Hepatitis C virus (HCV) infection is still a significant global health problem despite therapeutic advancements. Ribavirin and interferon therapy have been the sole available treatments for HCV infection for a number of years with low efficacy. Thus, currently, a number of therapeutic strategies are being used, including nanoparticles (NPs), micro‐RNAs such as small interfering RNA (siRNA), RNAi‐based gene silencing and antisense oligonucleotide‐based microRNA‐122, microRNA‐155, and short hairpin RNAs (shRNAs), and immunotherapeutic approaches such as anti‐programmed cell death 1(PD‐1), monoclonal antibodies (mAb or moAb), and monocyte‐derived dendritic cells (Mo‐DCs). Furthermore, direct‐acting antivirals (DAAs) and host‐targeting agents (HTA) were also the current therapeutic approaches with great efficacy. In spite of different clinical trials on HCV vaccine developments, nowadays there is no effective HCV vaccine in opposition to virus due to various challenges including genetic diversity, lack of immunocompetent small animal models, shortage of HCV vaccination testing alternatives, lack of an effective tissue culture method for replicating HCV, and inadequate knowledge regarding to immune responses against HCV infection. Nowadays, mRNA vaccine, recombinant viral vector, peptides vaccine, virus‐like particles, DNA vaccine, rational designed vaccine, and recombinant polyantigenic T‐cell‐based vaccine are novel promising candidates for HCV vaccine based on various clinical trials. This review summarizes the different therapeutic approaches and the advancements of vaccine candidates for HCV infection.

Hepatitis B virus (HBV)‐associated liver cancer is the third most prevalent cancer‐related cause of death worldwide. Different studies have been done on the histomolecular analysis of HBV induced‐liver cancer including epigenetics which are dynamic molecular mechanisms to control gene expression without altering the host deoxyribonucleic acid, genomics characterise the integration of the viral genome with host genome, proteomics characterise how gene modifies and results overexpression of proteins, glycoproteomics discover different glyco‐biomarker candidates and show glycosylation in malignant hepatocytes, metabolomics characterise how HBV impairs a variety of metabolic functions during hepatocyte immortalisation, exosomes characterise immortalised liver cells in terms of their differentiation and proliferation, and autophagy plays a role in the development of hepatocarcinogenesis linked to HBV infection.

The antigen recognition and immune response to acute and chronic hepatitis B virus (HBV) infections are the result of both the innate and adaptive immune response. The innate immune response comprises Dendritic Cells (DCs), which served as professional antigen-presenting cells and a bridge between innate and adaptive immunity, Kupffer cells and inflammatory monocytes for the continuous inflammation of hepatocyte, neutrophils for hepatic tissue damage due to acute inflammation, type I interferons (IFN), which induce an antiviral state on infected cells, directs natural killer (NK) cells to kill virally infected cells, reduces the population of infected cells, and promotes the effective maturation and site recruitment of adaptive immunity through the production of pro-inflammatory cytokines and chemokines. Through stimulating B cells, T-helper, and cytotoxic T cells, the adaptive immune system also protects against hepatitis B infection. During HBV infection, a network of cell types that can either play protective or harmful functions creates the anti-viral adaptive immune response. These many elements, such as ‎Cluster of differentiation four (CD4) T cells (traditionally known as helper T cells), are potent cytokine producers and necessary for the effective maturation of effector cytotoxic cluster of differentiation eight (CD8) T cells and B cell antibody production. By cytolytic and non-cytolytic processes, CD8 T cells are able to eliminate HBV-infected hepatocytes and directly detect virus-infected cells, and circulating CD4+ CD25+ regulatory T cells for the modulation of immune system. In order to avoid reinfection, B cells can produce antibodies that destroy free viral particles. Moreover, by presenting HBV antigens to helper T cells, B cells may also influence how well these cells operate.

Background: Hepatitis B vaccination is recommended for all children at birth within 24 hours or during childhood. Objective: This study was aimed to evaluate protective efficacy of hepatitis B vaccine and estimate the sero-prevalence of hepatitis B virus infection among vaccinated children. Materials and methods: A community-based cross-sectional study was conducted from March, 2021 to October, 2021 in Debre Markos town. A simple random sampling technique was used to select 165 fully vaccinated children aged 5–12 years old. A serum sample was used to determine hepatitis B surface antigen (HBsAg), anti-hepatitis B core antibody (anti-HBc), anti-hepatitis B surface antibody titer (anti-HBs) using ELISA. Results: The seroprevalence of HBsAg and anti-HBc anti-body was found to be 4.2% and 4.8% respectively. Of 165 fully vaccinated children, 129 (78.2%) had anti-HBs titer ≥ 10 mIU/ml. Among 129 sero-protected children, 76 (58.9%) were hypo-responders whereas the rest 53 (41.1%) were good responders. Those children within the age group of 5–7 years were 2.9 times (AOR: 2.873, 95% CI: 1.156, 7.141) (P<0.023) more likely to respond to HBV vaccine. Multivariate logistic regression revealed that children who were born from HBV positive mothers (AOR 3.917, 95% CI: 1.456, 5.365, P<0.027) and those who had history of injectable medications (AOR 9.232, 95% CI: 1.503, 11.697, P<0.016) were more likely to be HBsAg positive. Children who had history of hospital admission (AOR 6.973, 95% CI: 1.495, 8.530, P<0.013) were more likely to be anti-HBcAb positive. Conclusions: There was an intermediate prevalence of childhood HBV infection despite being vaccinated suggesting low protective efficacy of hepatitis B vaccine in the study area.

Background: In many low- and middle-income countries, including Ethiopia, dolutegravir (DTG)-based regimens are the preferred first-line regimens for people living with HIV (PLWH). However, there are concerns about hyperglycemia and, in certain circumstances, diabetes mellitus in individuals who have switched to DTG. Objective: To assess the prevalence and factors associated with hyperglycemia among PLWH on DTG-based antiretroviral therapy (ART). Design: An institutional-based cross-sectional study. Methods: The study was carried out from December 1, 2021 to February 30, 2022, and included 423 participants who were recruited via a simple random sampling technique. We enrolled PLWH aged 18 years or older who had been on DTG-based ART for more than 6 months. Data were collected by using an interviewer-administered structured questionnaire, medical card review, physical measurement, and biochemical measurements. Hyperglycemia was defined as a fasting blood glucose level ⩾110 mg/dl. Multivariable logistic regression was used to identify factors associated with hyperglycemia, using SPSS version 26.0 software. Variables with a p -value of <0.05 were considered statistically significant. Results: The prevalence of hyperglycemia among PLWH receiving DTG-based ART was 12.1% (95% CI: 9.2–15.1). Age (AOR = 1.04, 95% confidence interval (CI): 1–1.08, p = 0.036), BMI (AOR = 1.09, 95% CI: 1.01–1.17, p = 0.022), and triglyceride level (AOR = 2.44, 95% CI: 1.28–4.64, p = 0.006) were significant predictors of hyperglycemia among PLWH on DTG-based ART. Conclusion: Overall, our study revealed a high prevalence of hyperglycemia (12.1%) among PLWH receiving DTG-based ART. Age, BMI, and triglyceride levels were significant predictors of hyperglycemia. These findings underscore the importance of monitoring blood glucose levels in PLWH receiving DTG-based ART, with a special emphasis on patients with advanced age, increased BMI, and increased triglyceride levels.