Hepatitis a virus: Growth characteristics of in vivo and in vitro propagated wild and attenuated virus strains

1984 ◽  
Vol 14 (4) ◽  
pp. 373-386 ◽  
Author(s):  
Daniel W. Bradley ◽  
Charles A. Schable ◽  
Karen A. McCaustland ◽  
E. H. Cook ◽  
Bert L. Murphy ◽  
...  
Keyword(s):  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Growth Characteristics ◽  
Virus Growth ◽  
Attenuated Virus ◽  
Virus Strains

scholarly journals Effect of Ribavirin on Hepatitis A Virus Replication In Vitro

1992 ◽  
Vol 3 (2) ◽  
pp. 67-70 ◽  
Author(s):  
Rabindra K Chaudhary ◽  
Anton P Andonov
Keyword(s):  
Cell Growth ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Inhibitory Effect ◽  
Significant Inhibition ◽  
Virus Growth ◽  
Infectious Dose ◽  
Persistently Infected ◽  
Inoculum Dose

The effect of ribavirin on fetal Rhesus monkey kidney cells (FRhK-4) acutely or chronically infected with hepatitis A virus was studied. The effect of ribavirin on hepatitis A virus yield as detected by radioimmunoassay in acutely infected FRhK-4 cells was dependent on hepatitis A virus inoculum dose. Treatment with 100 μg/mL ribavirin completely inhibited hepatitis A virus growth in cultures infected with 100 to 800 tissue culture infectious dose 50 (TCID50) hepatitis A virus, but inocula of 800 to 1600 TCID50resulted in limited production of virus. The effect was time dependent and required more than 96 h of treatment to inhibit the virus completely. Ribavirin was less effective in treating cells persistently infected with hepatitis A virus, although there was significant inhibition of hepatitis A virus (82%) in persistently infected cells as well. Ribavirin had some inhibitory effect on cell growth; treatment with 25, 50 or 100 μg/mL ribavirin reduced cell growth by approximately 0, 20 and 40%, respectively.

Kinetics of hepatitis A virus replication in vivo and in vitro using negative-strand quantitative PCR

2009 ◽  
Vol 28 (10) ◽  
pp. 1167-1176 ◽  
Author(s):  
V. S. Paula ◽  
A. S. Perse ◽  
L. A. Amado ◽  
L. M. Morais ◽  
S. M. B. Lima ◽  
...  
Keyword(s):  
Quantitative Pcr ◽  
Virus Replication ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Negative Strand ◽  
Kinetics Of

Expression of Hepatitis A Virus Precursor Protein P3 in Vivo and in Vitro: Polyprotein Processing of the 3CD Cleavage Site

Virology ◽  
1994 ◽  
Vol 198 (2) ◽  
pp. 524-533 ◽  
Author(s):  
Michael Tesar ◽  
Inga Pak ◽  
Xi-Yu Jia ◽  
Oliver C. Richards ◽  
Donald F. Summers ◽  
...  
Keyword(s):  
Cleavage Site ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Precursor Protein ◽  
Polyprotein Processing

scholarly journals Molecular Cloning of cDNA from Hepatitis A Virus Strain HM-175 after Multiple Passages in vivo and in vitro

1986 ◽  
Vol 67 (8) ◽  
pp. 1741-1744 ◽  
Author(s):  
B. C. Ross ◽  
B. N. Anderson ◽  
A. G. Coulepis ◽  
M. P. Chenoweth ◽  
I. D. Gust
Keyword(s):  
Molecular Cloning ◽  
Virus Strain ◽  
Hepatitis A ◽  
Hepatitis A Virus

Efficient neutralizing activity of cocktailed recombinant human antibodies against hepatitis a virus infection in vitro and in vivo

2008 ◽  
Vol 80 (7) ◽  
pp. 1171-1180 ◽  
Author(s):  
Jingyuan Cao ◽  
Shufang Meng ◽  
Chuan Li ◽  
Yan Ji ◽  
Qingling Meng ◽  
...  
Keyword(s):  
Virus Infection ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Neutralizing Activity ◽  
Human Antibodies

scholarly journals Comparison of the anti-duck hepatitis A virus activities of phosphorylated and sulfated Astragalus polysaccharides

