“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.

scholarly journals Mechanisms of Hepatocellular Injury in Hepatitis A

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 861
Author(s):  
Minghang Wang ◽  
Zongdi Feng
Keyword(s):  
T Cells ◽  
Liver Injury ◽  
Hepatitis A ◽  
Acute Viral Hepatitis ◽  
Hepatitis A Virus ◽  
Current Knowledge ◽  
Cytotoxic T Cells ◽  
Host Factors ◽  
Hepatocellular Injury

Hepatitis A virus (HAV) infection is a common cause of acute viral hepatitis worldwide. Despite decades of research, the pathogenic mechanisms of hepatitis A remain incompletely understood. As the replication of HAV is noncytopathic in vitro, a widely accepted concept has been that virus-specific cytotoxic T cells are responsible for liver injury. However, accumulating evidence suggests that natural killer (NK) cells, NKT cells, and even non-HAV-specific CD8+ T cells contribute to liver damage during HAV infection. In addition, intrinsic death of virus-infected hepatocytes has been implicated as a cause of liver injury in a murine model of hepatitis A. Furthermore, genetic variations in host factors such as T cell immunoglobulin-1 (TIM1) and IL-18 binding protein (IL-18BP) have been linked to hepatitis A severity. This review summarizes the current knowledge of the mechanisms of hepatocellular injury in hepatitis A. Different mechanisms may be involved under different conditions and they are not necessarily mutually exclusive. A better understanding of these mechanisms would aid in diagnosis and treatment of diseases associated with HAV infection.

Influence of twenty potentially antiviral substances on in vitro multiplication of hepatitis a virus

1986 ◽  
Vol 6 (2) ◽  
pp. 103-112 ◽  
Author(s):  
Anders Widell ◽  
Bengt Göran Hansson ◽  
Bo Öberg ◽  
Erik Nordenfelt
Keyword(s):  
Hepatitis A ◽  
Hepatitis A Virus ◽  
In Vitro Multiplication

UV Light Inactivation of Hepatitis A Virus, Aichi Virus, and Feline Calicivirus on Strawberries, Green Onions, and Lettuce

2008 ◽  
Vol 71 (5) ◽  
pp. 908-913 ◽  
Author(s):  
VIVIANA R. FINO ◽  
KALMIA E. KNIEL
Keyword(s):  
Foodborne Pathogens ◽  
Hepatitis A ◽  
Fruits And Vegetables ◽  
Hepatitis A Virus ◽  
Uv Light ◽  
Mammalian Cell Culture ◽  
Aichi Virus ◽  
Feline Calicivirus ◽  
Virus Inactivation ◽  
Need To Evaluate

A majority of illnesses caused by foodborne viruses are associated with fresh produce. Fruits and vegetables may be considered high-risk foods, as they are often consumed raw without a specific inactivation step. Therefore, there is a need to evaluate nonthermal treatments for the inactivation of foodborne pathogens. This study investigates the UV inactivation of three viruses: feline calicivirus (a surrogate for norovirus), and two picornaviruses, hepatitis A virus and Aichi virus. Three produce types were selected for their different surface topographies and association with outbreaks. Green onions, lettuce, and strawberries were individually spot inoculated with 107 to 109 50% tissue culture infective doses (TCID50) of each virus per ml and exposed to UV light at various doses (≤240 mW s/cm2), and viruses were eluted using an optimized recovery strategy. Virus infection was quantified by TCID50 in mammalian cell culture and compared with untreated recovered virus. UV light applied to contaminated lettuce resulted in inactivation of 4.5 to 4.6 log TCID50/ml; for contaminated green onions, inactivation ranged from 2.5 to 5.6 log TCID50/ml; and for contaminated strawberries, inactivation ranged from 1.9 to 2.6 log TCID50/ml for the three viruses tested. UV light inactivation on the surface of lettuce is more effective than inactivation on the other two produce items. Consistently, the lowest results were observed in the inactivation of viruses on strawberries. No significant differences (P > 0.05) for virus inactivation were observed among the three doses applied (40, 120, and 240 mW s/cm2)on the produce, with the exception of hepatitis A virus and Aichi virus inactivation on green onions, where inactivation continued at 120 mW s/cm2 (P < 0.05).

Inhibition of hepatitis A virus replication in vitro by antiviral compounds

1990 ◽  
Vol 31 (2) ◽  
pp. 155-160 ◽  
Author(s):  
J. M. Crance ◽  
E. Biziagos ◽  
J. Passagot ◽  
H. van Cuyck-Gandré ◽  
R. Deloince
Keyword(s):  
Virus Replication ◽  
Hepatitis A ◽  
Hepatitis A Virus ◽  
Antiviral Compounds

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
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