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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of mouse L-2 fibroblasts with mouse hepatitis virus (MHV) results in strong inhibition of host cell protein synthesis. Since it has been suggested in other virus systems that translational control is modulated by changes in the intracellular ionic environment, we investigated the possible occurrence of similar changes during MHV infection. Membrane permeability to extracellular sodium ions was measured by culturing MHV-infected cells in the presence of 22Na+. Sodium influx into MHV-infected cells rose dramatically from 4 to 6 h post-infection. This influx correlated chronologically with the expression of MHV-mediated cell fusion. Cell fusion was blocked by the addition of a monoclonal antibody against the MHV E2 glycoprotein. This addition also resulted in a reduction in the normal influx of 22Na+, suggesting that E2 expression was responsible, directly or indirectly, for the increased permeability to sodium ions in infected cells. Cultures of MHV-infected cells were labelled with [35S]methionine in the presence of medium supplemented with sodium chloride at final concentrations ranging from 150 mM to 350 mM. Incorporation of radiolabel into proteins decreased with increasing NaCl concentration; however, the ratio of viral to cellular protein synthesis remained relatively constant. Similarly, alteration of intracellular Na+ and K+ levels by treatment of infected cells with ouabain had little effect on the pattern of viral/cellular protein synthesis. Using monoclonal anti-E2 antibody to inhibit Na+ influx, we demonstrated normal inhibition of host cell protein synthesis. We therefore conclude that MHV-induced shut-off of host translation is not mediated by changes in intracellular Na+ concentrations.
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PMID:Translational regulation in mouse hepatitis virus infection is not mediated by altered intracellular ion concentrations. 303 44

Epidemiological aspects of 400 consecutive in-patients with acute viral hepatitis, aged one to 81 years, were studied: 180 patients were less than 15 years old (mean age 6.9 years) and 220 were older (mean age 33.8 years). Serum hepatitis markers were detected by RIA. Hepatitis A (HA) was diagnosed in 188 patients (47.0%), ages ranging from one to 34 years (mean age 8.5 years), hepatitis B (HB) in 163 patients (40.8%), ages ranging from two to 72 years (mean age 32.7 years) and non-A, non-B hepatitis (NANBH) in 41 patients (10.2%), ages ranging from two to 81 years (mean age 35.4 years). Two patients had simultaneous HA and HB, and in six patients the etiology was not classified. In patients less than 15 years old, HA was the commonest type (91.1%), other etiologies having a low frequency; in the age group over 15 years, HB represented the most frequent type (70.0%), followed by NANBH (16.8%) and HA (10.9%). The probable source of infection was unknown in most of the cases (51%). With regard to HA, secondary contact was frequently reported and small outbreaks were registered. Parenteral exposure was the main probable source of HB and NANBH virus infections, the transmission frequently being iatrogenic. Drug abuse was a rare source of infection.
Infection
PMID:Epidemiological aspects of acute viral hepatitis in Portugal. 308 36

Eleven male fulminant hepatitis (FH) patients (mean age: 47.7 +/- 16 years) positive for hepatitis B surface antigen (HBsAg) but negative for IgM antibody to hepatitis B core antigen (IgM anti-HBc) were admitted consecutively to the Athens Hospital for Infectious Diseases between May 1981 and November 1983. Because of the absence of IgM anti-HBc, determined by an enzyme immunoassay, these patients were considered to be HBsAg carriers with a superimposed acute hepatitis. Three of the 11 patients received immunosuppressive chemotherapy during the six months before the onset of the acute hepatitis. None of the patients was homosexual or a drug addict. Infection with hepatitis A virus (HAV), hepatitis B virus (HBV), or hepatitis delta virus (HDV) was detected with serologic markers and/or molecular hybridization techniques. Fulminant hepatitis was attributed to spontaneous reactivation of chronic hepatitis B in four patients, chemotherapy-induced reactivation of chronic hepatitis B in three patients, HDV superinfection in one patient and possible superinfection by non-A, non-B agent(s), HDV, or HDV-like agents in three patients. Reactivation of chronic hepatitis B was an important cause of apparent acute hepatitis in heterosexual male HBsAg carriers from an area with a high prevalence of HBV infection.
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PMID:Fulminant hepatitis in asymptomatic hepatitis B surface antigen carriers in Greece. 309 15

