Echoviruses and Coxsackie B Viruses That Use Human Decay‐Accelerating Factor (DAF) as a Receptor Do Not Bind the Rodent Analogues of DAF

2000 ◽  
Vol 181 (1) ◽  
pp. 340-343 ◽  
Author(s):  
O. Brad Spiller ◽  
Ian G. Goodfellow ◽  
David J. Evans ◽  
Jeffrey W. Almond ◽  
B. Paul Morgan
2005 ◽  
Vol 79 (1) ◽  
pp. 655-660 ◽  
Author(s):  
Aaron M. Milstone ◽  
JenniElizabeth Petrella ◽  
Melissa D. Sanchez ◽  
Mariam Mahmud ◽  
J. Charles Whitbeck ◽  
...  

ABSTRACT Although many coxsackie B viruses interact with decay accelerating factor (DAF), attachment to DAF by itself is not sufficient to initiate infection. We examined the early events in infection that follow virus interaction with DAF, and with the coxsackievirus and adenovirus receptor (CAR). Interaction with soluble CAR in a cell-free system, or with CAR on the surfaces of transfected cells, induced the formation of A particles; interaction with soluble or cell surface DAF did not. The results suggest that CAR, but not DAF, is capable of initiating the conformational changes in the viral capsid that lead to release of viral nucleic acid.


2002 ◽  
Vol 83 (1) ◽  
pp. 45-52 ◽  
Author(s):  
O. Brad Spiller ◽  
Ian G. Goodfellow ◽  
David J. Evans ◽  
Stewart J. Hinchliffe ◽  
B. Paul Morgan

Coxsackie B viruses (CVB) are enteroviruses belonging to the family Picornaviridae. Serotypes 1, 3 and 5 of CVB bind to the human membrane complement regulator decay-accelerating factor (DAF) and the coxsackievirus/adenovirus receptor (CAR), using either or both as receptors. These viruses are known to infect pig cell lines, but the receptor(s) involved has not been identified. We have recently characterized the pig homologue of DAF and here explore the interactions of human DAF-binding CVB with pig homologues of DAF and CAR. CVB infection of three pig cell lines resulted in cytolysis, which could be not be blocked by anti-pig DAF antibodies. CVB bound to CHO cells transfected with human DAF, but not pig DAF. Modification of pig DAF by incorporation of the fourth short consensus repeat of human DAF did not confer CVB-binding capacity. CVB did bind CHO cells expressing pig or human CAR, and pre-incubation of pig cells with anti-CAR antibody blocked CVB infection.


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

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

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