Immune responses to H particles of poliovirus
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Virus-like particle
Monoclonal antibody 2F5 recognizing the ELDKWA epitope on HIV-1 gp41 has a significant neutralization potency against 90% of the investigated viruses of African, Asian, American, and European strains, but the antibody responses to the epitope 2F5 in HIV-1-infected individuals were very low. We attempted to induce high levels of epitope-specific antibodies to ELDKWA and its three mutated epitopes by candidate epitope vaccines. The four candidate epitope vaccines all induced strong antibody responses at dilutions from about 1:6,400 to 1:25,600. We tested the cross-reactions between these antisera and four epitope peptides. The ELDKWA-specific antisera showed strong cross-reactivity with three neutralizing-resistant mutated epitopes which contain changes in the D or K positions of the epitope sequence. Virus variants containing these changes could escape neutralization by monoclonal antibody 2F5. In immunoblotting analysis, the ELDKWA, ELDEWA, and ELEKWA epitope specific antibodies all recognized rsgp41 which confirms that the antibodies against both mutated epitopes, ELDEWA and ELEKWA, could cross-react with the native epitope on rsgp41. Although it is not clear whether the polyclonal antibodies induced by the ELDKWA epitope vaccine could neutralize the mutated viruses containing these mutated epitopes, it is conceivable that epitope vaccines based on mutated epitopes could induce strong antibody responses with predefined epitope specificity to neutralize mutated viruse containing the mutated epitope. An epitope vaccine, using different epitopes including mutated epitopes, could provide a new concept for developing a new vaccine against HIV-1.
Linear epitope
Polyclonal antibodies
Epitope mapping
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Summary Hepatitis B virus surface antigen ( HB s A g) plays an important role in maintaining the tolerance and may interfere with host innate and adaptive immune responses; therefore, novel therapeutic strategies to reduce HB s A g loads in patients infected with hepatitis B virus ( HBV ) are emerging as an attractive but challenging issue. Metformin could regulate hepatic metabolism while the latter interacts with HBV infection. We hypothesized that metformin could affect HB s A g expression and HBV replication and may work synergistically when combined with current antivirals. In our study, a notably inhibitory effect on HB s A g production, as well as a moderate inhibition in HBV replication and HB e A g expression was observed following metformin treatment. The 50% effective concentration ( EC 50 ) for extracellular HB s A g and intracellular HB s A g in HBV ‐producing H ep G 2.2.15 cells was 2.85 m m and 2.75 m m , respectively, with a similarly selective index of about 18. When administered in combination, metformin enhanced the inhibitory effects of interferon‐α2b on HB s A g expression and HBV replication and provided a complimentary role in HB s A g expression for lamivudine ( LMV ). This novel action of metformin derives partially from its inhibition on multiple HBV cis ‐acting elements. By the virtues of preferably hepatocyte distribution and safety profile, collectively, our results suggest that metformin would be potentially clinically helpful as an HB s A g production inhibitor.
HBeAg
Hepatitis B
cccDNA
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Epitope-vaccine is a newly developing vaccine which has many advantages comparied with to the traditional vaccine.The key step for designing epitope-vaccine is to screen epitopes.The epitope-screening methods include protein degration,peptide-probing scanning,epitope prediction by computer,et al.Usually,the epitope-vaccine needs combine some carriers to display immunologic activity,for example,lipid carriers,protein carriers,and adjuvant.In addition,researchers also use tandem repeat epitopes,conformational multiple antigen peptide(MAP) and epitope modifying to strengthen the immunological efficacity.The epitope-vaccine mainly contains viral epitope-vaccine,bacterial epitope-vaccine and epitope-vaccine for parasites.Although the researches on epitope-vaccine develop fast,some problems and challenges need to resolve impendingly.
