scholarly journals Evaluation of Factors Related to Growth of Rift Valley Fever Virus in Suspended Cell Cultures

1969 ◽  
Author(s):  
Jerry S. Walker ◽  
Richard C. Carter ◽  
Frederick Klein ◽  
Shirley E. Snowden ◽  
Ralph E. Lincoln
1969 ◽  
Vol 17 (5) ◽  
pp. 658-664 ◽  
Author(s):  
Jerry S. Walker ◽  
Richard C. Carter ◽  
Frederick Klein ◽  
Shirley E. Snowden ◽  
Ralph E. Lincoln

1969 ◽  
Vol 17 (5) ◽  
pp. 658-664
Author(s):  
Jerry S. Walker ◽  
Richard C. Carter ◽  
Frederick Klein ◽  
Shirley E. Snowden ◽  
Ralph E. Lincoln

2019 ◽  
Author(s):  
Belén Borrego ◽  
Ana I. de Ávila ◽  
Esteban Domingo ◽  
Alejandro Brun

ABSTRACTRift Valley fever virus (RVFV) is an emerging, mosquito-borne, zoonotic pathogen with recurrent outbreaks paying a considerable toll of human deaths in many African countries, for which no effective treatment is available. In cell culture studies and with laboratory animal models, the nucleoside analogue favipiravir (T-705) has demonstrated great potential for the treatment of several seasonal, chronic and emerging RNA virus infections of humans, suggesting applicability to control some viral outbreaks. Treatment with favipiravir was shown to reduce the infectivity of Rift Valley fever virus both in cell cultures and in experimental animal models, but the mechanism of this protective effect is not understood. In this work we show that favipiravir at concentrations well below the toxicity threshold estimated for cells is able to extinguish RVFV from infected cell cultures. Nucleotide sequence analysis has documented RVFV mutagenesis associated with virus extinction, with a significant increase in G to A and C to U transition frequencies, and a decrease of specific infectivity, hallmarks of lethal mutagenesis.


1988 ◽  
Vol 24 (2) ◽  
pp. 161-174 ◽  
Author(s):  
D. S. Ellis ◽  
P. V. Shirodaria ◽  
Elizabeth Fleming ◽  
D. I. H. Simpson

2019 ◽  
Vol 63 (8) ◽  
Author(s):  
Belén Borrego ◽  
Ana I. de Ávila ◽  
Esteban Domingo ◽  
Alejandro Brun

ABSTRACT Rift Valley fever virus (RVFV) is an emerging, mosquito-borne, zoonotic pathogen with recurrent outbreaks taking a considerable toll in human deaths in many African countries, for which no effective treatment is available. In cell culture studies and with laboratory animal models, the nucleoside analogue favipiravir (T-705) has demonstrated great potential for the treatment of several seasonal, chronic, and emerging RNA virus infections in humans, suggesting applicability to control some viral outbreaks. Treatment with favipiravir was shown to reduce the infectivity of Rift Valley fever virus both in cell cultures and in experimental animal models, but the mechanism of this protective effect is not understood. In this work, we show that favipiravir at concentrations well below the toxicity threshold estimated for cells is able to extinguish RVFV from infected cell cultures. Nucleotide sequence analysis has documented RVFV mutagenesis associated with virus extinction, with a significant increase in G to A and C to U transition frequencies and a decrease of specific infectivity, hallmarks of lethal mutagenesis.


1950 ◽  
Vol 5 (5) ◽  
pp. 243-247
Author(s):  
Minoru MATSUMOTO ◽  
Saburo IWASA ◽  
Motosige ENDO

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