scholarly journals A review regarding virology, etiology, prevalence and associated risk factors of Hepatitis A.

2020 ◽  
pp. 129-137

Hepatitis A is an infectious disorder of the liver prompted by Hepatovirus A virus (HAV). It is a kind of viral hepatitis. It has naked nucleocapsid virus with a single stranded, positive polarity RNA. It is devoid of virion polymerase and has a single serotype. Transmission is via fecal–oral route. In contrast to Hepatitis B virus and Hepatitis C virus, blood borne transmission of HAV is infrequent because viremia is short-term and of low titer. Mostly instances, have few or no signs, specifically in younger ones. The virus replicates in the gastrointestinal tract and then spreads to the liver during a short-term viremic period. HAV is not cytopathic for the hepatocyte. Hepatocellular injury is triggered by immune attack by the cytotoxic T cells. The time among the infection and signs, in patients that progress them, is among two and six weeks. When the signs occur, they commonly last 8 weeks and might encompass nausea, vomiting, diarrhea, jaundice, pain in abdomen and fever. Around 10 to 15 percent of patients undergo a recurrence of signs at some stage in the six months after the preliminary infection. Acute liver failure may also seldom occur, with this being extra regular in elderly. No antiviral medication is available. The most suitable test to diagnose acute infection is IgM antibody. Isolation of the virus from clinical samples is not done. Vaccine consists of killed virus. Administration of immune globulin in the course of the incubation can alleviate the disease.

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.


2014 ◽  
Vol 27 (1) ◽  
pp. 17-19 ◽  
Author(s):  
Dariusz Pachnia ◽  
Dorota Polz-Gruszka ◽  
Pawel Macielag ◽  
Malgorzata Polz-Dacewicz

Abstract Hepatitis A virus (HAV) is an hepatotropic human picornavirus that is associated only with acute infection of liver. This pathogen is mainly transmitted through the faecal-oral route, by person-to-person contact, and also contaminated drinking water and food. This reserach presenting the comparative seroepidemiological study (1990/1999/2012) on HAV infection was carried out in population from south-eastern Poland. Anti-HAV was tested in 613 subjects from 0 to over 60 years of age and the results were compared with those observed in 1990 and 1989/99. We also analyzed the number of vaccinations in the past decade and their role in preventing disease.


2000 ◽  
Vol 42 (4) ◽  
pp. 197-200 ◽  
Author(s):  
Isabel Takano OBA ◽  
Angela Maria Miranda SPINA ◽  
Cláudia Patara SARACENI ◽  
Marcílio Figueiredo LEMOS ◽  
Rita de Cássia Ferreira Andrade SENHORAS ◽  
...  

The possibility of detecting acute infection and immunity using body fluids that are easier to collect than blood, mainly in children, would facilitate the investigation and follow-up of outbreaks of hepatitis A (HAV). Our study was carried out to evaluate the detection of anti-HAV IgM, IgA and total antibodies in saliva using serum samples as reference. Forty three paired serum and saliva samples were analyzed. From this total, 24 samples were obtained from children and 1 from one adult during the course of acute hepatitis A; an additional 18 samples were obtained from health professionals from Adolfo Lutz Institute. The sensitivity to detect anti-HAV IgM was 100% (95%CI: 79.1 to 100.0%), employing saliva as clinical samples. In detecting anti-HAV IgA, the sensitivity was 80.8% (95%CI: 60.0 to 92.7%) and for the total antibodies was 82.1% (95%CI: 62.4 to 93.2%). The specificity was 100% for each. The rate of agreement was high comparing the results of serum and saliva samples for detecting HAV antibodies. We conclude that saliva is an acceptable alternative specimen for diagnosing acute hepatitis A infection, and for screening individuals to receive hepatitis A vaccine or immunoglobulin.


