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Advances in Experimental Medicine and... 2021Interactions between liver cells are closely regulated by Notch signaling. Notch signaling has been reported clinically related to bile duct hypogenesis in Alagille... (Review)
Review
Interactions between liver cells are closely regulated by Notch signaling. Notch signaling has been reported clinically related to bile duct hypogenesis in Alagille syndrome, which is caused by mutations in the Jagged1 gene. Notch activation and hepatocarcinogenesis are closely associated since cancer signaling is affected by the development of liver cells and cancer stem cells. Gene expression and genomic analysis using a microarray revealed that abnormalities in Notch-related genes were associated with the aggressiveness of liver cancer. This pattern was also accompanied with α-fetoprotein- and EpCAM-expressing phenotypes in vitro, in vivo, and in clinical tissues. Hepatitis B or C virus chronic infection or alcohol- or steatosis-related liver fibrosis induces liver cancer. Previous reports demonstrated that HBx, a hepatitis B virus protein, was associated with Jagged1 expression. We found that the Jagged1 and Notch1 signaling pathways were closely associated with the transcription of covalently closed circular hepatitis B virus DNA, which regulated cAMP response element-binding protein, thereby affecting Notch1 regulation by the E3 ubiquitin ligase ITCH. This viral pathogenesis in hepatocytes induces liver cancer. In conclusion, Notch signaling exerts various actions and is a clinical signature associated with hepatocarcinogenesis and liver context-related developmental function.
Topics: Hepatitis; Hepatitis B virus; Humans; Liver Neoplasms; Receptors, Notch; Repressor Proteins; Signal Transduction; Ubiquitin-Protein Ligases
PubMed: 33034027
DOI: 10.1007/978-3-030-55031-8_6 -
World Journal of Gastroenterology Dec 2021In 2016, the World Health Assembly adopted a Global Health Sector Strategy on viral hepatitis, with targets set for the years 2020 and 2030 to achieve hepatitis...
In 2016, the World Health Assembly adopted a Global Health Sector Strategy on viral hepatitis, with targets set for the years 2020 and 2030 to achieve hepatitis elimination. The main target of hepatitis elimination strategy is to reduce the incidence of hepatitis B virus (HBV) and hepatitis C virus (HCV) by 90% and mortality by 65% in 2030. In last 5 years, the number of people receiving HCV treatment has increased from 1 million to 9.4 million; however, this number is far from the 2030 target of 40 million people receiving HCV treatment. HBV and HCV incidence rates are down from 1.4 million to 1.1 million annual deaths but this is far from the 2030 target of < 0.5 million deaths. The coronavirus disease 2019 pandemic has severely affected the efforts in the fight against hepatitis. No major donor has committed to investing in the fight against hepatitis. Time is running out. There is a need to speed up efforts in the fight against hepatitis to achieve hepatitis elimination by 2030.
Topics: Antiviral Agents; COVID-19; Global Health; Hepacivirus; Hepatitis B; Hepatitis C; Hepatitis, Viral, Human; Humans; SARS-CoV-2
PubMed: 35068864
DOI: 10.3748/wjg.v27.i47.8199 -
Human Genetics Jun 2020In rare cases, hepatitis A virus (HAV) and hepatitis B virus (HBV) can cause fulminant viral hepatitis (FVH), characterized by massive hepatocyte necrosis and an... (Review)
Review
In rare cases, hepatitis A virus (HAV) and hepatitis B virus (HBV) can cause fulminant viral hepatitis (FVH), characterized by massive hepatocyte necrosis and an inflammatory infiltrate. Other viral etiologies of FVH are rarer. FVH is life-threatening, but the patients are typically otherwise healthy, and normally resistant to other microbes. Only a small minority of infected individuals develop FVH, and this is the key issue to be addressed for this disease. In mice, mouse hepatitis virus 3 (MHV3) infection is the main model for dissecting FVH pathogenesis. Susceptibility to MHV3 differs between genetic backgrounds, with high and low mortality in C57BL6 and A/J mice, respectively. FVH pathogenesis in mice is related to uncontrolled inflammation and fibrinogen deposition. In humans, FVH is typically sporadic, but rare familial forms also exist, suggesting that there may be causal monogenic inborn errors. A recent study reported a single-gene inborn error of human immunity underlying FVH. A patient with autosomal recessive complete IL-18BP deficiency was shown to have FVH following HAV infection. The mechanism probably involves enhanced IL-18- and IFN-γ-dependent killing of hepatocytes by NK and CD8 T cytotoxic cells. Proof-of-principle that FVH can be genetic is important clinically, for the affected patients and their families, and immunologically, for the study of immunity to viruses in the liver. Moreover, the FVH-causing IL18BP genotype suggests that excessive IL-18 immunity may be a general mechanism underlying FVH, perhaps through the enhancement of IFN-γ immunity.
