Adil A. Abdalla

Bio: Adil A. Abdalla is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Reflux esophagitis & Microscopic colitis. The author has an hindex of 6, co-authored 18 publications receiving 268 citations. Previous affiliations of Adil A. Abdalla include National Institutes of Health & Mayo Clinic.

The Mayo Dysphagia Questionnaire-30: Documentation of Reliability and Validity of a Tool for Interventional Trials in Adults with Esophageal Disease

Abstract: The aim of this study was to develop the Mayo Dysphagia Questionnaire-30 Day (MDQ-30), a tool to measure esophageal dysphagia, by adapting items from validated instruments for use in clinical trials, and assess its feasibility, reproducibility, and concurrent validity. Outpatients referred to endoscopy for dysphagia or seen in a specialty clinic were recruited. Feasibility testing was done to identify problematic items. Reproducibility was measured by test–retest format. Concurrent validity reflects agreement between information gathered in a structured interview versus the patients’ written responses. The MDQ-30, a 28-item instrument, took 10 min (range = 5–30 min) to complete. Four hundred thirty-one outpatients [210 (49%) men; mean age = 61 years] participated. Overall, most concurrent validity κ values for dysphagia were very good to excellent with a median of 0.78 (min 0.28, max 0.95). The majority of reproducibility κ values for dysphagia were moderate to excellent with a median κ value of 0.66 (min 0.07, max 1.0). Overall, concurrent validity and reproducibility κ values for gastroesophageal reflux disease (GERD) symptoms were 0.81 (95% CI = 0.72, 0.91) and 0.66 (95% CI = 0.55, 0.77), respectively. Individual item percent agreement was generally very good to excellent. Internal consistency was excellent. We conclude that the MDQ-30 is an easy-to-complete tool to evaluate reliably dysphagia symptoms over the last 30 days.

Effect of ribavirin on viral kinetics and liver gene expression in chronic hepatitis C

Abstract: Objective Ribavirin improves treatment response to pegylated-interferon (PEG-IFN) in chronic hepatitis C but the mechanism remains controversial. We studied correlates of response and mechanism of action of ribavirin in treatment of hepatitis C. Design 70 treatment-naive patients were randomised to 4 weeks of ribavirin (1000–1200 mg/d) or none, followed by PEG-IFNα-2a and ribavirin at standard doses and durations. Patients were also randomised to a liver biopsy 24 h before or 6 h after starting PEG-IFN. Hepatic gene expression was assessed by microarray and interferon-stimulated gene (ISG) expression quantified by nCounter platform. Temporal changes in ISG expression were assessed by qPCR in peripheral-blood mononuclear cells (PBMC) and by serum levels of IP-10. Results After 4 weeks of ribavirin monotherapy, hepatitis C virus (HCV) levels decreased by 0.5±0.5 log 10 (p=0.009 vs controls) and ALT by 33% (p Conclusions Ribavirin is a weak antiviral but its clinical effect seems to be mediated by a separate, indirect mechanism, which may act to reset IFN-responsiveness in HCV-infected liver.

Durability of Antibody Response Against Hepatitis B Virus in Healthcare Workers Vaccinated as Adults

Abstract: The implementation of vaccination programs worldwide against hepatitis B virus (HBV) has reduced the morbidity and mortality of acute and chronic HBV infection and the incidence of hepatocellular carcinoma, particularly in endemic regions [1–3]. Vaccination against HBV consists of 3 or 4 intramuscular injections of recombinant hepatitis B surface antigen (HBsAg) at varying schedules [4]. Response rates to primary vaccination are high, with 85%–100% of vaccinees developing antibody to HBsAg (anti-HBs) ≥10 mIU/mL [5], a level that is considered protective [5–9]. Factors found to be associated with nonresponse include male sex, increasing age at vaccination (>40 years old), obesity, alcoholism, smoking, and genetic factors [10–12]. Asymptomatic breakthrough infections (detected by the presence of antibody to hepatitis B core antigen [anti-HBc] or HBV DNA in serum) have been reported in vaccinated persons with a documented initial antibody response [13, 14]. Long-term follow-up studies of persons who were vaccinated as infants have reported absence of anti-HBs in 50%–70% of persons 15–30 years later [13, 15–18]. In contrast, data on the longevity of immunity afforded by hepatitis B vaccine in a healthy adult population are scarce. The few available studies in young adults who initially responded to a past primary vaccine series with antibody concentrations of ≥10 mIU/mL reported that 17%–50% have low or undetectable anti-HBs (reflecting anti-HBs loss) 10–15 years after vaccination [14, 19]. Whether low or undetectable levels of anti-HBs predispose to subsequent infection is unknown. Moreover, whether individuals may respond to a hepatitis B vaccine booster to maintain long-term protection is unknown. Current guidelines do not recommend booster doses, but the duration of long-term protection is unknown [4, 20]. Healthcare workers (HCWs) in the United States are mandated to receive hepatitis B vaccine and are at risk for hepatitis B through occupational exposure. Therefore, they would be an ideal population to assess durability of antibody response and long-term (≥10 years) vaccine protection and to determine response to a booster dose in those who did not maintain the immune response to primary vaccination as adults.

SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls.

Abstract: Memory T cells induced by previous pathogens can shape susceptibility to, and the clinical severity of, subsequent infections1. Little is known about the presence in humans of pre-existing memory T cells that have the potential to recognize severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here we studied T cell responses against the structural (nucleocapsid (N) protein) and non-structural (NSP7 and NSP13 of ORF1) regions of SARS-CoV-2 in individuals convalescing from coronavirus disease 2019 (COVID-19) (n = 36). In all of these individuals, we found CD4 and CD8 T cells that recognized multiple regions of the N protein. Next, we showed that patients (n = 23) who recovered from SARS (the disease associated with SARS-CoV infection) possess long-lasting memory T cells that are reactive to the N protein of SARS-CoV 17 years after the outbreak of SARS in 2003; these T cells displayed robust cross-reactivity to the N protein of SARS-CoV-2. We also detected SARS-CoV-2-specific T cells in individuals with no history of SARS, COVID-19 or contact with individuals who had SARS and/or COVID-19 (n = 37). SARS-CoV-2-specific T cells in uninfected donors exhibited a different pattern of immunodominance, and frequently targeted NSP7 and NSP13 as well as the N protein. Epitope characterization of NSP7-specific T cells showed the recognition of protein fragments that are conserved among animal betacoronaviruses but have low homology to 'common cold' human-associated coronaviruses. Thus, infection with betacoronaviruses induces multi-specific and long-lasting T cell immunity against the structural N protein. Understanding how pre-existing N- and ORF1-specific T cells that are present in the general population affect the susceptibility to and pathogenesis of SARS-CoV-2 infection is important for the management of the current COVID-19 pandemic.