Cytopathic feline leukemia viruses cause apoptosis in hemolymphatic cells.
Cytopathic feline leukemia viruses cause apoptosis in hemolymphatic cells.
复制标题
细胞病变猫白血病病毒导致血淋巴细胞凋亡。
DOI:
10.1007/978-3-642-79850-4_2
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发表时间:
1996
期刊:
影响因子:
--
通讯作者:
Neil,JC
中科院分区:
文献类型:
--
作者:
Rojko,JL;Hartke,JR;Cheney,CM;Phipps,AJ;Neil,JC
Certain isolates of the oncoretrovirus feline leukemia virus (FeLV) are strongly cytopathic for hemolymphatic cells. A major cytopathicity determinant is encoded by the SU envelope glycoprotein gp70. Isolates with subgroup C SU gp70 genes specifically induce apoptosis in hemolymphatic cells but not fibroblasts. In vitro exposure of feline T-cells to FeLV-C leads first to productive viral replication, next to virus-induced cell agglutination, and lastly to apogenesis. This in vitro phenomenon may explain the severe progressive thymic atrophy and erythroid aplasia which follow viremic FeLV-C infection in vivo. Inappropriate apoptosis induction has also been hypothesized to explain the severe thymicolymphoid atrophy and progressive immune deterioration associated with isolates of FeLV containing variant envelope genes. The influence of envelope hypervariability (variable regions 1 [Vr1] and 5 [Vr5] on virus tropism, viremia induction, neutralizing antibody development and cytopathicity is discussed. Certain potentially cytopathic elements in FeLV SU gp70 Vr5 may derive from replication-defective, poorly expressed, endogenous FeLVs. Other more highly conserved regions in FeLV TM envelope p15E may also influence apoptosis induction.