scholarly journals Hepatitis A Virus Survival on Drug Paraphernalia

2020 ◽  
Vol 41 (S1) ◽  
pp. s248-s248
Author(s):  
Magdalena Medrzycki ◽  
Michael A. Purdy

Background: The ongoing hepatitis A outbreak in the United States has concerned public health authorities since March 2017. The outbreak has already spread throughout 30 states and includes primarily homeless individuals and persons who use drugs, including persons who inject drugs (PWIDs). Contaminated drug injection paraphernalia and sharing of these items are suspected to be one of multiple causes of hepatitis A virus (HAV) transmission in those populations. Methods: We used a standard plaque assay to investigate HAV infectivity. Liquid suspensions of HAV were tested to examine the effects of time and temperature on viral infectivity. We also examined HAV survival on commonly used drug paraphernalia, such as needles, syringes, cookers, tourniquets, and cotton balls/filters frequently shared among PWIDs. We investigated the effect of low pH on HAV survival using citric acid, which is frequently used by PWIDs during dose preparation. We also compared the plaque assay results with those concurrently obtained by RT-PCR to establish whether viral HAV RNA levels could be used as surrogates for plaque assay results. Results: We found that HAV suspended in PBS at room temperature was able to infect FRhk4 cells for >17 weeks. HAV remained viable in syringes and needles (ie, semidry conditions) for up to 10 weeks depending on the size of the needles and the syringe dead volume. HAV survival in dry conditions on cooker, tourniquet, and cotton balls/filter surfaces did not exceed 4 weeks. HAV retained its infectivity for >10 weeks at pH as low as 2. PCR results suggest that RNA is amplified from both infectious and noninfectious HAV. Conclusions: Our findings show that HAV can survive and remain infective in the PWID setting for 4–10 weeks depending on the type of paraphernalia examined. These findings suggest that sharing drug paraphernalia by the homeless and PWIDs can potentially facilitate the transmission of HAV within these populations. Moreover, our results confirm that the plaque assay is currently the only reliable method to determine the infectivity of HAV in vitro.Funding: NoneDisclosures: None

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.


2021 ◽  
Vol 22 (15) ◽  
pp. 7906
Author(s):  
Alexey A. Komissarov ◽  
Maria A. Karaseva ◽  
Marina P. Roschina ◽  
Andrey V. Shubin ◽  
Nataliya A. Lunina ◽  
...  

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.


Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 861
Author(s):  
Minghang Wang ◽  
Zongdi Feng

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.


1986 ◽  
Vol 6 (2) ◽  
pp. 103-112 ◽  
Author(s):  
Anders Widell ◽  
Bengt Göran Hansson ◽  
Bo Öberg ◽  
Erik Nordenfelt

Transfusion ◽  
1998 ◽  
Vol 38 (6) ◽  
pp. 573-579 ◽  
Author(s):  
JM Soucie ◽  
BH Robertson ◽  
BP Bell ◽  
KA McCaustland ◽  
BL Evatt

1985 ◽  
Vol 48 (9) ◽  
pp. 815-823 ◽  
Author(s):  
GARY P. RICHARDS

Outbreaks of hepatitis A, Norwalk illness, and nonspecific viral gastroenteritis are associated with consumption of sewage-contaminated shellfish. Over 100 outbreaks have been reported in the United States during the past 50 years. Reported cases of shellfish-associated enteric virus illness are on the increase, whereas bacterial illness from shellfish is on the decline. As yet, there are no procedures for detecting hepatitis A virus, Norwalk virus and numerous other pathogenic viruses in environmental samples, but virus extraction and assay procedures for water and shellfish are available for the more easily cultivated enteric viruses. Current standards rely on bacterial indicators as a means to evaluate the sanitary quality of shellfish and their growing waters, but the adequacy of using bacteria as indicators of possible virus contamination is questionable. The feasibility of employing enteroviruses or rotaviruses as possible viral indiators is discussed. It is proposed that easily cultivated enteroviruses, such as poliovirus, be used as an interim indicator for the possible presence of human pathogenic viruses in seafoods, with the subsequent formulation of guidelines to limit the levels of virus contamination in shellfish.


2021 ◽  
Author(s):  
Kenrad E Nelson ◽  
Brittany L Kmush

Epidemics of infectious jaundice have been reported throughout recorded history. However, the proof that many of these outbreaks and individual cases of acute hepatitis were caused by a viral infection, the hepatitis A virus (HAV), did not appear until the 1960s. After the transmission of infection to marmosets and humans, the epidemiologic and virologic characteristics that differed between hepatitis A and hepatitis B virus infections were defined more clearly. After the development and licensure of hepatitis A vaccines in the 1990s, it became possible to implement an effective prevention program involving routine immunization of young children in the United States and several other Western countries. However, despite the dramatic efficacy of the childhood immunization program in reducing the incidence of acute hepatitis from HAV in the population, older children and adults remained susceptible. Significant morbidity continues to occur in the United States among international travelers, injection drug users, persons with underlying liver disease, and other high-risk populations. Since HAV is a global pathogen, the prevention of increasing morbidity from hepatitis A attributable to the incidence of clinically more severe disease increases in countries transitioning from high to intermediate or low endemic status is a major public health challenge. In this review, we discuss the epidemiology, virology, clinical characteristics, and prevention of hepatitis A infections. This review contains 8 figures, 3 tables and 89 references Key words: epidemiology, global impact, hepatitis A vaccine, hepatitis A virus, prevention, reservoirs, risk factors, treatment


Vox Sanguinis ◽  
1994 ◽  
Vol 67 (1) ◽  
pp. 24-28 ◽  
Author(s):  
James W. Mosley ◽  
Marek J. Nowicki ◽  
Carol K. Kasper ◽  
Elizabeth Donegan ◽  
Louis M. Aledort ◽  
...  

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