Hepatitis B Virus in Jordan: Prevalence, Incidence and Clearance From Cross-Sectional and Cohort Studies.

Hepatitis B virus (HBV) infection is a global health challenge, with the World Health Organization (WHO) targeting its elimination by 2030. Jordan lacks sufficient data on HBV epidemiology, including prevalence, incidence and clearance. This study addresses these gaps through a retrospective analysis of HBV testing data from 40,268 individuals collected at Biolab Diagnostic Laboratories (2010-2024).

Patterns and trends of hepatitis C virus infection in Jordan: an observational study.

Background: Hepatitis C virus (HCV) infection levels in Jordan remain uncertain. No HCV national population-based survey has ever been conducted in the country. To meet the World Health Organization's target of reducing HCV incidence to ≤5 per 100,000 people per year by 2030, it is essential to determine the infection levels, identify affected individuals and populations, and provide appropriate treatment using direct-acting antivirals to individuals carrying the virus.

A model for public-private partnership during the COVID-19 pandemic: Lessons from Biolab and public laboratories working in the Hashemite Kingdom of Jordan.

Introduction: The global COVID-19 pandemic overwhelmed national public health and laboratory capacity in Jordan and globally. In response, Biolab, a private laboratory group with 27 branches across Jordan, assisted with testing. Biolab was equipped to quickly increase molecular testing capacity without compromising quality or turnaround time, allowing them to contribute to national COVID-19 surveillance efforts.

Molecular characterization of patients with chronic hepatitis C virus infection in Jordan: implications on response to direct-acting antiviral therapy.

Objectives: To investigate the molecular characteristics of Hepatitis C Virus (HCV) detected in patients with chronic HCV infection in Jordan.

Methods: The study included 48 Jordanian treatment-naïve patients with active chronic HCV recruited from seven governorates. HCV genotype and the resistance-associated substitutions (RAS) profile were investigated by next-generation sequencing of the NS5B, NS5A, and NS3 regions of HCV.

Regional connectivity drove bidirectional transmission of SARS-CoV-2 in the Middle East during travel restrictions.

Regional connectivity and land travel have been identified as important drivers of SARS-CoV-2 transmission. However, the generalizability of this finding is understudied outside of well-sampled, highly connected regions. In this study, we investigated the relative contributions of regional and intercontinental connectivity to the source-sink dynamics of SARS-CoV-2 for Jordan and the Middle East.

Prevalence of IgE-mediated sensitization in patients with suspected food allergic reactions in Jordan.

Background: Despite the recognition of food allergies as a significant cause of morbidity and a growing public health burden worldwide, there are no epidemiological studies addressing food sensitization and allergy in Jordan.

Objective: To conduct an epidemiological study that retrospectively analyzes sensitization data from 3463 patients with suspected immunoglobulin E (IgE)-mediated food allergic reactions who performed specific IgE tests in our laboratories in Jordan.

Methods: Specific IgE (s-IgE) tests were analyzed for patients who performed enzyme allegro-sorbent testing based on either self-reported food allergy or upon physician's request.

Acute myeloid leukemia creates an arginase-dependent immunosuppressive microenvironment.

Acute myeloid leukemia (AML) is the most common acute leukemia in adults and the second most common frequent leukemia of childhood. Patients may present with lymphopenia or pancytopenia at diagnosis. We investigated the mechanisms by which AML causes pancytopenia and suppresses patients' immune response.

Host cell signalling and leishmania mechanisms of evasion.

Leishmania parasites are able to secure their survival and propagation within their host by altering signalling pathways involved in the ability of macrophages to kill pathogens or to engage adaptive immune system. An important step in this immune evasion process is the activation of host protein tyrosine phosphatase SHP-1 by Leishmania. SHP-1 has been shown to directly inactivate JAK2 and Erk1/2 and to play a role in the negative regulation of several transcription factors involved in macrophage activation.

Comparative study of the ability of Leishmania mexicana promastigotes and amastigotes to alter macrophage signaling and functions.

Leishmania alternates between two morphologically different stages, promastigotes and amastigotes. While the majority of reports focused on how the promastigote form can alter macrophage (Mphi) signaling and function, fewer reports investigated signaling alterations mediated by amastigotes, and there is a lack of comparative studies. In this study, we performed a comparison between the ability of both forms of the parasite to alter Mphi signaling and functions.

Identification of key cytosolic kinases containing evolutionarily conserved kinase tyrosine-based inhibitory motifs (KTIMs).

We previously reported that SHP-1 regulates IRAK-1 activity by binding to an ITIM-like motif found within its kinase domain, which we named kinase tyrosine-based inhibitory motif (KTIM). Herein, we further investigated the presence, number, location, and evolutionary time of emergence of potential KTIMs in many cytosolic kinases, all known to play important roles in the signalling and function of immune cells. We unveil that several kinases contain potential KTIMs, mostly located within their kinase domain and appearing predominantly at the level of early vertebrates becoming highly conserved thereafter.

Leishmania-induced IRAK-1 inactivation is mediated by SHP-1 interacting with an evolutionarily conserved KTIM motif.

Parasites of the Leishmania genus can rapidly alter several macrophage (MØ) signalling pathways in order to tame down the innate immune response and inflammation, therefore favouring their survival and propagation within their mammalian host. Having recently reported that Leishmania and bacterial LPS generate a significantly stronger inflammatory response in animals and phagocytes functionally deficient for the Src homology 2 domain-containing protein tyrosine phosphatase (SHP-1), we hypothesized that Leishmania could exploit SHP-1 to inactivate key kinases involved in Toll-like receptor (TLR) signalling and innate immunity such as IL-1 receptor-associated kinase 1 (IRAK-1). Here we show that upon infection, SHP-1 rapidly binds to IRAK-1, completely inactivating its intrinsic kinase activity and any further LPS-mediated activation as well as MØ functions.

Regulation of macrophage nitric oxide production by the protein tyrosine phosphatase Src homology 2 domain phosphotyrosine phosphatase 1 (SHP-1).

Nitric oxide (NO) is a potent molecule involved in the cytotoxic effects mediated by macrophages (MØ) against microorganisms. We previously reported that Src homology 2 domain phosphotyrosine phosphatase 1 (SHP-1)-deficient cells generate a greater amount of NO than wild-type cells in response to interferon-gamma (IFN-gamma). We also reported that the Leishmania-induced MØ SHP-1 activity is needed for the survival of the parasite within phagocytes through the attenuation of NO-dependent and NO-independent mechanisms.