Search bioRxiv⌕ Search

bioRxiv · 10.1101/385880

Epidemiological impact of hepatitis B vaccination in Monastir Tunisia (2000-17)

Abstract

Background: In 2016, the first global health sector strategy on viral hepatitis was endorsed with the goal of eliminating viral hepatitis as a public health threat by 2030. In Tunisia, effective vaccines for hepatitis B (HBV) have been added to the expanded programme of immunization (EPI) since July 1995 for new borns. We expected to have a decreasing trend in the prevalence rate of reported HBV. Our study aimed to address the epidemiological profile of HBV, to assess trends by age and gender in Monastir governorate over a period of 18 years according to immunization status and to estimate the burden (years lived with disability YLDs) of this pathology. Methods: We performed a descriptive cross sectional study of declared HBV from January 1, 2000 to December 31, 2017 defined as having positive serologic markers for HBs Ag. All declared patients were residents of Monastirs Governorate. EPI included two periods, the first between 1995 and 2006 following a three-dose schedule (3, 4, 9 months). The second PI cohort after 2006 following a three-dose schedule (0, 2, 6 months). Results: During 18 years, 1526 cases of HBV were declared in Monastir with a mean of 85 cases per year. We estimated a mean of 1699 declared cases per year of HBV in Tunisia. CPR was 16.85/100,000 inh being the higher in age group of 20-39 years and in men .ASR was 15.99/100,000 inh, being 35.5 in men and 8.69 in women. During the study period, declared cases among presumed immunized (PI) person against HBV were 32(2.0%). Among PI cases, 29 were from the first period and 3 were from the second. We established a negative trend over 18 years of hepatitis B. The age group of 20 to 39 was the most common with a sharply decline. Presumed not immunized (PNI) HBV cases are decreasing by years with a prediction of 35 cases in 2024. Reported HBV contributed to 1.26 YLDs per 100,000 inh. The highest rate of YLDs occurred at the age 20-39 (2.73 YLDs per 100,000 inh). During 18 years, YLDs were 114.45 in Monastir with a mean of 2293.65 YLDs of HBV in Tunisia. Conclusion, this study showed a law prevalence rate and a decreasing trend of HBV during 18 years showing an efficacy of immunization and confirming that the universal hepatitis B vaccination in Tunisia has resulted in progress towards the prevention and control of hepatitis B infection. These findings should be demonstrated in other Tunisian regions with a standardized serological profile.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Dhouib, W., Kacem, M., Samia, G., Maalel, I., Zemni, I., Abroug, H., Ben Salah, A., Chelly, S., Djobbi, A., Green, E., Sriha Belguith, A.. 2018-08-06. Epidemiological impact of hepatitis B vaccination in Monastir Tunisia (2000-17). https://doi.org/10.1101/385880

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

CD19-CAR T-cell therapy resets the EBV+ autoreactive B cell repertoire in autoimmune disease

Epstein-Barr virus (EBV) reprograms autoreactive B cells into activated antigen-presenting cells that drive pathogenic T- and B-cell responses in autoimmune disease. Using EBV B-cell sequencing (EBV-seq), we profiled EBV+ B cells in patients treated with CD19 chimeric antigen receptor (CAR) T cells (systemic lupus, n=6; idiopathic inflammatory myopathies, n=3; systemic sclerosis, n=3) or rituximab (n=15). CAR T cells, but not rituximab, depleted EBV+ B cells, resetting the repertoire toward a naive state: predominantly IgM+ with minimal somatic hypermutation. Post-rituximab B-cells remained class-switched, hypermutated, and activated. Monoclonal antibodies cloned from EBV+ B cells lost autoreactivity after CAR T cells but not rituximab. Sustained drug-free remission occurred in 8/12 CAR-treated but 0/15 rituximab-treated patients. EBV+ B cells were predominantly Latency III and resisted anti-CD20 and anti-CD19 antibodies, yet were killed by CAR T cells and T-cell engagers. CD19-CAR T-cell therapy resets the autoreactive EBV+ B-cell repertoire, which may underlie sustained drug-free remission.

immunology↗

A minimal two-residue C-terminal truncation of AID in adult-onset hyper-IgM syndrome type 2 (HIGM2)

Activation-induced cytidine deaminase (AID), encoded by AICDA, facilitates class-switch recombination (CSR) and somatic hypermutation (SHM) in activated B cells. Loss of AID function causes hyper-IgM syndrome type 2 (HIGM2). While typically autosomal recessive, three C-terminal truncation variants have been reported to act in autosomal dominant manner. We describe a novel heterozygous AICDA nonsense variant, c.589G>T (p.G197*), that truncates the final two C-terminal residues of AID and results in adult-onset HIGM2. Single-cell sequencing of primary patient B cells revealed a complete block in CSR and a [~]10-fold reduction in SHM. AICDA mRNA expression was balanced between wild-type and variant alleles, yet AID protein abundance was reduced to [~]56% with normal subcellular localization. Remarkably, inducible germinal center (iGB) cultures restored CSR in purified naive patient B cells. CRISPR-Cas9 editing of healthy donor B cells confirmed that the iGB platform can rescue B cells harboring heterozygous, but not homozygous, AICDA variants. These results demonstrate that even a two-amino-acid truncation at the AID C-terminus is sufficient to disrupt its function and cause HIGM2.

immunology↗

Defining the Functional Consequence of the Human Ocular Microbiome

The ocular surface is one of the body's most environmentally exposed mucosal barriers, yet it is considered low biomass and harbors orders of magnitude fewer bacteria than microbe-rich sites like the gut. This has cast doubt on whether a functional core ocular microbiome exists at all. Having previously defined a protective gd T cell and IL-17 axis engaged by the murine commensal Corynebacterium mastitidis, we asked whether human-derived bacteria could do the same. Pairing sequencing and culturomics of healthy human conjunctiva from two geographically distinct cohorts, we define a stable core microbiome and identify Corynebacterium bovis as a consistent eye-resident commensal rather than a transient contaminant. In humans, C. bovis elicits a non-pathogenic response marked by IL-17 secretion by {gamma}{delta} T cells and circulating C. bovis-specific IgG, which suggests commensalism rather than pathology. Colonizing mice with human C. bovis strains from Pittsburgh or Miami reproduced this program and conferred protection against ocular infection with Staphylococcus aureus. Together, these findings identify C. bovis as a human-derived ocular commensal that can drive protective {gamma}{delta} T cell immunity, translating a mechanism previously defined only in mice into human relevance and a rational target against sight-threatening infection.

immunology↗