Publications by Year: 1981

Wolf JL, Rubin DH, Finberg R, Kauffman RS, Sharpe AH, Trier JS, Fields BN. Intestinal M cells: a pathway for entry of reovirus into the host. Science. 1981;212 (4493) :471-2.Abstract
Thirty minutes after inoculation of reovirus type 1 into the intestinal lumen of the mouse, viruses were found adhering to the surface of intestinal M cells but not other epithelial cells. Within 1 hour, viruses were seen in the M cell cytoplasm and were associated with mononuclear cells in the intercellular space adjacent to the M cell. These findings suggest that M cells are the site where reovirus penetrates the intestinal epithelium.
Sharpe AH, Fields BN. Reovirus inhibition of cellular DNA synthesis: role of the S1 gene. J Virol. 1981;38 (1) :389-92.Abstract
Type 3 reovirus inhibits L cell DNA synthesis, whereas type 1 reovirus exerts little or no effect on L cell DNA synthesis. By using recombinant viruses containing both type 1 and type 3 double-standard RNA segments, we determined that one double-stranded RNA segment, the reovirus type 3 S1 double-stranded RNA segment which encodes the viral hemagglutinin, segregates with and is responsible for the capacity of reovirus type 3 to inhibit L cell DNA synthesis.
Ahmed R, Canning WM, Kauffman RS, Sharpe AH, Hallum JV, Fields BN. Role of the host cell in persistent viral infection: coevolution of L cells and reovoirus during persistent infection. Cell. 1981;25 (2) :325-32.Abstract
Mutant L cells, designated LR cells, were isolated after "curing" a persistently infected cell line (L/C) with antireovirus serum. The LR cells were shown to be virus-free; no reovirus was detectable by infectious center assays, plaque assays, presence of viral proteins, presence of viral dsRNA and immunofluorescence studies. Persistent infections were readily established n LR cells following infection with either cloned, low passage wild-type reovirus or cloned, low passage reovirus isolated from carrier cultures. Reovirus isolated from carrier cultures, however, grew much better than wild-type reovirus in LR cells and showed complete dominance over wild-type reovirus in coinfection experiments. Infection of LR cells with wild-type reovirus resulted in a low-level persistent infection with inefficient viral replication; these mutant L cells were partially resistant to infection with wild-type reovirus. In contrast, infection of the mutant L cells with virus isolated from the persistently infected cells resulted in a persistent infection accompanied with efficient viral replication. Infection of the original L cells with either wild-type reovirus or reovirus isolated from the persistently infected cells resulted in a lytic infection with no surviving cells. Thus the host cell plays a crucial role in the maintenance of persistent reovirus infection. Our results show that there is a coevolution of both mutant L cells and mutant reovirus during persistent infection.