Infant postexposure prophylaxis prevents perinatal hepatitis B (HepB) virus transmission and mortality and morbidity caused by chronic HepB virus infection. The US Perinatal Hepatitis B Prevention Program (PHBPP) identifies and manages infants born to HepB surface antigen–positive women.

It presents the first estimates of the long-term costs and outcomes of postexposure prophylaxis with the PHBPP. It analyzes the effects of the PHBPP, and alternative immunization scenarios, on health and economic outcomes for the 2009 US birth cohort. (Read the full article)

Duration of protection among children and adolescents who have received the recombinant hepatitis B (HB) vaccination series is known to be long. Less is known about duration of protection of the vaccination series after being administered during infancy.

A robust response to a challenge dose of HB vaccine among adolescents indicates prolonged duration of protection against disease; the addition of a booster dose of HB vaccine to the routine immunization schedule for adolescents appears unnecessary. (Read the full article)

Timely immunoprophylaxis and completion of the 3-dose hepatitis B vaccine series represents the cornerstone of perinatal hepatitis B prevention. Immunoprophylaxis for infants born to hepatitis B surface antigen–positive mothers reduces up to 95% of perinatal hepatitis B virus infections.

Despite recommended immunoprophylaxis, perinatal hepatitis B virus infection occurs among ~1% of infants. Infants born to mothers who are younger, hepatitis B e-antigen positive, or who have a high viral load or infants who receive <3 hepatitis B vaccine doses are at greatest risk of infection. (Read the full article)

Pediatric autoimmune hepatitis is an uncommon condition; children and youth can present with a diverse and insidious clinical course and biochemical features. Response to treatment is generally good, and transplantation is rarely needed.

This population-based study adds knowledge regarding the incidence of pediatric autoimmune hepatitis in Canada, as well as a description of diagnostic and therapeutic approaches among centers. Long-term outcomes are also described. (Read the full article)

The quinoline MK-571 is the most commonly used inhibitor of multidrug resistance protein-1 (MRP-1) but was originally developed as a cysteinyl leukotriene receptor 1 (CysLTR1) antagonist. While studying the modulatory effect of MRP-1 on anti-hepatitis C virus (HCV) direct acting-antivirals (DAA) efficiency, we observed an unexpected anti-HCV effect of compound MK-571 alone. This anti-HCV activity was characterized in Huh7.5 cells stably harboring a subgenomic genotype 1b replicon. A dose-dependent decrease of HCV RNA levels was observed upon MK-571 administration, with an EC₅₀ of 9±0.3 μM and a maximum HCV RNA level reduction of approximatively 1 Log₁₀. MK-571 also reduced the replication of the HCV full-length J6/JFH1 model in a dose-dependent manner. However, probenecid and apigenin homodimer (APN), two specific inhibitors of MRP-1, had no effect on HCV replication. In contrast, the CysLTR1 antagonists SR2640 increased HCV-SGR RNA levels in a dose-dependent manner, with a maximum increase of 10-fold. In addition, a combination of natural CysLTR1 agonist (LTD4) or antagonists (zafirlukast, cinalukast, and SR2640) with MK-571 completely reversed its antiviral effect, suggesting its anti-HCV activity is related to CysLTR1 rather to MRP-1 inhibition. In conclusion, we showed that MK-571 inhibits HCV replication in hepatoma cell cultures by acting as a CysLTR1 receptor antagonist, thus unraveling a new host-virus interaction in the HCV life cycle.

Updated Information: DPH Announces Potential Exposure at Two Additional Food Establishments and Updated Timeline DOVER – The Division of Public Health (DPH) announced today that employees and patrons of Buffalo Wild Wings located at 540 W. Main St., Middletown, may have been exposed to the hepatitis A virus between March 31 and April 10, 2019. When […]

he Division of Public Health (DPH) is providing updated information regarding a potential Hepatitis A exposure at a Buffalo Wild Wings food establishment in Middletown, which was announced on Thursday, April 11, 2019.