Forty-seven drug addicts with histologically verified chronic non-A, non-B hepatitis were followed up for at least 12 months (mean 58 +/- 34.5 months). The patients were young, mean age 25 years and predominantly of the male sex. Forty patients (85%) had chronic persistent hepatitis (CPH) in the first biopsy and seven (15%) had chronic active hepatitis with or without cirrhosis (CAH/C). Except for bilirubin levels, standard biochemical tests at the time of the biopsy did not differ significantly between the two histologic groups. Ten patients had repeated biopsies performed and in four of them a histologic progression was observed. Six patients with CAH had evidence of cirrhosis. No patient developed hepatic failure or died because of the liver disease. Two patients seemed to resolve biochemically during follow-up. The rather benign liver morphology contrasts with chronic NANBH after blood transfusion where chronic active hepatitis and cirrhosis are much more common. Age-dependent immunologic factors might to some extent explain these differences.
Infection
PMID:Chronic non-A, non-B hepatitis in drug addicts--a follow-up study. 313 84

The aetiology of sporadic acute hepatitis in Taiwan was studied in a consecutive series of 273 patients, 209 males and 64 females, aged from less than 1 to 73 years. Only eight patients (2.9%) had acute hepatitis A, 36 (13.2%) acute hepatitis B and 57 (20.9%) had acute non-A, non-B hepatitis (NANB). The remaining 172 patients (63.0%) were HBsAg positive but anti-HBc IgM negative and were classified as acute hepatitis in chronic HBsAg carriers. Age-specific analysis revealed that acute hepatitis types A and B accounted for 35% and 47%, respectively of acute hepatitis in patients below age 10, but their prevalence decreased dramatically with increasing age and remained quite low in patients over age 40. In contrast, acute hepatitis NANB occurred predominantly in the older patients. The prevalence of acute hepatitis NANB was 11 to 15% in patients below age 40, but increased gradually with increasing age thereafter. Of the patients over age 60, 58% had acute hepatitis NANB. Acute hepatitis in chronic HBsAg carriers accounted for 59 to 76% of acute hepatitis episodes in patients over age 10 and below age 60. Sex-specific analysis revealed that the prevalence of acute hepatitis A or B showed no significant sex difference, whereas acute hepatitis in chronic HBsAg carriers occurred predominantly in males and acute hepatitis NANB occurred predominantly in females. Of the acute hepatitis episodes in chronic HBsAg carriers about one-third was due to hepatitis Delta virus superinfection, while the remaining two-thirds were most likely acute exacerbations of the underlying hepatitis B virus infection and a few were due to non-A, non-B hepatitis superinfection.
Infection
PMID:The aetiology of acute hepatitis in Taiwan: acute hepatitis superimposed on HBsAg carrier state as the main aetiology of acute hepatitis in areas with high HBsAg carrier rate. 314 Dec 91

Liver biopsy specimens previously taken from 16 haemophilic patients with chronic non-A, non-B hepatitis were reviewed. The degree of fibrosis correlated with serum procollagen III peptide (sPIIIP) concentrations, measured both at the time of biopsy and 4.25 years later. Two patients with extremely high sPIIIP concentrations had collateral veins on computed tomography, suggesting portal hypertension. Twenty eight of 47 patients (60%) had splenomegaly on computed tomography, and of 28 patients in whom intravenous contrast medium was used, seven (25%) had collateral oesophageal veins. Serum procollagen III peptide estimations and computed tomography, both non-invasive investigations, indicated that hepatic fibrosis and portal hypertension had developed in a proportion of haemophilic patients with non-A, non-B hepatitis. Infection with the human immunodeficiency virus (HIV) may modify the course of this presumably cytopathic virus infection of the liver.
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PMID:Non-invasive investigation of liver disease in haemophilic patients. 314 33