2016 ◽  
Vol 242 (3) ◽  
pp. 344-353 ◽  
Author(s):  
Yixuan Wang ◽  
Yun Chen ◽  
Hongxu Du ◽  
Jingjing Yang ◽  
Ke Ming ◽  
...  
Keyword(s):  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Sodium Tripolyphosphate ◽  
Chlorosulfonic Acid ◽  
Polymerase Chain Reaction Method ◽  
Viral Multiplication ◽  
Duck Hepatitis ◽  
Antiviral Activities

Duck hepatitis A virus (DHAV) (Picornaviridae) causes an infectious disease in ducks which results in severe losses in duck industry. However, the proper antiviral supportive drugs for this disease have not been discovered. Polysaccharide is the main ingredient of Astragalus that has been demonstrated to directly and indirectly inhibit RNA of viruses replication. In this study, the antiviral activities of Astragalus polysaccharide (APS) and its derivatives against DHAV were evaluated and compared. APS was modified via the sodium trimetaphosphate and sodium tripolyphosphate (STMP-STPP) method and chlorosulfonic acid-pyridine method to obtain its phosphate (pAPS) and sulfate (sAPS), respectively. The infrared structures of APS, pAPS, and sAPS were analyzed with the potassium bromide disc method. Additionally, the antiviral activities were evaluated with the MTT ((4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide) method in vitro and the artificial inoculation method in vivo. The clinical therapy effects were evaluated by mortality rate, liver function-related biochemical indicators, and visual changes in pathological anatomy. The anti-DHAV proliferation effects of APS, pAPS, and sAPS on the viral multiplication process in cell and blood were observed with the reverse transcription-polymerase chain reaction method. The results revealed that pAPS inhibited DHAV proliferation more efficiently in the entire process of viral multiplication than APS and sAPS. Moreover, only pAPS significantly improved the survival rate to 33.5% and reduced the DHAV particle titer in the blood as well as liver lesions in clinical trials. The results indicated that pAPS exhibited greater anti-DHAV activity than APS and sAPS both in vitro and in vivo.

“In vitro” and in Animal Model Studies on a Double Virus- Inactivated Factor VIII Concentrate

1995 ◽  
Vol 74 (03) ◽  
pp. 868-873 ◽  
Author(s):  
Silvana Arrighi ◽  
Roberta Rossi ◽  
Maria Giuseppina Borri ◽  
Vladimir Lesnikov ◽  
Marina Lesnikov ◽  
...  
Keyword(s):  
Heat Treatment ◽  
Animal Model ◽  
Factor Viii ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Virus Inactivation ◽  
Enveloped Viruses ◽  
Model Studies ◽  
Heat Treated

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.

scholarly journals Individual Expression of Hepatitis A Virus 3C Protease Induces Ferroptosis in Human Cells In Vitro

2021 ◽  
Vol 22 (15) ◽  
pp. 7906
Author(s):  
Alexey A. Komissarov ◽  
Maria A. Karaseva ◽  
Marina P. Roschina ◽  
Andrey V. Shubin ◽  
Nataliya A. Lunina ◽  
...  
Keyword(s):  
Cell Death ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Proteolytic Enzymes ◽  
Morphological Changes ◽  
Human Cells ◽  
Mitochondrial Potential ◽  
3C Protease ◽  
Wide Range

Regulated cell death (RCD) is a fundamental process common to nearly all living beings and essential for the development and tissue homeostasis in animals and humans. A wide range of molecules can induce RCD, including a number of viral proteolytic enzymes. To date, numerous data indicate that picornaviral 3C proteases can induce RCD. In most reported cases, these proteases induce classical caspase-dependent apoptosis. In contrast, the human hepatitis A virus 3C protease (3Cpro) has recently been shown to cause caspase-independent cell death accompanied by previously undescribed features. Here, we expressed 3Cpro in HEK293, HeLa, and A549 human cell lines to characterize 3Cpro-induced cell death morphologically and biochemically using flow cytometry and fluorescence microscopy. We found that dead cells demonstrated necrosis-like morphological changes including permeabilization of the plasma membrane, loss of mitochondrial potential, as well as mitochondria and nuclei swelling. Additionally, we showed that 3Cpro-induced cell death was efficiently blocked by ferroptosis inhibitors and was accompanied by intense lipid peroxidation. Taken together, these results indicate that 3Cpro induces ferroptosis upon its individual expression in human cells. This is the first demonstration that a proteolytic enzyme can induce ferroptosis, the recently discovered and actively studied type of RCD.

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