Title: FDA Panel Urges Approval of Hepatitis C Drug
Category: Health News
Created: 4/28/2011 11:01:00 AM
Last Editorial Review: 4/28/2011 12:00:00 AM

Title: FDA Panel Backs 2 Hepatitis C Drugs
Category: Health News
Created: 4/29/2011 11:01:00 AM
Last Editorial Review: 4/29/2011 12:00:00 AM

Title: Opioid Crisis Means More Newborns With Hepatitis C, But Few Get Tested
Category: Health News
Created: 5/2/2018 12:00:00 AM
Last Editorial Review: 5/2/2018 12:00:00 AM

Title: Kentucky, Indiana Latest States with Hepatitis A Outbreaks
Category: Health News
Created: 5/2/2018 12:00:00 AM
Last Editorial Review: 5/3/2018 12:00:00 AM

Immune-competent animal models for the hepatitis C virus (HCV) are nonexistent, impeding studies of host-virus interactions and vaccine development. Experimental infection of laboratory rats with a rodent hepacivirus isolated from Rattus norvegicus (RHV) is a promising surrogate model due to its recapitulation of HCV-like chronicity. However, several aspects of rat RHV infection remain unclear, for instance, how RHV evades host adaptive immunity to establish persistent infection. Here, we analyzed the induction, differentiation, and functionality of RHV-specific CD8 T cell responses that are essential for protection against viral persistence. Virus-specific CD8 T cells targeting dominant and subdominant major histocompatibility complex class I epitopes proliferated considerably in liver after RHV infection. These populations endured long term yet never acquired antiviral effector functions or selected for viral escape mutations. This was accompanied by the persistent upregulation of programmed cell death-1 and absent memory cell formation, consistent with a dysfunctional phenotype. Remarkably, transient suppression of RHV viremia with a direct-acting antiviral led to the priming of CD8 T cells with partial effector function, driving the selection of a viral escape variant. These data demonstrate an intrinsic abnormality within CD8 T cells primed by rat RHV infection, an effect that is governed at least partially by the magnitude of early virus replication. Thus, this model could be useful in investigating mechanisms of CD8 T cell subversion, leading to the persistence of hepatotropic pathogens such as HCV.

IMPORTANCE Development of vaccines against hepatitis C virus (HCV), a major cause of cirrhosis and cancer, has been stymied by a lack of animal models. The recent discovery of an HCV-like rodent hepacivirus (RHV) enabled the development of such a model in rats. This platform recapitulates HCV hepatotropism and viral chronicity necessary for vaccine testing. Currently, there are few descriptions of RHV-specific responses and why they fail to prevent persistent infection in this model. Here, we show that RHV-specific CD8 T cells, while induced early at high magnitude, do not develop into functional effectors capable of controlling virus. This defect was partially alleviated by short-term treatment with an HCV antiviral. Thus, like HCV, RHV triggers dysfunction of virus-specific CD8 T cells that are vital for infection resolution. Additional study of this evasion strategy and how to mitigate it could enhance our understanding of hepatotropic viral infections and lead to improved vaccines and therapeutics.

Capsid assembly is a critical step in the hepatitis B virus (HBV) life cycle, mediated by the core protein. Core is a potential target for new antiviral therapies, the capsid assembly modulators (CAMs). JNJ-56136379 (JNJ-6379) is a novel and potent CAM currently in phase II trials. We evaluated the mechanisms of action (MOAs) and antiviral properties of JNJ-6379 in vitro. Size exclusion chromatography and electron microscopy studies demonstrated that JNJ-6379 induced the formation of morphologically intact viral capsids devoid of genomic material (primary MOA). JNJ-6379 accelerated the rate and extent of HBV capsid assembly in vitro. JNJ-6379 specifically and potently inhibited HBV replication; its median 50% effective concentration (EC₅₀) was 54 nM (HepG2.117 cells). In HBV-infected primary human hepatocytes (PHHs), JNJ-6379, when added with the viral inoculum, dose-dependently reduced extracellular HBV DNA levels (median EC₅₀ of 93 nM) and prevented covalently closed circular DNA (cccDNA) formation, leading to a dose-dependent reduction of intracellular HBV RNA levels (median EC₅₀ of 876 nM) and reduced antigen levels (secondary MOA). Adding JNJ-6379 to PHHs 4 or 5 days postinfection reduced extracellular HBV DNA and did not prevent cccDNA formation. Time-of-addition PHH studies revealed that JNJ-6379 most likely interfered with postentry processes. Collectively, these data demonstrate that JNJ-6379 has dual MOAs in the early and late steps of the HBV life cycle, which is different from the MOA of nucleos(t)ide analogues. JNJ-6379 is in development for chronic hepatitis B treatment and may translate into higher HBV functional cure rates.

