scholarly journals Zinc-Binding of the Cysteine-Rich Domain Encoded in the Open Reading Frame 1B of the RNA Polymerase Gene of Coronavirus

Author(s):  
Dongwan Yoo ◽  
Michael D. Parker ◽  
Graham J. Cox ◽  
Lorne A. Babiuk
1996 ◽  
Vol 318 (2) ◽  
pp. 459-462 ◽  
Author(s):  
Norman McKIE ◽  
Donna J DALLAS ◽  
Tracy EDWARDS ◽  
Jane F APPERLEY ◽  
Graham G. RUSSELL ◽  
...  

We have isolated a novel cDNA from human myeloma cells encoding a member of the reprolysin family of metalloproteinases. Derived amino acid sequence predicts a protein of approx. 76 kDa. The open reading frame predicts the presence of a leader peptide, a pro-peptide with a ‘cysteine switch’, a metalloproteinase domain, a disintegrin-like domain, a cysteine-rich domain, an epidermal growth factor-like domain and a putative transmembrane sequence. Expression of the mRNA for this metalloproteinase has been demonstrated in human myeloma cells.


2020 ◽  
Vol 6 (2) ◽  
Author(s):  
Wen Wang ◽  
Xian-Dan Lin ◽  
Hai-Lin Zhang ◽  
Miao-Ruo Wang ◽  
Xiao-Qing Guan ◽  
...  

Abstract To better understand the genetic diversity, host associations and evolution of coronaviruses (CoVs) in China we analyzed a total of 696 rodents encompassing 16 different species sampled from Zhejiang and Yunnan provinces. Based on reverse transcriptase PCR-based CoV screening of fecal samples and subsequent sequence analysis of the RNA-dependent RNA polymerase gene, we identified CoVs in diverse rodent species, comprising Apodemus agrarius, Apodemus chevrieri, Apodemus latronum, Bandicota indica, Eothenomys cachinus, Eothenomys miletus, Rattus andamanensis, Rattus norvegicus, and Rattus tanezumi. CoVs were particularly commonplace in A. chevrieri, with a detection rate of 12.44 per cent (24/193). Genetic and phylogenetic analysis revealed the presence of three groups of CoVs carried by a range of rodents that were closely related to the Lucheng Rn rat CoV (LRNV), China Rattus CoV HKU24 (ChRCoV_HKU24), and Longquan Rl rat CoV (LRLV) identified previously. One newly identified A. chevrieri-associated virus closely related to LRNV lacked an NS2 gene. This virus had a similar genetic organization to AcCoV-JC34, recently discovered in the same rodent species in Yunnan, suggesting that it represents a new viral subtype. Notably, additional variants of LRNV were identified that contained putative non-structural (NS)2b genes located downstream of the NS2 gene that were likely derived from the host genome. Recombination events were also identified in the open reading frame (ORF) 1a gene of Lijiang-71. In sum, these data reveal the substantial genetic diversity and genomic complexity of rodent-borne CoVs, and extend our knowledge of these major wildlife virus reservoirs.


10.1038/9893 ◽  
1999 ◽  
Vol 17 (6) ◽  
pp. 583-587 ◽  
Author(s):  
Tadashi Mizuta ◽  
Masatoshi Fujiwara ◽  
Toshifumi Hatta ◽  
Takayuki Abe ◽  
Naoko Miyano-Kurosaki ◽  
...  

Author(s):  
Hitoshi Inada ◽  
Motoaki Seki ◽  
Hiromichi Morikawa ◽  
Mitsuo Nishimura ◽  
Koh Iba

2007 ◽  
Vol 53 (10) ◽  
pp. 1133-1140 ◽  
Author(s):  
Safaa Lamhoujeb ◽  
Hugues Charest ◽  
Ismail Fliss ◽  
Solange Ngazoa ◽  
Julie Jean

Noroviruses are recognized as the most common cause of nonbacterial gastroenteritis worldwide. In this study, we investigated the molecular epidemiology of noroviral isolates in Canada from 2004 to 2005 by sequencing the RNA polymerase gene and capsid N-terminal/shell (N/S) domain. Norovirus genogroups I and II were thus found to have co-circulated in Canada during the studied period, with a higher incidence of genogroup II (95.7%). The GII-4 or Lordsdale subgroup was the predominant genotype, suggesting that norovirus genogroup II is the major cause of viral gastroenteritis in Canada, as it is in many other countries. Phylogenetic analyses of the RNA polymerase gene and the capsid N/S domain indicated different genotypes for 2 strains, suggesting probable genetic recombination. Sequencing of the norovirus polymerase gene may reflect actual classification but should be supported by sequence information obtained from the capsid gene.


Virus Genes ◽  
2007 ◽  
Vol 35 (3) ◽  
pp. 681-684 ◽  
Author(s):  
Cintia Lopes de Brito Magalhães ◽  
Bárbara Resende Quinan ◽  
Renata Franco Vianna Novaes ◽  
João Rodrigues dos Santos ◽  
Erna Geessien Kroon ◽  
...  

2000 ◽  
Vol 74 (17) ◽  
pp. 7834-7841 ◽  
Author(s):  
Cheng Huang ◽  
Katsuhiro Kiyotani ◽  
Yutaka Fujii ◽  
Noriko Fukuhara ◽  
Atsushi Kato ◽  
...  

ABSTRACT The V protein of Sendai virus (SeV) is nonessential to virus replication in cell culture but indispensable to viral pathogenicity in mice. The highly conserved cysteine-rich zinc finger-like domain in its carboxyl terminus is believed to be responsible for this viral pathogenicity. In the present study, we showed that the cysteine-rich domain of the SeV V protein could actually bind zinc by using glutathione-S-transferase fusion proteins. When the seven conserved cysteine residues at positions 337, 341, 353, 355, 358, 362, and 365 were replaced individually, the zinc-binding capacities of the mutant proteins were greatly impaired, ranging from 22 to 68% of that of the wild type. We then recovered two mutant SeVs from cDNA, which have V-C341S and V-C365R mutations and represent maximal and minimal zinc-binding capacities among the corresponding mutant fusion proteins, respectively. The mutant viruses showed viral protein synthesis and growth patterns similar to those of wild-type SeV in cultured cells. However, the mutant viruses were strongly attenuated in mice in a way similar to that of SeV VΔC, which has a truncated V protein lacking the cysteine-rich domain, by exhibiting earlier viral clearance from the mouse lung and less virulence to mice. We therefore conclude that the zinc-binding capacity of the V protein is involved in viral pathogenesis.


Sign in / Sign up

Export Citation Format

Share Document