndrome (GHDS). Development of the GHDS correlates with the virus's ability to replicate in the GH-producing cells and cause reduced levels of GH synthesis. LCMV strain WE infects few GH-producing cells and does not cause GHDS in C3H/St mice. We show here that clonal variants isolated from the GHDS-nil WE population are able to replicate at high levels in GH-producing cells and cause GHDS in C3H/St mice. These variants are stably maintained, but phenotypically silent, within the GHDS-nil WE population.
用淋巴细胞性脉络丛脑膜炎病毒(LCMV)阿姆斯特朗株持续感染C3H/St小鼠会导致生长紊乱和低血糖。宿主和病毒决定因素都导致了这种生长激素(GH)缺乏综合征(GHDS)。GHDS的发展与病毒在产生GH的细胞中复制的能力以及导致GH合成水平降低有关。LCMV株WE感染很少产生GH的细胞,并且不会在C3H/St小鼠中引起GHDS。我们在此表明,从无GHDS的WE群体中分离出的克隆变体能够在产生GH的细胞中高水平复制,并在C3H/St小鼠中引起GHDS。这些变体在无GHDS的WE群体中稳定维持,但表型沉默。