scholarly journals Hepatitis A Virus Codon Usage: Implications for Translation Kinetics and Capsid Folding

2018 ◽  
Vol 8 (10) ◽  
pp. a031781 ◽  
Author(s):  
Rosa M. Pintó ◽  
Francisco-Javier Pérez-Rodríguez ◽  
Lucia D’Andrea ◽  
Montserrat de Castellarnau ◽  
Susana Guix ◽  
...  
2013 ◽  
Vol 12 (3) ◽  
pp. 2306-2319 ◽  
Author(s):  
X.-X. Ma ◽  
Y.-P. Feng ◽  
L. Chen ◽  
Y.-Q. Zhao ◽  
J.-L. Liu ◽  
...  

2019 ◽  
Vol 11 (9) ◽  
pp. 2439-2456 ◽  
Author(s):  
Lucía D’Andrea ◽  
Francisco-Javier Pérez-Rodríguez ◽  
Montserrat de Castellarnau ◽  
Susana Guix ◽  
Enric Ribes ◽  
...  

AbstractHepatoviruses show an intriguing deviated codon usage, suggesting an evolutionary signature. Abundant and rare codons in the cellular genome are scarce in the human hepatitis A virus (HAV) genome, while intermediately abundant host codons are abundant in the virus. Genotype–phenotype maps, or fitness landscapes, are a means of representing a genotype position in sequence space and uncovering how genotype relates to phenotype and fitness. Using genotype–phenotype maps of the translation efficiency, we have shown the critical role of the HAV capsid codon composition in regulating translation and determining its robustness. Adaptation to an environmental perturbation such as the artificial induction of cellular shutoff—not naturally occurring in HAV infection—involved movements in the sequence space and dramatic changes of the translation efficiency. Capsid rare codons, including abundant and rare codons of the cellular genome, slowed down the translation efficiency in conditions of no cellular shutoff. In contrast, rare capsid codons that are abundant in the cellular genome were efficiently translated in conditions of shutoff. Capsid regions very rich in slowly translated codons adapt to shutoff through sequence space movements from positions with highly robust translation to others with diminished translation robustness. These movements paralleled decreases of the capsid physical and biological robustness, and resulted in the diversification of capsid phenotypes. The deviated codon usage of extant hepatoviruses compared with that of their hosts may suggest the occurrence of a virus ancestor with an optimized codon usage with respect to an unknown ancient host.


2003 ◽  
Vol 77 (1) ◽  
pp. 452-459 ◽  
Author(s):  
Glòria Sánchez ◽  
Albert Bosch ◽  
Rosa M. Pintó

ABSTRACT The number of synonymous mutations per synonymous site (Ks ), the number of nonsynonymous mutations per nonsynonymous site (Ka ), and the codon usage statistic (Nc ) were calculated for several hepatitis A virus (HAV) isolates. While Ks was similar to those of poliovirus (PV) and foot-and-mouth disease virus (FMDV), Ka was 1 order of magnitude lower. The Nc parameter provides information on codon usage bias and decreases when bias increases. The Nc value in HAV was about 38, while in PV and FMDV, it was about 53. The emergence of 22 rare codons in front of 8 in PV and 7 in FMDV was detected. Most of the conserved rare codons of the P1 region were strategically located at the carboxy borders of β barrels and α helices, their potential function being the assurance of proper folding of the capsid proteins through a decrease in the translation speed. This strategic location was not observed for amino acids encoded by the conserved rare codons of the 3D region. The percentage of bases with low pairing number values was higher in the latter region, suggesting a role of the conserved rare codons in the maintenance of RNA structure. Many of the rare codons in HAV are among the most frequent in humans, unlike in PV or in FMDV. This fact may be explained by the lack of cellular shutoff in HAV. One hypothesis is that HAV has evolved in order to avoid competition with its host for cellular tRNAs.


2011 ◽  
Vol 8 (1) ◽  
Author(s):  
Yiqiang Zhang ◽  
Yongsheng Liu ◽  
Wenqian Liu ◽  
Jianhua Zhou ◽  
Haotai Chen ◽  
...  

2014 ◽  
Vol 88 (9) ◽  
pp. 5029-5041 ◽  
Author(s):  
M. I. Costafreda ◽  
F. J. Perez-Rodriguez ◽  
L. D'Andrea ◽  
S. Guix ◽  
E. Ribes ◽  
...  

2011 ◽  
Vol 157 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Lucía D’ Andrea ◽  
Rosa M. Pintó ◽  
Albert Bosch ◽  
Héctor Musto ◽  
Juan Cristina

2010 ◽  
Vol 6 (3) ◽  
pp. e1000797 ◽  
Author(s):  
Lluís Aragonès ◽  
Susana Guix ◽  
Enric Ribes ◽  
Albert Bosch ◽  
Rosa M. Pintó

2007 ◽  
Vol 127 (2) ◽  
pp. 158-163 ◽  
Author(s):  
Rosa M. Pintó ◽  
Lluis Aragonès ◽  
M. Isabel Costafreda ◽  
Enric Ribes ◽  
Albert Bosch

Author(s):  
Charles D. Humphrey ◽  
E. H. Cook ◽  
Karen A. McCaustland ◽  
Daniel W. Bradley

Enterically transmitted non-A, non-B hepatitis (ET-NANBH) is a type of hepatitis which is increasingly becoming a significant world health concern. As with hepatitis A virus (HAV), spread is by the fecal-oral mode of transmission. Until recently, the etiologic agent had not been isolated and identified. We have succeeded in the isolation and preliminary characterization of this virus and demonstrating that this agent can cause hepatic disease and seroconversion in experimental primates. Our characterization of this virus was facilitated by immune (IEM) and solid phase immune electron microscopic (SPIEM) methodologies.Many immune electron microscopy methodologies have been used for morphological identification and characterization of viruses. We have previously reported a highly effective solid phase immune electron microscopy procedure which facilitated identification of hepatitis A virus (HAV) in crude cell culture extracts. More recently we have reported utilization of the method for identification of an etiologic agent responsible for (ET-NANBH).


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