Peptide vaccine
Epitope mapping
Linear epitope
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This study was conducted by the International Consortium for Blood Safety (ICBS) to identify high-quality test kits for detection of hepatitis B virus (HBV) surface antigen (HBsAg) for the benefit of developing countries.The 70 HBsAg test kits from around the world were evaluated comparatively for their clinical sensitivity, analytical sensitivity, sensitivity to HBV genotypes and HBsAg subtypes, and specificity using 394 (146 clinical, 48 analytical and 200 negative) ICBS Master Panel members of diverse geographical origin comprising the major HBV genotypes A-F and the HBsAg subtypes adw2,4, adr and ayw1-4.Seventeen HBsAg enzyme immunoassay (EIA) kits had high analytical sensitivity <0.13 IU/ml, showed 100% diagnostic sensitivity, and were even sensitive for the various HBV variants tested. An additional six test kits had high sensitivity (<0.13 IU/ml) but missed HBsAg mutants and/or showed reduced sensitivity to certain HBV genotypes. Twenty HBsAg EIA kits were in the sensitivity range of 0.13-1 IU/ml. The other eight EIAs and the 19 rapid assays had analytical sensitivities of 1 to >4 IU/ml. These assays were falsely negative for 1-4 clinical samples and 17 of these test kits showed genotype dependent sensitivity reduction. Analytical sensitivities for HBsAg of >1 IU/ml significantly reduce the length of the HBsAg positive period which renders them less reliable for detecting HBsAg in asymptomatic HBV infections. Reduced sensitivity for HBsAg with genetic diversity of HBV occurred with genotypes/subtypes D/ayw3, E/ayw4, F/adw4 and by S gene mutants. Specificity of the HBsAg assays was >or=99.5% in 57 test kits and 96.4-99.0% in the remaining test kits.Diagnostic efficacy of the evaluated HBsAg test kits differed substantially. Laboratories should therefore be aware of the analytical sensitivity for HBsAg and check for the relevant HBV variants circulating in the relevant population.
Hepatitis B
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Rationale & ObjectiveHepatitis B virus (HBV) transmission in hemodialysis units has become a rare event since implementation of hemodialysis-specific infection control guidelines: performing hemodialysis for hepatitis B surface antigen (HBsAg)-positive patients in an HBV isolation room, vaccinating HBV-susceptible (HBV surface antibody and HBsAg negative) patients, and monthly HBsAg testing in HBV-susceptible patients. Mutations in HBsAg can result in false-negative HBsAg results, leading to failure to identify HBsAg seroconversion from negative to positive. We describe 4 unique cases of HBsAg seroconversion caused by mutant HBV infection or reactivation in hemodialysis patients.Study DesignFollowing identification of a possible HBsAg seroconversion and mutant HBV infection, public health investigations were launched to conduct further HBV testing of case patients and potentially exposed patients. A case patient was defined as a hemodialysis patient with suspected mutant HBV infection because of false-negative HBsAg testing results. Confirmed case patients had HBV DNA sequences demonstrating S-gene mutations.Setting & ParticipantsCase patients and patients potentially exposed to the case patient in the respective hemodialysis units in multiple US states.Results4 cases of mutant HBV infection in hemodialysis patients were identified; 3 cases were confirmed using molecular sequencing. Failure of some HBsAg testing platforms to detect HBV mutations led to delays in applying HBV isolation procedures. Testing of potentially exposed patients did not identify secondary transmissions.LimitationsLack of access to information on past HBsAg testing platforms and results led to challenges in ascertaining when HBsAg seroconversion occurred and identifying and testing all potentially exposed patients.ConclusionsMutant HBV infections should be suspected in patients who test HBsAg negative and concurrently test positive for HBV DNA at high levels. Dialysis providers should consider using HBsAg assays that can also detect mutant HBV strains for routine HBV testing. Hepatitis B virus (HBV) transmission in hemodialysis units has become a rare event since implementation of hemodialysis-specific infection control guidelines: performing hemodialysis for hepatitis B surface antigen (HBsAg)-positive patients in an HBV isolation room, vaccinating HBV-susceptible (HBV surface antibody and HBsAg