Different Forms Of Hepatitis Research Articles

Hepatitis-virus-positive patients management in dental office.

Hepatitis is a condition characterized by inflammation of the liver, which can be caused by several viruses including hepatitis A, B, C, D and E. This condition can affect the oral health of patients and increase the risk of complications during dental management. The clinical management of hepatitis patients in the dental setting requires a comprehensive and individualized approach to ensure safety and optimal treatment outcomes. This article aims to provide a comprehensive overview of the current literature on the dental management of patients with different forms of hepatitis. The article focuses on the specific challenges associated with dental treatments in hepatitis patients, including increased risk of infection and bleeding. Additionally, the article provides recommendations for dental practitioners, including infection control measures, communication with medical providers, and the use of prophylactic antibiotics. The authors show that the dental management of patients with hepatitis requires a thorough understanding of the specific challenges associated with this condition, as well as the implementation of appropriate preventive measures to ensure the safety and well-being of these patients. Further research is needed to better understand the impact of hepatitis on oral health and the most effective approaches to managing dental treatments in this patient population.

Identification of a Shared Cytochrome p4502E1 Epitope Found in Anesthetic Drug-Induced and Viral Hepatitis.

Cytochrome p4502E1 (CYP2E1) autoantibodies are biomarkers for drug-induced hepatitis and chronic hepatitis C. However, major histocompatibility-restricted CYP2E1 epitopes associated with these diseases have not been identified. We hypothesized that CYP2E1 epitopes associated with different types of hepatitis may be shared and may impact immune responses and metabolism. SYFPEITHI epitope prediction identified CYP2E1 candidate epitopes that would be recognized by MHC II haplotypes. Candidate epitopes were tested for induction of hepatitis and CYP2E1 autoantibodies in mice and recognition by sera from patients with anesthetic drug-induced and viral hepatitis. Human liver cells treated with epitope hybridoma serum were analyzed for mitochondrial stress. CYP2E1 activity was measured in human microsomes similarly treated. Epitope antibodies in viral hepatitis sera were analyzed using linear regression to uncover associations with liver pathology. A P value of <0.05 was considered significant. One epitope (Gly113-Leu135) induced hepatitis and CYP2E1 autoantibodies in mice after modification of Lys123 (P < 0.05). Gly113-Leu135 antiserum recognized mitochondria and endoplasmic reticula (P < 0.05), upregulated HSP27 (P < 0.01) and mitochondrial oxidative stress via complex 1 inhibition (P < 0.001), and inhibited CYP2E1 activity. Gly113-Leu135 IgG4 detected in viral hepatitis sera was associated with severe hepatic fibrosis (P = 0.0142). We found a novel CYP2E1 epitope that was detected in anesthetic and viral hepatitis and that triggered hepatitis in mice. Our findings may improve understanding of hepatic immune responses triggered by metabolism or viruses.IMPORTANCE Drug-induced hepatitis is the leading reason that an approved drug is removed from the commercial market. Halogenated anesthetics can induce hepatitis in susceptible persons, and cytochrome p4502E1 (CYP2E1) enzymes responsible for their metabolism induce antibodies in addition to hepatitis. CYP2E1 antibodies detected in anesthetic hepatitis patients have been detected in patients with viral hepatitis, suggesting that these different forms of hepatitis could develop immune reactions to a common segment or epitope of CYP2E1. We have found a common MHC-restricted CYP2E1 epitope in anesthetic and viral hepatitis that is a dominant epitope in anesthetic hepatitis and is significantly associated with fibrosis in patients with viral hepatitis. Along with conformational epitopes, our identification of MHC-restricted CYP2E1 epitopes can be used to develop specific diagnostic tests for drug-induced or viral hepatitis or associated fibrosis or to predict individuals at risk for developing these diseases or their sequelae.