We reviewed laboratory-acquired infections occurring in Utah from 1978 through 1982. Written and telephone interviews of supervisors of 1,191 laboratorians revealed an estimated annual incidence of 3 laboratory-acquired infections per 1,000 employees. Infections, in order of frequency, included hepatitis B (clinical cases), shigellosis, pharyngitis, cellulitis, tuberculosis (skin test conversion), conjunctivitis, and non-A, non-B hepatitis. One-half of large laboratories (over 25 employees), but only 12% of smaller laboratories, reported infections. The annual incidence, however, at smaller laboratories was more than three times greater than at large laboratories (5.0 versus 1.5 per 1,000; P less than 0.05, chi-square test). Microbiologists were at greatest risk of infection, with an incidence of almost 1%, followed by generalists and phlebotomists. Shigellosis was acquired only by microbiologists and accounted for more than half of their infections. The most common laboratory-acquired infection, hepatitis B, affected a microbiologist, a hematologist, a phlebotomist, a pulmonary blood gas technician, and a blood bank technologist who died from her illness. Clinical cases of hepatitis B occurred at a rate 10 times higher than the rate in the general U.S. population. The incidence of tuberculosis skin test conversion was intermediate between rates reported for hospital employees and for the state of Utah.
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PMID:Infections acquired in clinical laboratories in Utah. 315

Seromarkers for hepatitis A, B and D were used to determine the cause of acute hepatitis in 94 children (age 2 to 14 years) prospectively studied when they were admitted to Embaba Fever Hospital in Cairo, Egypt, between January and April 1983. The diagnoses were: hepatitis A (4%), hepatitis B (33%), acute hepatitis in HBsAg carriers (10%), dual infections with A and B (2%), and hepatitis non-A, non-B (NANB) (50%). Past hepatitis A was diagnosed in 96%. Among acute hepatitis B infections, 17% (5 of 29 tested) had anti-delta antibody; of HBsAg positive persons, 15% (6 of 40) were HBeAg positive. Two patients had simultaneous presence of HBsAg and antiHBs. For differential diagnosis, clinical, epidemiological, and biochemical findings were evaluated but did not distinguish hepatitis B from NANB hepatitis. Males predominated for HBV infections. No risk factors were found for 58% of HBV and 70% of NANB infections; of the remaining patients, 42% percent of HBV and 30% of NANB infections were associated with injections or surgery but none with transfusion or known contact with hepatitis cases.
Infection
PMID:The etiology of acute hepatitis in hospitalized children in Cairo Egypt. 321 88

Expression of hepatitis delta virus (HDV) markers was investigated in sera from 310 patients with acute hepatitis, 63 chronic hepatitis B surface antigen (HBsAg) carriers and 76 drug addicts positive for at least one serological hepatitis B virus (HBV) marker. Acute HDV infection occurred in 17.1% of the patients with acute hepatitis. Among 40 cases of coinfection, hepatitis was severe in ten and fulminant in three. Only two of the 13 superinfected patients showed a severe hepatitis, but a high percentage (78%) of them developed chronic hepatitis one year after HDV infection. Also in our area parenteral drug addiction represents the main factor of risk for HDV infection. The high prevalence of HDV infection in our area points to the necessity for serological screening for HDV markers in patients with acute and chronic hepatitis.
Infection 1988
PMID:Clinical features of hepatitis delta virus infection in a northern Italian area. 322 May 79

We describe here two cases of delta hepatitis (a coinfection and a superinfection) presenting as acute HBsAg-negative hepatitis. The first patient, a parenteral drug abuser, had a biphasic course of the disease, with HBsAg detectable transiently only during the relapse. Testing for delta markers on stored sera gave evidence of HBV/HDV coinfection. The other patient, a hospital nurse, chronic asymptomatic carrier of HBsAg, developed fulminant hepatitis with the transient appearance of antibody to HBsAg. She survived massive liver necrosis, and serological analysis of HDV markers documented a hepatitis delta virus superinfection. These cases demonstrate the possible substantial repression of HBV gene products exerted by the replication of delta virus, with a likely misdiagnosis if delta markers are not determined in serial serum samples.
Infection 1988
PMID:A possible misdiagnosis in patients presenting with acute HBsAg-negative hepatitis: the role of hepatitis delta virus. 322 May 81


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