Prevalence of Serological Markers of Viruses in Patients of Acute Hepatitis.

Infections due to hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV) and hepatitis E (HEV) viruses are the major causes of hepatitis and are associated with significant morbidity and mortality in developing countries like Bangladesh. The aim of this study was to assess the distribution pattern of serological markers in patients of acute viral hepatitis. This was a hospital based observational cross sectional study among purposively selected 107 patients admitted with acute viral hepatitis in the Department of Medicine, Mymensingh Medical College Hospital, Mymensingh, Bangladesh from April 2017 to September 2017. Data were collected by face-to-face interview of the patients, clinical assessment and investigations of biochemical and serological parameters using a structured questionnaire. Descriptive analysis was done using the analytic software SPSS version 21.0. The mean age of the patients was 33.35±12.97 years. Majority was male (68.2%), Muslim (87.9%), married (72.9%) and came from urban area (63.6%) with different level of educational qualifications. The prevalence of viral hepatitis is higher in male (68.22%) than female (31.78%). The common clinical presentations were dark coloured urine (100.0%), yellow colouration of the sclera (100.0%), anorexia (90.6%), nausea/vomiting (79.4%) and abdominal pain (68.2%). Of the 107 patients, 51.40% (n=55) had acute viral E hepatitis, 36.40% (n=39) had acute viral B hepatitis, 12.15% (n=13) had acute viral A hepatitis. Mixed infection with both hepatitis E and A viruses was 1.87% (n=2). HEV and HBV are common in relatively older age while HAV is common in relatively younger age to cause acute viral hepatitis. The study revealed a high prevalence of HEV followed by HBV and HAV in the Bangladeshi population suspected of having suffered from acute viral hepatitis.

IL-6 promotes CD4+ T-cell and B-cell activation during Plasmodium infection.

Humoral immunity develops in the spleen during blood-stage Plasmodium infection. This elicits parasite-specific IgM and IgG, which control parasites and protect against malaria. Studies in mice have elucidated cells and molecules driving humoral immunity to Plasmodium, including CD4+ T cells, B cells, interleukin (IL)-21 and ICOS. IL-6, a cytokine readily detected in Plasmodium-infected mice and humans, is recognized in other systems as a driver of humoral immunity. Here, we examined the effect of infection-induced IL-6 on humoral immunity to Plasmodium. Using P. chabaudi chabaudi AS (PcAS) infection of wild-type and IL-6-/- mice, we found that IL-6 helped to control parasites during primary infection. IL-6 promoted early production of parasite-specific IgM but not IgG. Notably, splenic CD138+ plasmablast development was more dependent on IL-6 than germinal centre (GC) B-cell differentiation. IL-6 also promoted ICOS expression by CD4+ T cells, as well as their localization close to splenic B cells, but was not required for early Tfh-cell development. Finally, IL-6 promoted parasite control, IgM and IgG production, GC B-cell development and ICOS expression by Tfh cells in a second model, Py17XNL infection. IL-6 promotes CD4+ T-cell activation and B-cell responses during blood-stage Plasmodium infection, which encourages parasite-specific antibody production.