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Zoonoses ◽  
2022 ◽  
Vol 2 (1) ◽  
Author(s):  
Zhangyan Zhao ◽  
Haicheng Tang ◽  
Feng Li

Background: Every year, approximately 800,000 people die from liver diseases associated with hepatitis B virus (HBV) infection. Complications outside the liver are common, such as fungal lung infections and viral infections. These complications may be associated with poor immune function, thus making clinical treatment difficult and increasing the risk of death. Therefore, HBV-infection-related liver diseases are worthy of clinical attention and further research. Case summary: We report a case of HBeAg-negative chronic hepatitis B in which the patient received entecavir as an anti-HBV treatment after liver dysfunction. During the treatment, the patient was diagnosed with measles and severe viral pneumonia. After comprehensive treatment, including active antiviral medications and mechanical ventilation, the patient recovered and was discharged. Conclusion: HBV infection causes liver damage, affects immune function, and is likely to be associated with viral infections such as measles. Consequently, infections may lead to complications, such as severe viral pneumonia, that endanger patients’ lives. To decrease complications and mortality, better understanding of the disease is necessary to enable early diagnosis.


2022 ◽  
Vol 8 ◽  
Author(s):  
Young Chang ◽  
Soung Won Jeong ◽  
Jae Young Jang

Hepatitis B virus (HBV) reactivation associated with various therapeutic interventions is an important cause of morbidity and mortality in patients with current or resolved HBV infection. Because no curative treatment for HBV infection is yet available, there are many individuals at risk for HBV reactivation in the general population. Populations at risk for HBV reactivation include patients who are currently infected with HBV or who have been exposed to HBV in the past. HBV reactivation and its potential consequences is a concern when these populations are exposed to anti-cancer chemotherapy, immunosuppressive or immunomodulatory therapies for the management of various malignancies, rheumatologic diseases, inflammatory bowel disease, or solid-organ or hematologic stem cell transplantation. Accordingly, it has become important to understand the basics of HBV reactivation and the mechanisms by which certain therapies are more susceptible to HBV reactivation. This review aims to raise the awareness of HBV reactivation and to understand the mechanisms and the risks of HBV reactivation in various clinical settings.


Hepatology ◽  
2022 ◽  
Author(s):  
Sourina Pal ◽  
Debangana Dey ◽  
Bidhan Chandra Chakraborty ◽  
Madhuparna Nandi ◽  
Mousumi Khatun ◽  
...  

2022 ◽  
Author(s):  
Yue Jia ◽  
Jingjing Zhang ◽  
Lingfei Mo ◽  
Bomiao Ju ◽  
Nan Hu ◽  
...  

Abstract Background The rates of hepatitis B virus (HBV) infection in rheumatoid arthritis (RA) patients were controversial when considering the reported outcomes. It was speculated that HBV infection status altered after suffering from RA, and variations over HBV infection rates became apparent. Methods To compare the positive proportions of hepatitis B e antigen (HBeAg) and HBV DNA, a case-control study was performed between the 27 chronic hepatitis B (CHB) patients with RA and the 108 age-and gender-matched CHB patients. In addition, the positive rates of hepatitis B surface antigen (HBsAg) and hepatitis B core antibody (anti-HBc) were surveyed among the 892 RA patients. Results Compared to the CHB patients, the CHB patients with RA exhibited lower rates of HBeAg positivity (11.1% vs. 35.2%, P = 0.003), HBV DNA positivity (37.0% vs. 63.9%, P = 0.007) and ALT elevation (11.1% vs. 35.2%, P = 0.024). In the 892 RA patients, the prevalence of HBsAg (3.0%) was lower than that of China national data (7.2%), whereas the anti-HBc positive rate of 44.6% was higher than that of 34.1%. Conclusion HBV infection status altered after suffering from RA. Compared to the matched CHB patients, low positive proportions of HBeAg and HBV DNA were observed for CHB patients with RA.