Viral Hepatites in Dental Practice: Risks and Prevention

Objective: To discuss the epidemiological aspects of viral hepatites in dental professionals, with emphasis of the forms of transmission and prevention. Method: Narrative review of the literature on risks and prevention of the hepatites types in dental practice. Results: Hepatites are a group of inflammatory liver diseases with several etiologies, among which the most common are those caused by the A-E hepatotropic viruses. Hepatites A and E have acute and self-limited clinical presentation. Hepatites B and C may become chronic and progress to cirrhoses. The signs and symptoms of hepatites are similar and their evolution to the chronic form is silent or oligosymptomatic, which makes the disease being diagnosed incidentally, frequently at an advance stage. The early diagnosis increases the chances of chances of cure. Health professionals are at higher risk of having hepatites, especially those causes by the B and C viruses. Conclusion: Dentists, in their daily practice, are more exposed to accidents with cutting and perforating instruments, being thus a group with high risk of contamination. It is possible that other agents causing different forms of hepatitis or other diseases are identified in the future. The adoption of the universal infection control measures is and will always be essential for controlling transmissible diseases in dental facilities.

Lyme Disease—Current State of Knowledge: Different Symptoms

There are four different species of human pathogen Borrelia in Europe (in central Europe, mainly Borrelia afzelii and Borrelia garinii), whereas the United States has only one (Borrelia burgdorferi). The vectors (ticks) on the two continents also differ. The result is that manifestations of disease or constellations of symptoms of in Germany/Europe occasionally significantly differ from the US (1). Acrodermatitis chronica atrophicans, comparatively common in these parts, is almost unknown in the US, as is borrelial lymphocytoma. Erythema migrans, arthritis, neuroborreliosis, and other manifestations often take a different clinical course in the US as they do in Europe. Because of these differences—some of them very pronounced—different preventive approaches (2) have been developed: In the US, a vaccine that was actually successful and effective against B burgdorferi was taken off the market in 2001 because of side effects and lacking economic viability. Currently, antibiotic treatment with a single dose of 200 mg doxycyclin, orally administered within 72 hours after the tick bite, seems promising in the US—in contrast to Germany. In terms of differential diagnoses and therapeutic strategy, the undifferentiated term Lyme borreliosis for all tickborne borrelioses, which was adopted perhaps slightly too uncritically from the Anglo-American literature, is confusing. For this reason, in 2003, I proposed a differentiation of currently (still) unified terminology into distinct variants of the infectious disease (3), such as has been the case for the different forms of hepatitis for a long time. But more is required: an interdisciplinary consensus (guideline) for is needed in order to provide more detailed definitions of the occurring clinical entities of this infection with its many facets, which is often the subject of controversial discussions or used as an exclusion diagnosis, and to put this on a more differentiated footing.

Primary Hepatitis in Dogs: A Retrospective Review (2002–2006)

Little is known about etiology, disease progression, treatment outcome, survival time, and factors affecting prognosis in dogs with primary hepatitis (PH). To review retrospectively different forms of hepatitis in a referral population, by the World Small Animal Veterinary Association Standardization criteria. One-hundred and one dogs examined for histologically confirmed PH between 2002 and 2006. Dogs with nonspecific reactive hepatitis were excluded. Retrospective study. Medical records were reviewed for prevalence, signalment, clinical and clinicopathologic manifestation, outcome, survival time, and prognostic factors for shortened survival. PH occurred in 0.5% of dogs in this referral population. Acute (AH) and chronic hepatitis (CH) were diagnosed in 21 and 67 dogs, respectively. Progression from AH to CH occurred in 5/12 of the repeatedly sampled dogs. CH was idiopathic in 43 (64%) dogs, and was associated with copper accumulation in 24 (36%) dogs. Median survival time was longer in dogs with AH than in dogs with CH (either idiopathic or copper associated), and dogs with lobular dissecting hepatitis had the shortest survival time. Prognostic factors predicting shortened survival were associated with decompensated liver function and cirrhosis at initial examination. The majority of PH in dogs is CH. Previous studies appear to have underestimated the etiologic role of copper in both AH and CH. Prognosis is reduced in dogs with hepatic cirrhosis or cirrhosis-related clinical findings. Further research into etiology and treatment effectiveness in all PH forms is needed.

