D. Hamamdzic et al., Reovirus triggers cell type-specific proinflammatory responses dependent on the autocrine action of IFN-beta, AM J P-LUNG, 280(1), 2001, pp. L18-L29
Citations number
59
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Resident cells of the respiratory and gastrointestinal tracts, including ep
ithelial and fibroblast cells, are the initial sites of entry for many vira
l pathogens. We investigated the role that these cells play in the inflamma
tory process in response to infection with reovirus 1/L. In A549 human bron
chial or HT-29 human colonic epithelial cells, interferon (IFN)-beta, regul
ated on activation T cell expressed and secreted (RANTES), IFN-gamma -induc
ible protein (IP)-10, and interleukin-8 were upregulated regardless of whet
her cells were infected with replication-competent or replication-deficient
reovirus 1/L. However, in CCD-34Lu human lung fibroblast cells, IFN-beta,
IP-10, and RANTES were expressed only after infection with replication-comp
etent reovirus 1/L. Expression of interleukin-8 in CCD-34Lu fibroblast cell
s was viral replication independent. This differential expression of IFN-be
ta, RANTES, and IP-10 was shown to be due to the lack of induction of IFN r
egulatory factor-1 and -2 in CCD-34Lu fibroblast cells treated with replica
tion-deficient reovirus 1/L. We have shown that cytokine and/or chemokine e
xpression may not be dependent on viral replication. Therefore, treatment o
f viral infections with inhibitors of replication may not effectively allev
iate inflammatory mediators because most viral infections result in the gen
eration of replication-competent and replication-deficient virions in vivo.