2022 ◽  
Vol 12 ◽  
Author(s):  
Jing Ouyang ◽  
Silvere D. Zaongo ◽  
Xue Zhang ◽  
Miaomiao Qi ◽  
Aizhen Hu ◽  
...  

Hepatitis B virus (HBV) co-infection is fairly common in people living with HIV (PLWH) and affects millions of people worldwide. Identical transmission routes and HIV-induced immune suppression have been assumed to be the main factors contributing to this phenomenon. Moreover, convergent evidence has shown that people co-infected with HIV and HBV are more likely to have long-term serious medical problems, suffer more from liver-related diseases, and have higher mortality rates, compared to individuals infected exclusively by either HIV or HBV. However, the precise mechanisms underlying the comorbid infection of HIV and HBV have not been fully elucidated. In recent times, the human gastrointestinal microbiome is progressively being recognized as playing a pivotal role in modulating immune function, and is likely to also contribute significantly to critical processes involving systemic inflammation. Both antiretroviral therapy (ART)-naïve HIV-infected subjects and ART-treated individuals are now known to be characterized by having gut microbiomic dysbiosis, which is associated with a damaged intestinal barrier, impaired mucosal immunological functioning, increased microbial translocation, and long-term immune activation. Altered microbiota-related products in PLWH, such as lipopolysaccharide (LPS) and short-chain fatty acids (SCFA), have been associated with the development of leaky gut syndrome, favoring microbial translocation, which in turn has been associated with a chronically activated underlying host immune response and hence the facilitated pathogenesis of HBV infection. Herein, we critically review the interplay among gut microbiota, immunity, and HIV and HBV infection, thus laying down the groundwork with respect to the future development of effective strategies to efficiently restore normally diversified gut microbiota in PLWH with a dysregulated gut microbiome, and thus potentially reduce the prevalence of HBV infection in this population.


2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Shelina Moonsamy ◽  
Melinda Suchard ◽  
Pavitra Pillay ◽  
Nishi Prabdial-Sing

Abstract Background Hepatitis B virus (HBV), a global public health threat, is targeted for elimination by 2030. As national HBV prevalence and incidence is lacking for South Africa, our study aimed to provide such data in the public health sector. Methods We analysed laboratory-confirmed HBV data from 2015 to 2019 to determine annual prevalence and incidence rates of HBV infection per 100,000 population, HBsAg and anti-HBc IgM test positivity rates, and HBsAg and anti-HBc IgM testing rates per 100,000 population. Time trend and statistical analyses were performed on HBsAg and anti-HBc IgM test positivity rates. Results The national prevalence rate of HBV infection per 100,000 population increased from 56.14 in 2015 to 67.76 in 2019. Over the five years, the prevalence rate was higher in males than females, highest amongst individuals 25 to 49 years old and highest in Gauteng province. The HBsAg test positivity rate dropped from 9.77% in 2015 to 8.09% in 2019. Over the five years, the HBsAg test positivity rate was higher in males than females, amongst individuals 25 to 49 years old and amongst individuals of Limpopo province. Amongst HBsAg positive children under 5 years old, the majority (65.7%) were less than a year old. HBsAg testing rates per 100,000 population were higher in females under 45 years of age and in males 45 years and above. The national incidence rate of acute HBV infection per 100,000 population dropped from 3.17 in 2015 to 1.69 in 2019. Over the five-year period, incidence rates were similar between males and females, highest amongst individuals 20 to 39 years old and highest in Mpumalanga province. Amongst individuals 20 to 24 years old, there was a substantial decline in the incidence and anti-HBc IgM test positivity rates over time. Anti-HBc IgM testing rates per 100,000 population were higher in females under 40 years of age and in males 40 years and above. Conclusion Critical to hepatitis B elimination is strengthened infant vaccination coverage and interruption of vertical transmission. Transmission of HBV infection in adults may be reduced through heightened awareness of transmission routes and prevention measures.


Author(s):  
Kemal Fariz Kalista ◽  
Maryati Surya ◽  
Silmi Mariya ◽  
Diah Iskandriati ◽  
Irsan Hasan ◽  
...  

