Hepatitis "A"--new developments

International Journal of Pharmacy & Integrated Health Sciences

Viral HepatitisEvery one of us has heard the word “hepatitis” and considered it a fatal disease. “Viral hepatitis” is the inflammation of the liver that is caused by a nasty family of viruses. Due to hepatitis, it is estimated that globally 1.34 million people died per year and it is also reported that about 80% of cases of liver cancer are only caused by hepatitis B and Hepatitis C together. The number of patients having this infection is amplifying each year, which is quite an alarming situation (1). Viral Hepatitis Modes of TransmissionHAV (Hepatitis A Virus) transmitted by the contaminated water (fecal-oral route), and for HBV (Hepatitis B Virus) and HBC (Hepatitis C Virus)There are mainly four modes of transmission, these are;1. Via blood2. Through sexually contact3. Through needle sharing during drug administration and4. From an infected mother to baby.Further, health care professionals who are dealing with the patients and their sample are also at higher risk.

Dooley/Sherlock's Diseases of the Liver and Biliary System, 2011

Anatomical abnormalities of the liver, 4 Anatomy of the biliary tract, 5 Surface marking, 6 Methods of examination, 6 Microanatomy of the liver, 7 Hepatic ultrastructure (electron microscopy) and organelle functions, 11 Functional heterogeneity of the liver, 15 Dynamics of the hepatic microenvironment in physiology and disease, 16 Hepatocyte death and regeneration, 17 References, 18

Journal of General Virology, 1988

Virus-like particles (VLPs) with a mean diameter of 32 nm were recovered from the stools of three acute phase cases ofenterically transmitted non-A, non-B hepatitis (ET-NANBH) occurring in the Soviet Union, North Africa and North America. VLPs from two of these cases were studied in detail and were shown to react specifically with antibody in acute phase sera obtained from other cases of ET-NANBH in Asia, the Soviet Union, North Africa and North America. Partially purified VLPs were found to sediment at 183S in sucrose gradients and to cross-react with antibody in acute phase sera from geographically isolated cases of ET-NANBH. The latter virus preparations were also used to document the seroconversion of experimentally ET-NANBHinfected cynomolgus macaques to 32 nm VLPs. Our findings indicate that one virus or class of viruses is responsible for the majority of ET-NANBH. Enterically transmitted non-A, non-B hepatitis (ET-NANBH) has been documented to occur in epidemic or sporadic fashion in India (

Archives of Disease in Childhood, 1989

Over a period of three and a half years, 348 consecutive children with acute hepatitis were studied. There were 205 boys and 143 girls aged from 3 months to 12 years old. The most common type was hepatitis A, of which there were 281 cases, 81% of the total; there were 41 in the under 4 years old age group (63% of that group), 99 in the 5-8 year old age group (87% of that group) and 141 in the 8-12 year old age group (83% of that group). Hepatitis B occurred in 29 (8% of the total), and non-A, non-B hepatitis occurred in 35 (10%). All the children with hepatitis A and all but one with hepatitis B recovered. There were three deaths from fulminant hepatitis, one in the group with hepatitis B and two with non-A, non-B. Clearance of the hepatitis B surface antigen was fast, by six months 26 patients having cleared the antigen and 21 (77%) being positive for hepatitis B surface antibody. One patient became a carrier of hepatitis B surface antigen.

