Effects of double combinations of enterovirus replication inhibitors against Coxsackie B viruses

2022 ◽  
Vol 65 (04) ◽  
pp. 411-419
Author(s):  
Adelina Stoyanova ◽  
Angel S. Galabov
1963 ◽  
Vol 12 (1) ◽  
pp. 29-41 ◽  
Author(s):  
Reinhard Wigand ◽  
Albert B. Sabin

1982 ◽  
Vol 101 (4) ◽  
pp. 647-648 ◽  
Author(s):  
C.S. Bartsocas ◽  
C.J. Papadatos ◽  
M. Lab ◽  
N. Spyrou ◽  
B. Krikelis ◽  
...  

2004 ◽  
Vol 78 (6) ◽  
pp. 2948-2955 ◽  
Author(s):  
M. Steven Oberste ◽  
Silvia Peñaranda ◽  
Mark A. Pallansch

ABSTRACT RNA recombination has been shown to occur during circulation of enteroviruses, but most studies have focused on poliovirus. To examine the role of recombination in the evolution of the coxsackie B viruses (CVB), we determined the partial sequences of four genomic intervals for multiple clinical isolates of each of the six CVB serotypes isolated from 1970 to 1996. The regions sequenced were the 5′-nontranslated region (5′-NTR) (350 nucleotides [nt]), capsid (VP4-VP2, 416 nt, and VP1, ∼320 nt), and polymerase (3D, 491 nt). Phylogenetic trees were constructed for each genome region, using the clinical isolate sequences and those of the prototype strains of all 65 enterovirus serotypes. The partial VP1 sequences of each CVB serotype were monophyletic with respect to serotype, as were the VP4-VP2 sequences, in agreement with previously published studies. In some cases, however, incongruent tree topologies suggested that intraserotypic recombination had occurred between the sequenced portions of VP2 and VP1. Outside the capsid region, however, isolates of the same serotype were not monophyletic, indicating that recombination had occurred between the 5′-NTR and capsid, the capsid and 3D, or both. Almost all clinical isolates were recombinant relative to the prototype strain of the same serotype. All of the recombination partners appear to be members of human enterovirus species B. These results suggest that recombination is a frequent event during enterovirus evolution but that there are genetic restrictions that may influence recombinational compatibility.


1978 ◽  
Vol 86 (5) ◽  
pp. 1493-1496
Author(s):  
Ya. E. Khesin ◽  
A. M. Amchenkova ◽  
N. E. Gulevich ◽  
A. N. Narovlyanskii

2000 ◽  
Vol 181 (1) ◽  
pp. 340-343 ◽  
Author(s):  
O. Brad Spiller ◽  
Ian G. Goodfellow ◽  
David J. Evans ◽  
Jeffrey W. Almond ◽  
B. Paul Morgan

2004 ◽  
Vol 74 (2) ◽  
pp. 291-299 ◽  
Author(s):  
George Orthopoulos ◽  
Kathy Triantafilou ◽  
Martha Triantafilou

1989 ◽  
Vol 3 (2) ◽  
pp. 103-108 ◽  
Author(s):  
Marianne Alksnis ◽  
Michael Lindberg ◽  
Per Stålhandske ◽  
Hans Hultberg ◽  
Ulf Pettersson

2009 ◽  
Vol 84 (1) ◽  
pp. 254-260 ◽  
Author(s):  
Jennifer P. Wang ◽  
Anna Cerny ◽  
Damon R. Asher ◽  
Evelyn A. Kurt-Jones ◽  
Roderick T. Bronson ◽  
...  

ABSTRACT Coxsackie B viruses (CVB) are enteroviruses that have been associated with a variety of human diseases, including myocarditis. In the present study, we found that MDA5 and its adaptor molecule MAVS are critical for type I interferon responses to CVB, since the absence of either MAVS or MDA5 leads to deficient type I interferon production and early mortality in mice infected with CVB. Pancreatic and hepatic necrosis were observed on histopathological examination of MAVS and MDA5 knockout mice infected with CVB. Inflammatory cytokine production in response to systemic CVB infection was independent of MAVS. Surprisingly, virus titers were not elevated in MAVS-deficient mice, despite significant reductions in type I interferon levels. These data highlight the importance of type I interferon in host defense and provide insight on the mechanisms of innate immune responses following coxsackievirus infection.


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