scholarly journals Antigenic and genetic variation in cytopathic hepatitis A virus variants arising during persistent infection: evidence for genetic recombination.

1991 ◽  
Vol 65 (4) ◽  
pp. 2056-2065 ◽  
Author(s):  
S M Lemon ◽  
P C Murphy ◽  
P A Shields ◽  
L H Ping ◽  
S M Feinstone ◽  
...  
2003 ◽  
Vol 84 (12) ◽  
pp. 3191-3201 ◽  
Author(s):  
Mauro Costa-Mattioli ◽  
Anna Di Napoli ◽  
Virginie Ferré ◽  
Sylviane Billaudel ◽  
Raul Perez-Bercoff ◽  
...  

Knowledge of the molecular biology of hepatitis A virus (HAV) has increased exponentially since its identification. HAV exploits all known mechanisms of genetic variation to ensure survival, including mutation and genetic recombination. HAV has been characterized by the emergence of different genotypes, three human antigenic variants and only one major serotype. This paper reviews the genetic variability and molecular epidemiology of HAV. Its evolutionary mechanisms are described with particular emphasis on genetic recombination and HAV mutation rate. Genotypic classification methods are also discussed.


1991 ◽  
Vol 163 (2) ◽  
pp. 286-292 ◽  
Author(s):  
B. H. Robertson ◽  
B. Khanna ◽  
O. V. Nainan ◽  
H. S. Margolis

2002 ◽  
Vol 83 (9) ◽  
pp. 2183-2192 ◽  
Author(s):  
Verena Gauss-Müller ◽  
Yuri Y. Kusov

Unlike other picornaviruses, hepatitis A virus (HAV) replicates so inefficiently in cell culture that the study of its RNA biosynthesis presents a major experimental challenge. To assess viral RNA replication independent of particle formation, a subgenomic replicon representing a self-replicating RNA was constructed by replacing the P1 domain encoding the capsid proteins with the firefly luciferase sequence. Although translation of the HAV replicon was as efficient as a similar poliovirus replicon, the luciferase activity derived from replication of the HAV construct was more than 100-fold lower than that of poliovirus. The replication capacity of the HAV replicon was clearly demonstrated by its ability to recombine genetically with a non-viable, full-length HAV genome that served as capsid donor and thus to rescue a fully infectious virus. In contrast to a replication-deficient replicon, co-expression of the genetically marked and replication-competent HAV replicon with several lethally mutated HAV genomes resulted in the successful rescue of infectious HAV with a unique genetic marker. Our data suggest: (i) that autonomous HAV RNA replication does not require sequences for the HAV structural proteins; and (ii) that low-level genome replication can unequivocally be demonstrated by the rescue of infectious virus after co-expression with non-viable genomes.


1984 ◽  
Vol 65 (3) ◽  
pp. 609-615 ◽  
Author(s):  
A. Vallbracht ◽  
L. Hofmann ◽  
K. G. Wurster ◽  
B. Flehmig

2012 ◽  
Vol 27 (4) ◽  
pp. 248-253 ◽  
Author(s):  
Jiming Gao ◽  
Junhao Chen ◽  
Xingkui Si ◽  
Zhijing Xie ◽  
Yanli Zhu ◽  
...  

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).


Author(s):  
D.R. Jackson ◽  
J.H. Hoofnagle ◽  
A.N. Schulman ◽  
J.L. Dienstag ◽  
R.H. Purcell ◽  
...  

Using immune electron microscopy Feinstone et. al. demonstrated the presence of a 27 nm virus-like particle in acute-phase stools of patients with viral hepatitis, type A, These hepatitis A antigen (HA Ag) particles were aggregated by convalescent serum from patients with type A hepatitis but not by pre-infection serum. Subsequently Dienstag et. al. and Maynard et. al. produced acute hepatitis in chimpanzees by inoculation with human stool containing HA Ag. During the early acute disease, virus like particles antigenically, morphologically and biophysically identical to the human HA Ag particle were found in chimpanzee stool. Recently Hilleman et. al. have described similar particles in liver and serum of marmosets infected with hepatitis A virus (HAV). We have investigated liver, bile and stool from chimpanzees and marmosets experimentally infected with HAV. In an initial study, a chimpanzee (no.785) inoculated with HA Ag-containing stool developed elevated liver enzymes 21 days after exposure.


Author(s):  
C.D. Humphrey ◽  
T.L. Cromeans ◽  
E.H. Cook ◽  
D.W. Bradley

There is a variety of methods available for the rapid detection and identification of viruses by electron microscopy as described in several reviews. The predominant techniques are classified as direct electron microscopy (DEM), immune electron microscopy (IEM), liquid phase immune electron microscopy (LPIEM) and solid phase immune electron microscopy (SPIEM). Each technique has inherent strengths and weaknesses. However, in recent years, the most progress for identifying viruses has been realized by the utilization of SPIEM.


1995 ◽  
Vol 74 (03) ◽  
pp. 868-873 ◽  
Author(s):  
Silvana Arrighi ◽  
Roberta Rossi ◽  
Maria Giuseppina Borri ◽  
Vladimir Lesnikov ◽  
Marina Lesnikov ◽  
...  

SummaryTo improve the safety of plasma derived factor VIII (FVIII) concentrate, we introduced a final super heat treatment (100° C for 30 min) as additional virus inactivation step applied to a lyophilized, highly purified FVIII concentrate (100 IU/mg of proteins) already virus inactivated using the solvent/detergent (SID) method during the manufacturing process.The efficiency of the super heat treatment was demonstrated in inactivating two non-lipid enveloped viruses (Hepatitis A virus and Poliovirus 1). The loss of FVIII procoagulant activity during the super heat treatment was of about 15%, estimated both by clotting and chromogenic assays. No substantial changes were observed in physical, biochemical and immunological characteristics of the heat treated FVIII concentrate in comparison with those of the FVIII before heat treatment.


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