Background: Hepatitis B virus (HBV) infection is still one of the biggest health problems in the world, which could lead to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Treatment for HBV infection has not yet achieved a functional cure. More studies are needed to investigate human HBV (HuHBV), but the scarcity of animal models for HuHBV infection became a barrier. Recently, many studies have shown that Tupaia are suitable for the study of HuHBV. The purpose of this study was to develop a primary tupaia hepatocyte (PTH) culture from T. javanica, a species of Tupaia found in Indonesia, and to prove that HuHBV can replicate in the PTH.Method: In vitro experimental study using PTH isolated from five wild adult T. javanica in Primate Research Center, IPB University. HuHBV was taken from humans with HBsAg and HBV-DNA (+). PTH cells then were infected with HuHBV after reaching 80% confluence. Observation on PTH cells was done everyday for 20 days. Qualitative and quantitative HBsAg were measured using a CMIA while HBV-DNA and cccDNA were measured by RT-PCR.Results: A cytopathic effect was seen on day post infection (DPI)-16. HBsAg and HBV-DNA were detected from DPI-2 until DPI-18, with HBV-DNA level peaked on DPI-12. cccDNA concentration was fluctuating from DPI-2 until DPI-20 with highest level on DPI-16.Conclusion: HuHBV could infect and replicate in PTH from T. javanica can be infected with HuHBV and HuHBV can replicate in the PTH from T. javanica.


2022 ◽  
Author(s):  
Toshitada Takemori ◽  
Akiko Sugimoto-Ishige ◽  
Hironori Nishitsuji ◽  
Yushi Futamura ◽  
Michishige Harada ◽  
...  

Hepatitis B virus (HBV) infects 240 million people worldwide. Current therapy profoundly suppresses HBV replication but requires long-term maintenance therapy. Therefore there is still a medical need for an efficient HBV cure. HBV enters host cells by binding via the preS1-domain of the viral L protein to the Na + /Taurocholate Cotransporting Polypeptide (NTCP). Thus, NTCP should be a key target for the development of anti-HBV therapeutics. Indeed, Myrcludex B, a synthetic form of the myristoylated preS1 peptide, effectively reduces HBV/HDV infection and has been approved as Hepcludex® in Europe for the treatment of patients with chronic hepatitis D virus (HDV) infection. We established a monoclonal antibody (mAb) N6HB426-20 that recognizes the extracellular domain of human NTCP and blocks HBV entry in vitro into human liver cells but has much less of an inhibitory effect on bile acid uptake. In vivo , administration of the N6HB426-20 mAb prevented HBV viremia for an extended period of time after HBV inoculation in a mouse model system without strongly inhibiting bile acid absorption. Among the extracellular loops (ECLs) of NTCP, regions of amino acids (aa) 84-87 in ECL1 and aa 157-165 near ECL2 of transmembrane domain 5 are critically important for HBV/HDV infection. Epitope-mapping and the 3D model of the NTCP structure suggested that the N6HB426-20 mAb may recognize aa 276/277 at the tip of ECL4 and interfere with an binding of HBV to the aa 84-87 region. In summary, we identified an in vivo neutralizing NTCP-targeting antibody capable of preventing HBV infection. Further improvements in efficacy of this drug will pave the way for its clinical applications. IMPORTANCE A number of entry inhibitors are being developed to enhance the treatment of HBV patients with oral nucleos(t)ide analogues (NA). To amplify the effectiveness of NA therapy, several efforts have been made to develop therapeutic mAbs with neutralizing activity against HBs antigens. However, the neutralizing effect of these mAbs may be muted by a large excess of HBsAg-positive noninfectious particles in the blood of infected patients. The advantage of NTCP-targeted HBV entry inhibitors is that they remain effective regardless of viral genotype, viral mutations and the presence of subviral particles. Although N6HB426-20 requires a higher dose than Myrcludex to obtain equivalent suppression of HBV in a model mouse system, it maintained the inhibitory effect for a long time post administration in proportion to the half-life of an IgG mAb. We believe that further improvements will make this antibody a promising treatment option for patients with chronic hepatitis B.