Fecal excretion of hepatitis A virus (HAV) in 18 patients with HAV infection was evaluated by enzyme immunoassay (EIA) to detect viral antigen and by reverse transcription-PCR amplification followed by ethidium bromide staining (PCR-ETBr) or nucleic acid hybridization (PCR-NA) to detect viral genetic material. A gradation of sensitivity was observed in the detection of virus by the three methods. In persons who had detectable virus, serial stool samples were found to be positive by EIA for up to 24 days after the peak elevation of liver enzymes. Viral genetic material could be detected by PCR-ETBr for up to 34 days and by PCR-NA for up to 54 days after the peak elevation of liver enzymes. After intravenous inoculation of tamarins with stool suspensions categorized as highly reactive for HAV (positive by EIA, PCR-ETBr, and PCR-NA), moderately reactive (positive by PCR-ETBr and PCR-NA), or weakly reactive (positive by PCR-NA), only tamarins infected with highly reactive stool suspensions (EIA positive) developed HAV infection. We conclude that positivity of stool specimens for HAV by PCR-ETBr or PCR-NA indicates a lower potential for infectivity, compared to that of EIA-positive stools. Hepatitis A virus (HAV) is most commonly transmitted by the fecal-oral route. Several aspects of the pathogenesis of HAV infection, including the duration of HAV excretion in stool and the duration of infectivity, are not fully characterized. In addition, the relationship between detection of HAV genetic material in stool and infectivity has not been established. During an outbreak of hepatitis A in an institution for the developmentally disabled in August 1990, we collected serial stool specimens from patients with HAV infection. These stool specimens were evaluated for the presence of HAV and for infectivity in tamarins. The objectives of these studies were (i) to assess the duration of HAV excretion detected by enzyme immunoassay (EIA) and the PCR in adults and (ii) to evaluate the relationship between detection of HAV antigens and genetic material in stools and animal infectivity. MATERIALS AND METHODS Patient identification and specimen collection. In August and September 1990, an outbreak of hepatitis A occurred among residents at an institution for the developmentally disabled in Boulder County, Montana. Overall, 36 of 174 residents at the institution developed HAV infection, defined as positivity for immunoglobulin M antibody to HAV (IgM anti-HAV). The average age of the patients was 39 years (range, 28 to 59 years). In a retrospective cohort study conducted to identify risk factors for the acquisition of hepatitis A, frozen strawberries were implicated as the source of infection. The details of this outbreak investigation have been presented in a previous publication (10). At the outset of the outbreak investigation, 13 residents were identified with symptomatic acute hepatitis A, and immune globulin (IG) was administered to 143 other residents determined to be susceptible by serologic testing. These residents were then monitored by weekly serologic testing for liver enzyme elevations and hepatitis A markers, for up to 8 weeks. During the subsequent 2 weeks, an additional 23 (16%) of these 143 residents became positive for IgM anti-HAV (Abbott Laboratories, North Chicago, Ill.). Of these 23 residents, 7 (30%) had symptomatic HAV infection (jaundice), and 16 (70%) were identified by IgM anti-HAV seroconversion. IgM anti-HAV is found only associated with acute cases of HAV and would therefore not be present in the IG. Serum specimens were tested at the Hepatitis Branch, Centers for Disease Control and Prevention, for total and IgM anti-HAV by EIA (Abbott Laboratories). Virus detection. For patients with elevated liver enzymes, stool specimens were collected and evaluated for evidence of HAV. Stool suspensions were prepared at a 20% (wt/vol) concentration in phosphate-buffered saline (pH 7.4) and clarified by centrifugation at 7,000 g for 10 min at 4°C. Virus antigen was detected by EIA with rabbit anti-HAV as the capture antibody and hyperimmune chimpanzee anti-HAV serum as the detector antibody (16). The presence of viral nucleic acid was determined by immunocapture of the virus followed by reverse transcription-PCR amplification using primers targeted to the VP1 amino terminus (13). Amplified products were separated by agarose gel electrophoresis followed by detection with ethidium bromide staining (ETBr) or nucleic acid hybridization (NA) (12). Animal infectivity of virus antigen of RNA-positive stools. Six anti-HAV-negative tamarins, Saguinus mystax, were divided into three groups of two animals each. The animals were cared for and housed under Association for the Assessment and Accreditation of Laboratory Animal Care International, Inc.-approved animal husbandry conditions at the Animal Resources Branch, Scientific Resources Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, as outlined in the Guide for the Care and Use of Laboratory Animals prepared by the National Academy of Sciences and published by the National Institutes of Health. Each group was intravenously inoc-ulated with a different stool specimen from patient 1. Intravenous inoculations were used to ensure optimal infectivity. The stool specimens were categorized by the level of detectable viral antigen or RNA. Group 1 was inoculated with 1 ml of filtered human stool suspension that was positive for viral antigen, as determined by EIA, and contained viral nucleic acid as determined by a strong ETBr band. Group 2 was inoculated with 1 ml of stool suspension that did not contain sufficient viral antigen to be detected by EIA but did contain viral nucleic acid, as determined by PCR amplification, and resulted in a weak band by ETBr. The third group of tamarins were inoculated with 1 ml of stool suspension that did not contain sufficient viral antigen for EIA detection but was positive for viral nucleic acid, as determined by PCR amplification followed by NA (PCR-NA). Serum specimens were collected twice a week and tested for liver enzyme levels and total anti-HAV (HAVAB; Abbott laboratories). Stools, collected daily and pre

