CHARACTERIZATION OF THE INFECTION OF AEDES-ALBOPICTUS CELL CLONES BY SINDBIS-VIRUS

Citation
Ar. Karpf et al., CHARACTERIZATION OF THE INFECTION OF AEDES-ALBOPICTUS CELL CLONES BY SINDBIS-VIRUS, Virus research, 50(1), 1997, pp. 1-13
Citations number
27
Categorie Soggetti
Virology
Journal title
ISSN journal
01681702
Volume
50
Issue
1
Year of publication
1997
Pages
1 - 13
Database
ISI
SICI code
0168-1702(1997)50:1<1:COTIOA>2.0.ZU;2-K
Abstract
We have investigated the infection of Aedes albopictus (mosquito) cell clones by Sindbis virus. Variation in the multiplicity of infection ( MOI) from ranges of 50-0.00005 pfu/cell was determined to have no effe ct on the progression of the infection to high acute phase titer, sugg esting that intracellular factors alone are responsible for the restri ction of virus production seen as the infection enters the persistent phase. While persistently infected (over 1 year post infection) cell c lones are morphologically indistinct from uninfected cells, they do di splay a uniform 30% reduction in growth rate compared with uninfected cells of the same clone. Using flow cytometry-based DNA content analys is, we found that persistent Sindbis virus infection induces distinct cytological effects on these cells, including an increase in apoptosis and polyploidy in one clone and cell cycle phase effects in another. Finally, the observation that the number of cells in persistently infe cted cell cultures which are productively infected closely approximate s the number of cells dying by apoptosis prompted us to investigate th e role that cell death may play in the maintenance of the persistent i nfection. Persistently infected cell cultures which were artificially induced into apoptosis by short 45 degrees C heat treatments do not di splay increased Sindbis virus production. This result does not support the hypothesis that infection sensitivity induced by random apoptosis in persistently infected cell cultures is responsible for the long-te rm maintenance of the persistent infection. (C) 1997 Elsevier Science B.V.