negative) patients, and monthly HBsAg testing in HBV-susceptible patients. Mutations in HBsAg can result in false-negative HBsAg results, leading to failure to identify HBsAg seroconversion from negative to positive. We describe 4 unique cases of HBsAg seroconversion caused by mutant HBV infection or reactivation in hemodialysis patients. Following identification of a possible HBsAg seroconversion and mutant HBV infection, public health investigations were launched to conduct further HBV testing of case patients and potentially exposed patients. A case patient was defined as a hemodialysis patient with suspected mutant HBV infection because of false-negative HBsAg testing results. Confirmed case patients had HBV DNA sequences demonstrating S-gene mutations. Case patients and patients potentially exposed to the case patient in the respective hemodialysis units in multiple US states. 4 cases of mutant HBV infection in hemodialysis patients were identified; 3 cases were confirmed using molecular sequencing. Failure of some HBsAg testing platforms to detect HBV mutations led to delays in applying HBV isolation procedures. Testing of potentially exposed patients did not identify secondary transmissions. Lack of access to information on past HBsAg testing platforms and results led to challenges in ascertaining when HBsAg seroconversion occurred and identifying and testing all potentially exposed patients. Mutant HBV infections should be suspected in patients who test HBsAg negative and concurrently test positive for HBV DNA at high levels. Dialysis providers should consider using HBsAg assays that can also detect mutant HBV strains for routine HBV testing.
Seroconversion
Hepatitis B
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Hepatitis B
Orthohepadnavirus
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Linear epitope
Bovine herpesvirus 1
Epitope mapping
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Summary. Occult hepatitis B virus (HBV) infection is characterized by the absence of detectable hepatitis B surface antigen (HBsAg) in the serum, despite detectable HBV DNA. Investigations of the mechanisms underlying the development of occult HBV infection are lacking in the current literature, although viral mutations in the surface region, resulting in decreased HBsAg expression or secretion, represent one potential mechanism. Wild‐type HBsAg expression vectors were constructed from genotype‐matched chronic HBV sequences. Site‐directed mutagenesis was then utilized to introduce three genotype A mutations – M103I, K122R and G145A – associated with occult HBV infection in vivo , alone and in combination, into the wild‐type HBsAg vectors. Transfection of Huh7 and HepG2 cell lines was performed, and cell culture supernatants and cell lysates were collected over 7 days to assess the effects of these mutations on extracellular and intracellular HBsAg levels. The G145A mutation resulted in significantly decreased extracellular and intracellular HBsAg expression in vitro . The most pronounced reduction in HBsAg expression was observed when all three mutations were present. The mutations evaluated in vitro in the current study resulted in decreased HBsAg expression and potentially increased hepatic retention and/or decreased hepatic secretion of synthesized HBsAg, which could explain the lack of HBsAg detection that is characteristic of occult HBV infection in vivo .
Occult
Hepatitis B
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Objective To observe the HBsAg and HBcAg expression in the renal tissue in hepatitis B virus associated glomerulonephritis(HBV-GN) . Methods We selected 50 cases of HBV-GN as research group and the other randomly selected 20 cases of non-HBV-GN(NHBV-GN) as control group and used indirect immunofluorescence assay to detect the HBsAg and HBcAg expression in the renal puncture biopsies. Results The HBsAg and HBcAg-positive particles in the HBV-GN renal tissue could be detected,with the positive rates of 70%(35/50) and 24%(12/50) ,while HBsAg and HBcAg failed to be detected in the kidney tissue of 20 cases of NHBV-GN,with a significant difference between the two groups(P0.05) . Conclusion The immune fluorescence detection of HBsAg and HBcAg is an important indicator in the diagnosis of HBV-GN. HBV plays an important role in the kidney tissue infection and replication and the pathogenesis of HBV-GN.
HBcAg
Hepatitis B
Immunofluorescence
Pathogenesis
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