Topics: Cytokines; Hepadnaviridae; Hepatitis, Viral, Human; Humans
PubMed: 32285199
DOI: 10.1007/s00439-020-02166-y -
Journal of Medical Virology Jan 2022Hepatitis, a significant cause of mortality worldwide, results in around 1.34 million deaths each year globally. Africa is not exempt from the plague of Hepatitis....
Hepatitis, a significant cause of mortality worldwide, results in around 1.34 million deaths each year globally. Africa is not exempt from the plague of Hepatitis. Around 100 million estimated individuals are infected with Hepatitis B or C. Egypt has the highest prevalence of cases of Hepatitis followed by Cameroon and Burundi. The continent is severely affected by the onset of the COVID-19 pandemic, as the virus has added an additional burden on the already fragile continent. With the pandemic, it is presumable that Hepatitis like other viral diseases will pose a threat to collapsing healthcare system. Therefore, for Africa to become more resilient in the face of such menaces, including Hepatitis, further prevention policies are required to be implemented.
Topics: COVID-19; Developing Countries; Egypt; Health Services Accessibility; Hepacivirus; Hepatitis B virus; Hepatitis B, Chronic; Hepatitis C, Chronic; Humans; Liver; Prevalence; SARS-CoV-2
PubMed: 34506635
DOI: 10.1002/jmv.27330 -
Journal of Tropical Pediatrics Jan 2022The hepatitis A virus (HAV) is the most frequent global causes of vaccine-preventable viral hepatitis. Since Somalia is regarded as highly endemic for hepatitis A, the...
BACKGROUND
The hepatitis A virus (HAV) is the most frequent global causes of vaccine-preventable viral hepatitis. Since Somalia is regarded as highly endemic for hepatitis A, the hepatitis A vaccine was not included in the World Health Organization's expanded immunization program. The purpose of this study was to determine the prevalence of hepatitis A infection in the Somalia capital, Mogadishu.
METHODS
The serological results of 1153 individuals presenting to the Mogadishu Training and Research Hospital between January 2019 and January 2021 were examined retrospectively to evaluate the presence of anti-HAV IgG and IgM. The seroprevalence of anti-HAV IgG and IgM was analyzed on the basis of age and sex. The seroprevalence of anti-HAV IgG was also compared among the 11-year age group.
FINDINGS
The seroprevalence of anti-HAV IgG and IgM did not vary significantly between the sexes. Overall, the seroprevalence of anti-HAV IgG was 67.6%. The percentage of seropositivity for anti-HAV IgG was highest in adults aged ≥41 years (88.9%) and lowest in children aged 1-2 years (29.4%). Estimated age at midpoint of population immunity was 5 years which is compatible high endemicity. In addition, a significant rate of hepatitis A infection was also observed in the adolescent age group.
CONCLUSIONS
This study confirms the high HAV endemicity in Mogadishu. These data will be useful towards planning preventive and control measures by improving the sanitation programs in Mogadishu. Furthermore, prospective studies are needed to confirm these findings and evaluate urban-rural heterogeneity.