History of U.S. Military Contributions to the Study of Viral Hepatitis

Epidemic jaundice, although known by armies since ancient times, became a concern of the U.S. military only after outbreaks occurred during World War II. Early work by military investigators defined, for the first time, the existence of two different forms of hepatitis. Subsequently, investigators described the effective prevention of symptomatic hepatitis using immune serum globulin. Military researchers contributed to the isolation of and testing for the virus of infectious hepatitis, work that was then instrumental in the designing and fielding of a hepatitis A vaccine. Hepatitis B contributions included the elaboration of community-based epidemiology and description of the efficacy of immune serum globulin prophylaxis. Most recently, studies on hepatitis E defined the epidemiology, performed genomic sequencing, and developed a DNA vaccine currently being tested against the disease. Major research contributions to the understanding of and protection against viral hepatitis have been made by the military medical establishment over the past 60 years.

Sequence heterogeneity of TT virus and closely related viruses.

TT virus (TTV) is a recently discovered infectious agent originally obtained from transfusion-related hepatitis. However, the causative link between the TTV infection and liver disease remains uncertain. Recent studies demonstrated that genome sequences of different TTV strains are significantly divergent. To assess genetic heterogeneity of the TTV genome in more detail, a sequence analysis of PCR fragments (271 bp) amplified from open reading frame 1 (ORF1) was performed. PCR fragments were amplified from 5 to 40% of serum specimens obtained from patients with different forms of hepatitis who reside in different countries (e.g., China, Egypt, Vietnam, and the United States) and from normal human specimens obtained from U.S. residents. A total of 170 PCR fragments were sequenced and compared to sequences derived from the corresponding TTV genome region deposited in GenBank. Genotypes 2 and 3 were found to be significantly more genetically related than any other TTV genotype. Moreover, three sequences were shown to be almost equally related to both genotypes 2 and 3. These observations suggest a merger of genotypes 2 and 3 into one genotype, 2/3. Additionally, five new groups of TTV sequences were identified. One group represents a new genotype, whereas the other four groups were shown to be more evolutionary distant from all known TTV sequences. The evolutionary distances between these four groups were also shown to be greater than between TTV genotypes. The phylogenetic analysis suggested that these four new genetic groups represent closely related yet different viral species. Thus, TTV exists as a "swarm" of at least five closely related but different viruses. These observations suggest a high degree of genetic complexity within the TTV population. The finding of the additional TTV-related species should be taken into consideration when the association between TTV infections and human diseases of unknown etiology is studied.

Characterization of humoral and CD4+ cellular responses after genetic immunization with retroviral vectors expressing different forms of the hepatitis B virus core and e antigens.

The humoral and CD4+ cellular immune responses in mice following genetic immunization with three retroviral vectors encoding different forms of hepatitis B virus core antigen (HBcAg) and e antigen (HBeAg) were analyzed. The retroviral vectors induced expression of intracellular HBcAg (HBc[3A4]), secreted HBeAg (HBe[5A2]), or an intracellular HBcAg-neomycin phosphoryltransferase fusion protein (HBc-NEO[6A3]). Specific antibody levels and immunoglobulin G isotype restriction were highly dependent on both the host major histocompatibility complex and the transferred gene. Humoral and CD4+ cellular HBcAg and/or HBeAg (HBc/eAg)-specific immune responses following retroviral vector immunization were of a lower magnitude but followed the same characteristics compared with those after immunization with HBc/eAg in adjuvant. Two factors influenced the humoral responses. First, in vivo depletion of CD8+ cells in HBc-NEO[6A3]-immunized H-2k mice abrogated both HBcAg-specific antibodies and in vitro-detectable cytotoxic T lymphocytes. Second, priming of H-2b mice with an HBc/eAg-derived T-helper (Th) peptide in adjuvant prior to retroviral vector immunization greatly enhanced the HBc/eAg-specific humoral responses to all three vectors, suggesting that insufficient HBc/eAg-specific CD4+ Th-cell priming limits the humoral responses. In conclusion, direct injection of retroviral vectors seems to be effective in priming HBc/eAg-specific CD8+ but comparatively inefficient in priming CD4+ Th cells and subsequently specific antibodies. However, the limited HBc/eAg-specific CD4+ cell priming can effectively be circumvented by prior administration of a recombinant or synthetic form of HBc/eAg in adjuvant.

