Hueffer Karsten, Govindasamy Lakshman, Agbandje-McKenna Mavis, Parrish Colin R
James A. Baker Institute, Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
J Virol. 2003 Sep;77(18):10099-105. doi: 10.1128/jvi.77.18.10099-10105.2003.
Feline panleukopenia virus (FPV) and its host range variant, canine parvovirus (CPV), can bind the feline transferrin receptor (TfR), while only CPV binds to the canine TfR. Introducing two CPV-specific changes into FPV (at VP2 residues 93 and 323) endowed that virus with the canine TfR binding property and allowed canine cell infection, although neither change alone altered either property. In CPV the reciprocal changes of VP2 residue 93 or 323 to the FPV sequences individually resulted in modest reductions in infectivity for canine cells. Changing both residues in CPV to the FPV amino acids blocked the canine cell infection, but that virus was still able to bind the canine TfR at low levels. This shows that both CPV-specific changes control canine TfR binding but that binding is not always sufficient to mediate infection.
猫泛白细胞减少症病毒(FPV)及其宿主范围变体犬细小病毒(CPV)能够结合猫转铁蛋白受体(TfR),而只有CPV能与犬TfR结合。在FPV的VP2残基93和323处引入两个CPV特异性变化,赋予了该病毒与犬TfR结合的特性,并使其能够感染犬细胞,尽管单独一个变化都不会改变这两种特性。在CPV中,将VP2残基93或323分别替换为FPV序列,会导致对犬细胞的感染性适度降低。将CPV中的这两个残基都替换为FPV的氨基酸会阻断对犬细胞的感染,但该病毒仍能够低水平结合犬TfR。这表明CPV的这两个特异性变化都控制着与犬TfR的结合,但结合并不总是足以介导感染。