Canadian Journal of Infectious Diseases and Medical Microbiology

Hepatitis A virus (HAV) is one of the well-known viruses that cause hepatitis all around the globe. Although this illness has decreased in developed countries due to extensive immunization, numerous developing and under-developed countries are struggling with this virus. HAV infection can be spread by oral-fecal contact, and there are frequent epidemics through nutrition. Improvements in socioeconomic and sanitary circumstances have caused a shift in the disease’s prevalence worldwide. Younger children are usually asymptomatic, but as they become older, the infection symptoms begin to appear. Symptoms range from slight inflammation and jaundice to acute liver failure in older individuals. While an acute infection may be self-limiting, unrecognized persistent infections, and the misapplication of therapeutic methods based on clinical guidelines are linked to a higher incidence of cirrhosis, hepatocellular carcinoma, and mortality. Fortunately, most patients recover within two months ...

Journal of Medical Virology, 1992

Hepatitis E virus (HEV), a positive-strand RNA agent, has been associated with enterically transmitted non-A, non-B hepatitis in Asia, Africa, and Mexico. To evaluate the role of HEV in an outbreak of hepatitis in Pakistan, we used immune electron microscopy to detect 1) antibody to HEV, for evidence of infection, and 2) virus, to determine the pattern of HEV excretion. Paired sera from 2 patients were assayed for antibody by using reference HEV: one seroconverted, an atypical finding for HEV infections; the other had high levels of anti-HEV in both sera. Virus particles with the size (29 x 31 nm) and morphology of HEV were detected in feces from 10 of 85 patients and serologically identified as HEV by using reference antibodies from an HEV-infected chimpanzee. One of these HEV-containing specimens was collected 9 days before the onset of jaundice; it was among feces from 38 outpatients with nonspecific symptoms and biochemical hepatitis, 12 of whom subsequently developed jaundice. The other 9 feces with HEV were among 36 collected within 7 days of the onset of acute icteric hepatitis; all 11 feces from days 8 to 15 were negative for HEV. Fecal concentrations of HEV appeared t o be lower than those of many enteric viruses: only one specimen contained as many as 5 particles per EM grid square. It is concluded that HEV was etiologically associated with the epidemic and was predominantly excreted at very low levels during the first week of jaundice. Reyes et al. 19901 (Ticehurst, Neill, and Reyes, unpublished data). Like certain caliciviruses [for reviews, see Schaffer, 19791, HEV has a sedimentation coefficient of 183 S [Bradley et al., 1988al and was detected a t densities of 1.29 g/cm3 in potassium tartrateiglycerol [Bradley, 1990a,b] and 1.35 gicm3 in CsCl [Balayan et al., 19831; it was of interest KEY WORDS: enterically transmitted non-A, non-B (ET-NANB) hepatitis; epidemic, immune electron microscopy (IEM), antibody, virus particles -8 1992 WILEY-LISS, INC.

Hepatitis A is mainly transmitted by consuming food and water contaminated with feces or by direct physical contact with an infected person. It is also called "dirty hand disease". It can also be transmitted by consuming raw shellfish from sewage-contaminated water and by consuming frozen fruits and vegetables, and sexual transmission is also possible. Symptoms can range from mild to severe and can include fever, loss of appetite, diarrhea, nausea, abdominal pain, dark color of urine, light stools, and jaundice. Not all infected people have symptoms, and they occur more often in adults than in children. Hepatitis A is contagious two to four weeks before symptoms develop and for several days thereafter. People with hepatitis B or C can become carriers of the virus after recovery, even if chronic disease does not develop and symptoms are not present. Hot water and thorough cleaning of items used by patients is important to prevent the spread of infection.