The “priming” effect of Pre-S1 antigen on human leucocytes in different forms of hepatitis B infection

The “priming” effect of Pre-S1 antigen on human leucocytes in different forms of hepatitis B infection

The “priming” effect of Pre-S1 antigen on human leucocytes in different forms of hepatitis B infection

The “priming” effect of Pre-S1 antigen on human leucocytes in different forms of hepatitis B infection

A soluble form of the adhesion receptor CD58 (LFA-3) is present in human body fluids.

The human adhesion receptor CD58 (LFA-3) is expressed on most human cell types. Here we report on a soluble form of CD58 (sCD58) in human serum, human urine, and culture supernatants of several cell lines. sCD58 partially purified from human serum, from supernatant of the Hodgkin cell line L428, and purified sCD58 from human urine were found to have a molecular mass of 40-70 kDa under denaturating conditions (sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting). However, gel filtration of sCD58 purified from human urine gave a molecular mass of 118-166 kDa, suggesting a noncovalent homotrimer conformation or its association with other molecules. Using an enzyme-linked immunosorbent assay specific for CD58 we found that sera from patients suffering from different forms of hepatitis contained elevated sCD58 levels (n = 108). Accordingly, there was a fivefold increase of supernatant sCD58 when the hepatocellular carcinoma cell line Hep G2 was incubated with 25 ng/ml recombinant tumor necrosis factor-alpha in vitro. In contrast, sCD58 serum levels of 337 additional patients suffering from various other immunological disorders were not found to be raised. At high concentrations sCD58 binds to CD2-positive cells and inhibits rosette formation of human T cells to human erythrocytes. Thus, local release of large quantities of naturally occurring sCD58 may interfere with intercellular adhesion in vivo.

Detection of pre-S 1 proteins in peripheral blood mononuclear cells from patients with HBV infection

The presence of pre-S 1 proteins in peripheral blood mononuclear cell (PBMC) samples from 115 patients with different forms of hepatitis B virus (HBV) infection was investigated by Western blot. Among 67 chronic HBsAg carriers, HBV antigens were detected in the PBMC in 80% for HBsAg, 27% for HBc/e Ag and 34% for pre-S 1 proteins. The detection of pre-S 1 proteins in PBMC was significantly associated with the presence of serum markers of HBV replication (HBV DNA and/or DNA polymerase). In the group of 48 consecutive patients negative for serum HBsAg, but positive for anti-HBc with or without anti-HBs, HBsAg and pre-S 1 proteins could be detected in PBMC. This finding was more frequent among anti-HIV-positive patients (77 and 23% of the cases, respectively) than in the negative ones (23 and 4% of the cases, respectively). The detection of HBV DNA and polyadenylated RNA in some of the PBMC samples positive for HBV proteins suggests that these proteins may be expressed in PBMC, especially during intense HBV replication. In patients negative for serum HBsAg, PBMC may constitute a reservoir of HBV.

Different forms of hepatitis B virus DNA and expression of HBV antigens in peripheral blood mononuclear cells in chronic hepatitis B

The presence of both hepatitis B virus (HBV) DNA and HBV antigens (HBsAg, HBeAg) was assessed in peripheral blood mononuclear cells (PBMC) from 32 patients chronically infected with HBV. Three different molecular forms of HBV DNA were observed: free monomers (5), high-molecular-weight free concatemers (11), and integrated HBV DNA (9). The HBV DNA patterns in the PBMC were different from those found in liver and did not correlate with any specific profile of serum HBV markers. When the same PBMC were assayed for HBsAg, 22 of the 25 HBV DNA positive samples, but only three of the seven HBV DNA negative samples, were positive. By contrast, none of the PBMC samples from five healthy HBV vaccine recipients gave any positive signal in the HBV DNA or HBsAg assays. In some patients, T and B cells, monocytes, and polymorphonuclear (PMN) cells were assayed separately, showing that the DNA pattern was similar for these different leucocytes subsets and ruling out the possibility that these patterns might reflect PMN cell contamination. Thus, in chronic HBV infection, 87.5% (28/32) of patients were found to contain at least one HBV marker in their PBMC, and a strong correlation was found between the presence of HBV DNA and viral antigens, suggesting a specific expression of HBV encoded proteins.