Topics: Adolescent; Adult; Child; Child, Preschool; Hepatitis A; Hepatitis A Antibodies; Humans; Infant; Retrospective Studies; Seroepidemiologic Studies; Somalia
PubMed: 35134249
DOI: 10.1093/tropej/fmac009 -
Liver International : Official Journal... Aug 2023Hepatitis D viral infection in humans is a disease that requires the establishment of hepatitis B, relying on hepatitis B surface Ag and host cellular machinery to... (Review)
Review
Hepatitis D viral infection in humans is a disease that requires the establishment of hepatitis B, relying on hepatitis B surface Ag and host cellular machinery to replicate and propagate the infection. Since its discovery in 1977, substantial progress has been made to better understand the hepatitis D viral life cycle, pathogenesis and modes of transmission along with expanding on clinical knowledge related to prevention, diagnosis, monitoring and treatment. The availability of serologic diagnostic assays for hepatitis D infection has evolved over time with current widespread availability, improved detection and standardized reporting. With human migration, the epidemiology of hepatitis D infection has changed over time. Thus, the ability to use diagnostic assays remains essential to monitor the global impact of hepatitis D infection. Separately, while liver biopsy remains the gold standard for the staging of this rapidly progressive and severe form of chronic viral hepatitis, there is an unmet need for clinical monitoring of chronic hepatitis D infection for management of progressive disease. Thus, exploration of the utility of non-invasive fibrosis markers in hepatitis D is ongoing. In this review, we discuss the virology, the evolution of diagnostics and the development of non-invasive markers for the detection and monitoring of fibrosis in patients with hepatitis D infection.
Topics: Humans; Hepatitis Delta Virus; Hepatitis D; Hepatitis D, Chronic; Hepatitis B; Hepatitis B virus; Fibrosis
PubMed: 36621853
DOI: 10.1111/liv.15515 -
La Revue de Medecine Interne Oct 2022Viral hepatitis A is characterized by a wide range of clinical pictures ranging from a completely unapparent infection to a fulminant, potentially fatal hepatitis or the... (Review)
Review
Viral hepatitis A is characterized by a wide range of clinical pictures ranging from a completely unapparent infection to a fulminant, potentially fatal hepatitis or the classical icteric form. Hepatitis A can develop in an unusual way and extrahepatic manifestations (neurological, renal, haematological, cholecystitis, acute pancreatitis, vasculitis, etc.) can occasionally complicate the course of the disease. Although hepatitis A infection was identified in the early 1970s, there are few or no studies assessing the actual frequency of these complications. They have been studied mainly through clinical case reports. Currently, since the disease has become more common in adults, these complications are being increasingly observed. We present an update on extrahepatic complications during hepatitis A, which should be known by both specialist doctors (infectiologists internists, hepatologists and others) and general practitioners.
Topics: Acute Disease; Adult; Hepatitis A; Humans; Pancreatitis; Vasculitis
PubMed: 35906107
DOI: 10.1016/j.revmed.2022.07.007 -
Current Opinion in Virology Feb 2022
Topics: Antiviral Agents; Hepatitis, Chronic; Hepatitis, Viral, Human; Humans
PubMed: 34861638
DOI: 10.1016/j.coviro.2021.10.008 -
Gastroenterology Clinics of North... Jun 2020
Topics: Cholangitis; Global Health; Hepatitis, Viral, Human; Humans
PubMed: 32389371
DOI: 10.1016/j.gtc.2020.01.015 -
Viruses Jan 2023Viral hepatitis is an infection of human hepatocytes resulting in liver damage. Dual infection of two hepatotropic viruses affects disease outcomes. The hepatitis A... (Review)
Review
Viral hepatitis is an infection of human hepatocytes resulting in liver damage. Dual infection of two hepatotropic viruses affects disease outcomes. The hepatitis A virus (HAV) and hepatitis E virus (HEV) are two enterically transmitted viruses; they are single-stranded RNA viruses and have common modes of transmission. They are transmitted mainly by the fecal-oral route and ingestion of contaminated food, though the HAV has no animal reservoirs. The HAV and HEV cause acute self-limiting disease; however, the HEV, but not HAV, can progress to chronic and extrahepatic infections. The HAV/HEV dual infection was reported among acute hepatitis patients present in developing countries. The impact of the HAV/HEV on the prognosis for acute hepatitis is not completely understood. Studies showed that the HAV/HEV dual infection increased abnormalities in the liver leading to fulminant hepatic failure (FHF) with a higher mortality rate compared to infection with a single virus. On the other hand, other reports showed that the clinical symptoms of the HAV/HEV dual infection were comparable to symptoms associated with the HAV or HEV monoinfection. This review highlights the modes of transmission, the prevalence of the HAV/HEV dual infection in various countries and among several study subjects, the possible outcomes of this dual infection, potential model systems for studying this dual infection, and methods of prevention of this dual infection and its associated complications.
Topics: Humans; Hepatitis E virus; Hepatitis A virus; Hepatitis A; Hepatitis E
PubMed: 36851512
DOI: 10.3390/v15020298