Author(s):  
Tri Nugraha Susilawati ◽  
Winda Rahayuningtyas ◽  
Triyanta Yuli Pramana

Background: A persistent infection of hepatitis B virus (HBV) can cause liver cirrhosis and hepatocarcinoma even though the virus itself is non-cytopathic and does not cause cell injury. It has been asserted that liver injury in chronic HBV infection is attributed to the host immune system responding to HBV infection. Cytokines have a critical role in mediating immune responses to viral infection. This study aimed to determine the correlation between the levels of serum IFN-γ, IL-2, IL-17, and TNF- α with the progress of chronic HBV infection that was determined through provisional diagnosis, patient’s age, and the levels of serum transaminases.Method: Blood samples were collected from patients with chronic hepatitis B and the levels of serum IFN-γ, IL-2, IL-17, and TNF-α were measured by using ELISA. The correlation between each cytokine levels and the provisional diagnosis, patient’s age, and serum transaminases were analyzed by using the Spearman correlation test with a p value of 0.05 is considered as statistically significant.Results: A total of 47 samples were collected from patients with chronic hepatitis B (n=38), chronic hepatitis B with liver cirrhosis (n = 6), and chronic hepatitis B with hepatocellular carcinoma (nc = 3). A significant correlation was found between the levels of serum IFN-γ and aspartate aminotransferase (AST) (p = 0.04).Conclusion: The increase of serum IFN-γ and AST levels may highlight the importance of these particular cytokine and liver transaminase in the immune response to chronic HBV infection since IFN-γ is capable to induce apoptotic cell death which promotes AST release and facilitates liver injury.


2022 ◽  
Author(s):  
Garima Garg ◽  
Meenu MN ◽  
Kajal Patel ◽  
Shashank Purwar ◽  
Sramana Mukhopadhyay ◽  
...  

Background: The role of sodium taurocholate co-transporting polypeptide (NTCP), in facilitating the binding of Hepatitis B virus (HBV) on surface of hepatocytes is well documented. Expression of NTCP in extra hepatic cells may make these cells susceptible to HBV infection and support cellular proliferation akin to hepatocytes. Placental replication of HBV is not well explored. In this study we have assessed the expression of NTCP and HBV replication markers (HBeAg, HBcAg, and HBV DNA) in placental cells, to investigate if these cells act as host for HBV. Methods: Fourty one HBsAg+ve pregnant women along with 10 healthy controls were enrolled after obtaining informed consent. The HBV DNA in placenta was detected by qPCR using primers for X and core ORF. Expression of NTCP in placenta was analyzed by qRT-PCR and further investigated by immunohistochemistry (IHC) along with HBV replication biomarkers, HBeAg, and HBcAg. Results: HBsAg positive subjects were divided in two groups on the basis of viral load [High Viral Load (HVL) Group; viral load ≥2000IU/ml, Low Viral Load (LVL) Group; viral load <2000IU/ml] according to INASL guidelines 2018. HBV infected females showed increased expression of NTCP in trophoblasts of placenta compared to control group (HVL 3.69,SE 0.13 Vs Control 1.74,SE 0.15, p=0.0117). Furthermore, significant difference in NTCP expression was also observed between HVL and LVL group (HVL 3.69,SE 0.13 Vs LVL 1.98,SE 0.17, p=0.022) and positively correlated with the maternal HBV DNA load. Membranous and/or cytoplasmic immunostaining of NTCP, and cytoplasmic staining of HBeAg and HBcAg in trophoblasts along with presence of HBV DNA indicated that trophoblasts are not only susceptible to HBV infection but may also be a site for viral replication. Conclusions: This is the pioneer study, which demonstrates expression of NTCP on placenta which may facilitate the entry of HBV. Furthermore, the study establishes the presence of HBeAg in placenta of patients without circulating HBeAg, indicating these cells may act as replication host/reservoir. This pioneering finding hints at the possibility of exploring the potential of NTCP blocking strategies in preventing vertical transmission of HBV.


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