β-Hexosaminidase Level in Serum from Patients with Viral Hepatitis as a Measure of Reticuloendothelial Function

The lysosomal enzyme beta-hexosaminidase was elevated in different forms of hepatitis. The enzyme level was correlated to the aminotransferases in the acute stage of hepatitis A and B. In hepatitis B there was also a correlation to ALP and bilirubin. In chronic hepatitis B a significant correlation was found only to ALAT. The elevated beta-hexosaminidase levels are attributed to defective non-parenchymal liver cell function in hepatitis.

Autolymphocytotoxins (CoCoCy) in different forms of hepatitis and cirrhosis (author's transl)

Sera of altogether 282 patients with different forms of hepatitis and cirrhosis were screened for cold reacting complement dependant auto-lympho-cytotoxins (CoCoCy). These antibodies are 19S-IgM-immunoglobins and have no HLA-antigen-specificity. CoCoCy occurred in 48% of the patients with chronic aggressive hepatitis (CAH), in 14% of the patients with chronic persistent hepatitis (CPH) and in intermediate rates in the sera of patients with acute hepatitis. No correlations was found between CoCoCy and hepatitis B-antigen (HB-Ag). CoCoCy could be demonstrated also in 20% of the sera of a HB-Ag-positive and in 6% of a HB-Ag-negative control group. The serum concentration of CoCoCy is low. CoCoCy seems to be of T-cell-specificity and to reflect the overall-immunoreactivity without relation to the specificity of the antigenic stimulus. Thus demonstration of CoCoCy may be of pathogeneic and pathodynamic rather than of diagnostic interest.

Cellular localization of hepatitis-associated antigen in livers of patients with different forms of hepatitis.

The livers of 49 persons who died from different forms of hepatitis were examined by immunofluorescence (IFL) and electron microscopy. Hepatitis-associated antigen (HAA) was found by IFL in 40% of cases of subacute hepatitis, 54% of cases of chronic aggressive hepatitis, and 31.6% of cases of postnecrotic cirrhosis of the liver. The antigen was not found in any of the nine cases of acute fatal and fulminant hepatitis. Typical HAA particles were identified in the nuclei of hepatocytes in all cases of chronic aggressive hepatitis and postnecrotic cirrhosis studied by electron microscopy. Combined immunofluorescent and histologic studies revealed an inverse correlation between the amount of HAA and the extent and severity of parenchymal changes in the liver and the presence of HAA in body fluids. The results provide additional evidence that subacute hepatitis and the different types of chronic hepatitis, including hepatic cirrhosis, are etiologically related to HAA. Epidemiologic, immunologic, and physicochemical data strongly suggest that hepatitis-associated antigen (HAA) is intimately related to the etiologic agent of acute viral hepatitis or that it may be the

Platelet aggregation test in the study of hepatitis.

The platelet aggregation test (PLA) can be used as an indicator of Australia antigen or antibody in the serum. 1,2 The reaction of Au antigen-Au antibody complexes with human platelets changes the pattern of sedimentation of platelets on microplates. 2 This method has also been used to detect other antibodies and antigens. 3 When PLA was used to study hepatitis sera, it was soon found that many of these sera reacted directly with platelets without any added antibody or antigen. Earlier studies show that this can be a sign of the presence of immune complexes in the blood. 4 The possibility of immune complexes in severe hepatitis cases has recently been under special consideration. 5 This paper presents the results of 93 cases of different forms of hepatitis, 49 other diseases, and 99 blood donors. Special consideration is given to the direct reactivity of sera. The detection of the

Australia antigen immune complexes in patients with different forms of hepatitis.

In 1969, Shulman and Barker [1] and Purcell et al. [2] found, by measurement of anticomplementary activity, that Australia (Au) antigen immune complexes (Au/AuAb) are present in sera of patients with acute viral hepatitis (AVH). This observation was confirmed by electron microscopy in the same year by Almeida and Waterson [3], who observed particles of Au antigen covered by antibody. These important findings prompted us to analyze additional sera obtained from patients with different forms of hepatitis. For this purpose, we adapted the immunofluorescent test (IFT), using as a substrate liver obtained at autopsy from a leukemic patient who had large quantities of Au antigen.