2010 ◽  
Vol 151 (28) ◽  
pp. 1132-1136 ◽  
Author(s):  
István Tornai

A krónikus vírushepatitisek jelentik ma a legismertebb okokat a hepatocellularis carcinoma (HCC) kialakulásában. A krónikus B- és C-vírus-hepatitis a májrákok körülbelül 40-50%-át okozza. A nyugati típusú társadalmakban a HCC előfordulása folyamatosan növekvő tendenciát mutat. Az alkohol számít a környezeti tényezők közül a legfontosabbnak, bár az alkoholfogyasztás a legtöbb országban csökken. Ez aláhúzza az egyéb környezeti tényezők fontosságát is. Az elfogyasztott alkoholmennyiséggel egyenes arányban növekszik a cirrhosis és a következményes HCC gyakorisága nőkben és férfiakban egyaránt. A kémiai anyagok közül a legismertebb a Kínában és Afrikában elterjedt aflatoxin, amely a gabonaféléket szennyező mycotoxin. Hasonló területeken endémiás, mint a hepatitis B-vírus, együtt szinergista hatást fejtenek ki. A dohányzás is egyértelműen bizonyított hepatocarcinogen hatással rendelkezik. Ez is jelentősen fokozódik, ha alkoholfogyasztással vagy vírushepatitisszel társul. Társadalmilag talán a legfontosabb az elhízás, a következményes nem alkoholos zsírmáj, illetve steatohepatitis és a 2-es típusú cukorbetegség, amelyek prevalenciája egyre fokozódik. Feltehetően ezek állnak a növekvő HCC-gyakoriság hátterében. Az inzulinrezisztencia és az oxidatív stressz képezik a legfontosabb patogenetikai lépéseket a májsejtkárosodásban. További fontos rizikótényező az orális fogamzásgátlók elterjedt használata. Egyes foglalkozások esetén a tartós szervesoldószer-expozíció is növeli a HCC rizikóját. Védelmet jelenthetnek az antioxidánsok, a szelén, a gyógyszerek közül a statinok és a feketekávé-fogyasztás.


2018 ◽  
Vol 69 (3) ◽  
pp. 747-751 ◽  
Author(s):  
Daniela Gabriela Badita ◽  
Iulia Ioana Stanescu ◽  
Andra Balcangiu Stroescu ◽  
Dan Piperea Sianu ◽  
Daniela Miricescu ◽  
...  

Viral hepatitis represents a major health problem worldwide. Approximately 1.4 million people are infected with hepatitis A virus every year, although given that most of the cases evolve asymptomatically the real number could be even higher. At the same time, hepatitis B virus affects up to 30% of the world population and represents one of the main causes of cirrhosis and hepatocellular carcinoma. Thus, it is very important to understand the physiopathology of viral hepatitis A and B not only for the diagnosis, but also for the therapeutic protocol. The present research aimed to determine if HAV and HBV can alter serum and salivary levels of total protein and of 2 important electrolytes: calcium and potassium.


2017 ◽  
Vol 89 ◽  
pp. 14-21 ◽  
Author(s):  
Vincent Thibault ◽  
Annabelle Servant-Delmas ◽  
Thoai Duong Ly ◽  
Anne-Marie Roque-Afonso ◽  
Syria Laperche

2019 ◽  
pp. 1-8 ◽  
Author(s):  
Alba J. Kihn-Alarcón ◽  
María F. Toledo-Ponce ◽  
Angel Velarde ◽  
Ximing Xu

PURPOSE Guatemala has the highest mortality and incidence of liver cancer in Central and South America. The aim of this study is to describe the extent of liver cancer in the country from 2012 to 2016 and the associated risk factors. METHODS A secondary analysis was performed using liver cancer mortality and morbidity data and data on risk factors, such as hepatitis B virus infection, cirrhosis, and alcoholism. RESULTS Analysis revealed that liver cancer causes approximately 20% of cancer deaths in the country, is more frequent in the population older than age 65 years old, and is increasing in those age 30 to 44 years. More than 25% of deaths occurred in the North and West regions. The incidence of major risk factors for development of liver cancer has decreased. CONCLUSION The high mortality of liver cancer compared with its incidence indicates that most patients are diagnosed at late stages. To reduce the burden of liver cancer, creation of strategies for earlier detection is needed.


2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Nikolaos P. Karidis ◽  
Ioanna Delladetsima ◽  
Stamatios Theocharis

Chronic hepatitis C virus (HCV) infection may eventually lead to progressive liver fibrosis and cirrhosis through a complex, multistep process involving hepatocyte death and regeneration. Despite common pathogenetic pathways present in all forms of liver cirrhosis irrespective of etiology, hepatocyte turnover and related molecular events in HCV-induced cirrhosis are increasingly being distinguished from even “similar” causes, such as hepatitis B virus- (HBV-) related cirrhosis. New insights in HCV-induced hepatocellular injury, differential gene expression, and regenerative pathways have recently revealed a different pattern of progression to irreversible parenchymal liver damage. A shift to the significant role of the host immune response rather than the direct effect of HCV on hepatocytes and the imbalance between antiapoptotic and proapoptotic signals have been investigated in several studies but need to be further elucidated. The present review aims to comprehensively summarize the current evidence on HCV-induced hepatocellular turnover with a view to outline the significant trends of ongoing research.


Sign in / Sign up

Export Citation Format

Share Document