scholarly journals Hematopoietic Cancer Cell Lines Can Support Replication of Sabin Poliovirus Type 1

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Dinja Oosterhoff ◽  
Gerard van de Weerd ◽  
Gerco van Eikenhorst ◽  
Tanja D. de Gruijl ◽  
Leo A. van der Pol ◽  
...  

Viral vaccines can be produced in adherent or in suspension cells. The objective of this work was to screen human suspension cell lines for the capacity to support viral replication. As the first step, it was investigated whether poliovirus can replicate in such cell lines. Sabin poliovirus type 1 was serially passaged on five human cell lines, HL60, K562, KG1, THP-1, and U937. Sabin type 1 was capable of efficiently replicating in three cell lines (K562, KG1, and U937), yielding high viral titers after replication. Expression of CD155, the poliovirus receptor, did not explain susceptibility to replication, since all cell lines expressed CD155. Furthermore, we showed that passaged virus replicated more efficiently than parental virus in KG1 cells, yielding higher virus titers in the supernatant early after infection. Infection of cell lines at an MOI of 0.01 resulted in high viral titers in the supernatant at day 4. Infection of K562 with passaged Sabin type 1 in a bioreactor system yielded high viral titers in the supernatant. Altogether, these data suggest that K562, KG1, and U937 cell lines are useful for propagation of poliovirus.

2003 ◽  
Vol 77 (11) ◽  
pp. 6541-6545 ◽  
Author(s):  
Hein J. Boot ◽  
Daniella T. J. Kasteel ◽  
Anne-Marie Buisman ◽  
Tjeerd G. Kimman

ABSTRACT The emergence of circulating vaccine-derived poliovirus (cVDPV) strains in suboptimally vaccinated populations is a serious threat to the global poliovirus eradication. The genetic determinants for the transmissibility phenotype of polioviruses, and in particularly of cVDPV strains, are currently unknown. Here we describe the fecal excretion of wild-type poliovirus, oral polio vaccine, and cVDPV (Hispaniola) strains after intraperitoneal injection in poliovirus receptor-transgenic mice. Both the pattern and the level of fecal excretion of the cVDPV strains resemble those of wild-type poliovirus type 1. In contrast, very little poliovirus was present in the feces after oral polio vaccine administration. This mouse model will be helpful in elucidating the genetic determinants for the high fecal-oral transmission phenotype of cVDPV strains.


2009 ◽  
Vol 139 (1) ◽  
pp. 22-31 ◽  
Author(s):  
Isabel Olivares ◽  
Alicia Ballester ◽  
Luis Lombardia ◽  
Orlando Dominguez ◽  
Cecilio López-Galíndez

1977 ◽  
Vol 23 (3) ◽  
pp. 811-815 ◽  
Author(s):  
J B Milstien ◽  
J R Walker ◽  
L J Eron

Author(s):  
Youfeng Yang ◽  
Christopher J. Ricketts ◽  
Cathy D. Vocke ◽  
J. Keith Killian ◽  
Hesed M. Padilla‐Nash ◽  
...  

Virology ◽  
1984 ◽  
Vol 139 (2) ◽  
pp. 403-407 ◽  
Author(s):  
Christine Bellocq ◽  
Henri Agut ◽  
Sylvie Van Der Werf ◽  
Marc Girard

2001 ◽  
Vol 75 (17) ◽  
pp. 7944-7955 ◽  
Author(s):  
Noriko Nakajima ◽  
Richard Lu ◽  
Alan Engelman

ABSTRACT Functional retroviral integrase protein is thought to be essential for productive viral replication. Yet, previous studies differed on the extent to which integrase mutant viruses expressed human immunodeficiency virus type 1 (HIV-1) genes from unintegrated DNA. Although one reason for this difference was that class II integrase mutations pleiotropically affected the viral life cycle, another reason apparently depended on the identity of the infected cell. Here, we analyzed integrase mutant viral infectivities in a variety of cell types. Single-round infectivity of class I integration-specific mutant HIV-1 ranged from <0.03 to 0.3% of that of the wild type (WT) across four different T-cell lines. Based on this approximately 10-fold influence of cell type on mutant gene expression, we examined class I and class II mutant replication kinetics in seven different cell lines and two primary cell types. Unexpectedly, some cell lines supported productive class I mutant viral replication under conditions that restricted class II mutant growth. Cells were defined as permissive, semipermissive, or nonpermissive based on their ability to support the continual passage of class I integration-defective HIV-1. Mutant infectivity in semipermissive and permissive cells as quantified by 50% tissue culture infectious doses, however, was only 0.0006 to 0.005% of that of WT. Since the frequencies of mutant DNA recombination in these lines ranged from 0.023 to <0.093% of the WT, we conclude that productive replication in the absence of integrase function most likely required the illegitimate integration of HIV-1 into host chromosomes by cellular DNA recombination enzymes.


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