Cytopathic feline leukemia viruses cause apoptosis in hemolymphatic cells.
Prog Mol Subcell Biol
; 16: 13-43, 1996.
Article
em En
| MEDLINE
| ID: mdl-8822790
ABSTRACT
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 glucoprotein 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 thymico-lymphoid 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.
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Base de dados:
MEDLINE
Assunto principal:
Infecções Tumorais por Vírus
/
Linfócitos
/
Apoptose
/
Vírus da Leucemia Felina
/
Infecções por Retroviridae
Idioma:
En
Ano de publicação:
1996
Tipo de documento:
Article