Hepatitis C virus (HCV) is an important and underreported infectious disease, causing chronic infection in ~71 million people worldwide. The limited host range of HCV, which robustly infects only humans and chimpanzees, has made studying this virus in vivo challenging and hampered the development of a desperately needed vaccine. The restrictions and ethical concerns surrounding biomedical research in chimpanzees has made the search for an animal model all the more important. In this review, we discuss different approaches that are being pursued toward creating small animal models for HCV infection. Although efforts to use a nonhuman primate species besides chimpanzees have proven challenging, important advances have been achieved in a variety of humanized mouse models. However, such models still fall short of the overarching goal to have an immunocompetent, inheritably susceptible in vivo platform in which the immunopathology of HCV could be studied and putative vaccines development. Alternatives to overcome this include virus adaptation, such as murine-tropic HCV strains, or the use of related hepaciviruses, of which many have been recently identified. Of the latter, the rodent/rat hepacivirus from Rattus norvegicus species-1 (RHV-rn1) holds promise as a surrogate virus in fully immunocompetent rats that can inform our understanding of the interaction between the immune response and viral outcomes (i.e., clearance vs. persistence). However, further characterization of these animal models is necessary before their use for gaining new insights into the immunopathogenesis of HCV and for conceptualizing HCV vaccines.

The infection is being eliminated as a public health threat by countries that introduce widespread testing and treatment for those at risk

The Justice Department announced today that it has reached a settlement with the University of Medicine and Dentistry of New Jersey School under the Americans with Disabilities Act.

Several drugs approved for the treatment of hepatitis C viral infection have been identified as potential candidates against COVID-19 caused by the SARS-CoV-2 coronavirus, according to a study based on extensive calculations using supercomputer simulations.

Researchers from Johannes Gutenberg University Mainz (JGU) in Germany simulated the way that about 42,000 different substances listed in open databases bind to certain proteins of SARS-CoV-2, and thereby inhibit the penetration of the virus into the human body or its multiplication. Using the powerful MOGON II supercomputer operated by JGU and the Helmholtz Institute Mainz, the researchers made more than 30 billion single calculations within two months.

They found that compounds from the four hepatitis C drugs simeprevir, paritaprevir, grazoprevir, and velpatasvir have a high affinity to bind SARS-CoV-2 very strongly and may therefore be able to prevent infection. "This computer simulation method is known as molecular docking and it has been recognised and used for years. It is much faster and less expensive than lab experiments," said Professor Thomas Efferth from JGU, lead author of the study published in the Bulletin of the World Health Organization. "As far as we know, we were the first to have used molecular docking with SARS-CoV-2. And it is fantastic news that we have found a number of approved hepatitis C drugs as promising candidates for treatment," Efferth said.

The results are also supported by the fact that both SARS-CoV-2 and the hepatitis C virus are a virus of the same type, a so-called single-stranded RNA virus, explained Efferth. According to the researchers, a natural substance from the Japanese honeysuckle (Lonicera japonica), which has been used in Asia against various other diseases for some time now, might be another strong candidate against SARS-CoV-2. "Our research results now need to be checked in laboratory experiments and clinical studies," said Efferth. Molecular docking had already been used successfully in the search for active substances against the coronaviruses MERS-CoV and SARS-CoV, he added.

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Hepatitis B and C viral control was found to improve kidney transplant survival rates, stated study published in the Journal of Hepatology. Renal

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Survival rate of patients who received a heart transplant from a donor with hepatitis C to those who received hearts from donors without the disease was similar.

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Only around five percent of the babies born to mothers with hepatitis C are themselves infected by the disease. A possible reason for this low figure

Patent holder and pharma major Gilead, announced voluntary licences with seven generic drug manufacturers in India to s

The Republican senator from Kentucky received a booster for Hepatitis A, one year after his trip to Guatemala.

Berlin, May 5: Several drugs approved for the treatment of hepatitis C viral infection have been identified as potential candidates against COVID-19 caused by the SARS-CoV-2 coronavirus, according to a study based on extensive calculations using supercomputer simulations.

Viral hepatitis is the name given to a viral infection that causes liver inflammation and damage. There are different types of hepatitis viruses that infect the liver out of which hepatitis A, B and C are the most common.

Viral hepatitis is the name given to a viral infection that causes liver inflammation and damage. There are different types of hepatitis viruses that infect the liver out of which hepatitis A, B and C are the most common.

Interview with Anthony S. Fauci, MD, author of Sofosbuvir and Ribavirin for Hepatitis C Genotype 1 in Patients With Unfavorable Treatment Characteristics: A Randomized Clinical Trial

Interview with Mark S. Sulkowski, MD, author of Sofosbuvir and Ribavirin for Hepatitis C in Patients With HIV Coinfection

Interview with Melissa A Simon, MD MPH, USPSTF member and coauthor of Screening for Hepatitis B Virus Infection in Pregnant Women: US Preventive Services Task Force Reaffirmation Recommendation Statement

Interview with Michael J. Barry, MD, Task Force member and coauthor of Screening for Hepatitis C Virus Infection in Adolescents and Adults: US Preventive Services Task Force Recommendation Statement

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