HBV virus.pptx. Virology.

Medical research

1. HEPATITIS B VIRUS

2. Presentation layout INTRODUCTION (MORPHOLOGY AND GENOME) LABORATORY DIAGNOSIS VIRAL REPLICATION TREATMENT PATHOGENESIS PREVENTION EPIDEMIOLOGY CLINICAL FEATURES COMPLICATIONS HOST IMMUNE RESPONSE

3. INTRODUCTION The causes of hepatitis (inflammation of the liver) are varied and include viruses, bacteria, and protozoa, as well as drugs and toxins (eg, isoniazid, carbon tetrachloride, and ethanol). The clinical symptoms and course of acute viral hepatitis can be similar, regardless of etiology, and determination of a specific cause depends primarily on the use of laboratory tests. Hepatitis may be caused by at least five viruses, including hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and hepatitis E virus (HEV) belonging to different virus families Hepatitis B virus (HBV ) virion, also known as Dane particle, contains an incomplete double stranded DNA genome, a core protein (HBcAg), viral DNA polymerase (reverse transcriptase), and surface protein (HBsAg). HBV replication is unique in the sense that it utilizes reverse transcriptase enzyme to convert its pre-genomic RNA into genomic partially double stranded DNA. HBV is the cause of what was formerly known as “serum hepatitis” just to distinguish it from “infectious hepatitis” (HAV).

4. Hepatitis B virus (HBV) is a member of the hepadnavirus family It's a partially double stranded DNA virus Spherical double shell Enveloped virus Size is about 42 nm Contains HBsAg,HBcAg,HBeAg ,HBx and viral DNA polymerase (reverse transcriptase) Contains 3200 nucleoside

5. VIRAL REPLICATION STRATEGY HBV has a tropism for the liver, however the receptor & mechanism of viral entry is unknown Attachment to hepatocytes is mediated by the envelope protein via the surface antigen (HBsAg) After entry, the partial ds DNA is transported to the nucleus, where it is transcribed to viral mRNA using host cell RNA polymerase The viral mRNA is transported to the cytoplasm where viral proteins such as core & envelope proteins, full length viral RNA and reverse transcriptase are made In addition, the full length viral RNA acts as a template for viral DNA synthesis which is catalyzed by reverse transcriptase enzyme During viral maturation & assembly, HbsAg containing membrane of the endoplasmic reticulum or golgi apparatus is wrapped over the nucleocapsid core of the virion and are released by exocytosis

6. PATHOGENESIS OF HEPATITIS B VIRUS TRANSMISSION Transmitted through: Sexual contact Sharing needles and syringes (injectable drugs ) Blood and blood derived products Vertical transmission ( Mother to child ) INCUBATION PERIOD Incubation period ranges from 30-90days, average 60-90 days

7. In the past, hepatitis B was known as posttransfusion hepatitis or as hepatitis associated with the use of illicit parenteral drugs (serum hepatitis). However, over the last few years it has become clear that the major mode of acquisition is through close personal contact with body fluids of infected individuals. HBsAg has been found in most body fluids, including saliva,semen, and cervical secretions. Under experimental conditions, as little as 0.0001 mL of infectious blood has produced infection Immunological responses of the host are largely involved in the pathogenesis of HBV — Accumulation of immune complexes that activate the complement system — Accumulation of these immune complexes causes damage to the kidneys . CTLs cause damage to liver by destroying infected cells. In chronic active hepatitis B, the continued presence of inflammatory foci of infection results in necrosis of hepatocytes, collapse of the reticular framework of the liver, and progressive fibrosis. The increasing fibrosis can result in the syndrome of postnecrotic hepatic cirrhosis

8. Epidemiology Hepatitis B infection is found globally WHO as of 2019 estimated that 296 million people were living with chronic Hepatitis B infection with about 1.5 million new infections each year More than 820 000 people die of Hepatitis B complications such liver cirrhosis and Hepatocellular carcinoma as of 2019 The highest prevalence is sub saharan Africa and East Asia were about 5% to 10% of the adult population.

9. Epidemiology cont.. Majority of the infected are asymptomatic.. North america and western Europe have less than 1% of their population infected.. About 10% of people living with HIV are chronic carriers of hepatitis B Hepatitis is a preventable infection by use of safe vaccine that are available.

10. CLINICAL MANIFESTATIONS The clinical picture of hepatitis is very variable, patients present with the following symptoms: Fever Loss of appetite Joint pain Jaundice ,dark urine and clay colored stool. Fatigue Nausea and vomiting

11. Chronic Hepatitis Liver Cirrhosis ( Stellate cells activation) Liver Cancer (hepatocellular carcinoma) Liver failure and Hepatic Decompensation Extrahepatic Manifestation Death COMPLICATIONS

12. Host Immune Response 1. Innate Immune Response: Phagocytes : Cells such as macrophages and dendritic cells recognize HBV particles and engulf them through a process called phagocytosis. Natural Killer (NK) Cells: NK cells are a type of lymphocyte that can directly kill virus-infected cells. Interferons : Infected cells produce interferons, which are signaling proteins that inhibit viral replication and enhance the immune response.

13. Host immune response Inflammatory Response : HBV infection triggers inflammation at the site of infection, leading to recruitment of immune cells to the liver. 2. Adaptive Immune Response: T-Cell Response: Hepatitis B-specific cytotoxic T lymphocytes (CTLs) recognize and kill infected liver cells displaying viral proteins on their surface. This helps eliminate the virus from the liver. Immune Memory : Memory T Cells: After the acute infection is resolved, some T cells develop into memory T cells as well as B cell Memory

14. Laboratory Diagnosis Diagnosing of hepatitis B Virus typically involves a combination of medical history assessment, physical examination, and laboratory tests. Laboratory tests include ; Hepatitis B core antibody (anti-HBs)> detects antibodies to the core antigen of HBV Hepatitis B surface antigen (HBsAg)> used to determine immunity to Hepatitis B from past infections or vaccinations Hepatitis B e antigen (HBeAg)>detect a protein produced by HBV during active viral replication Hepatitis B viral load> measures the amount of HBV in DNA in the blood Liver function tests>measure levels of liver enzymes (such as ALT and AST) and bilirubin, which can indicate liver inflammation and damage. Imagining studies>ultraSounds, computer Tomography (CT) or Magnetic resonance imaging (MRI) Liver biopsy

15. TREATMENT On the basis of severity (acute; chronic) Acute hepatitis B -no specific treatment for acute hepatitis B -high calorie diet is recommended - considerations: · Immunosuppressed · Patients with rapid deteriorating liver function · Cirrhosis · Complications (ascites, hepatic encephalopathy, or haemorrhage)

16. TREATMENT cont.. Chronic hepatitis B -pegylated or regular interferon-alpha (some) -Antivirals · -Lamivudine (3TC)- potent inhibitor of HIV reverse transcriptase · -Entecavir, telbivudine- nucleoside analogs · -Adefovir, tenofovir – nucleotide analogs Note: these antivirals inhibit viral replication and may reduce viral load but do not cure HBV infection

17. PREVENTION OF HEPATITIS B Screening of blood and plasma product donors for HBsAg , anti-HBcAg, and HBV DNA Screening of pregnant women and treatment of exposed newborns with hepatitis b immune globulin HBV vaccine Safe sex practice and avoidance of needle stick injuries Avoid sharing personal hygiene items Weight management

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