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Hepatitisinflammation of the liver: causes

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drugs toxins alcohol viral infections (A, B, C, D, E) other infections (parasites, bacteria) physical damage

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Liver Functions:

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Stores sugar needed for energy Absorbs good nutrients Breaks down poisons (toxins) and drugs Makes important proteins that help build new tissue and repair broken tissue Produces bile, which helps remove waste from the body

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Acute Hepatitis:

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Short-term hepatitis. Body's immune system clears the virus from the body within 6 months

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Chronic Hepatitis:

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Long-term hepatitis. Infection lasts longer than 6 months because the body's immune system cannot clear the virus from the body

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Hepatitis A: Incubation period

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30 days on average (range 15-50 days) infectious latter half of incubation period while asymptomatic through 1 week after having jaundice.

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Hepatitis A: Symptoms

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A person may have all, some or none of these: Nausea Loss of appetite Vomiting Fatigue Fever Dark urine Pale stool Jaundice Stomach pain Side pain

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Hepatitis A: How do you get it?

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Feces (stool) on hands that gets on food or in water Contaminated shellfish Sex A person is most contagious 2 weeks before they feel sick Not spread by kissing, sneezing, saliva

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Hepatitis A: Diagnosis and Treatment

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Blood test No medicine or treatment to make it go away Rest, fluids, treatment of symptoms Most people recover completely and become immune to reinfection

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Hepatitis A: Prevention

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Shot of immune globulin up to 2 weeks after exposure Good hand washing Cook food well Good diaper hygiene Only drink clean water VACCINE!!!

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Hepatitis A: Who needs immune globulin?

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Living with someone with Hep A Eaten food handled by someone with Hep A Sexual contact with person with Hep A Traveling to an area where Hep A is common Child or employee at a child care program where someone else has Hep A

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Hepatitis B: What is it?

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Hep B is a serious disease caused by a virus that infects the liver Can cause lifelong infection, cirrhosis (liver scarring), liver cancer, liver failure and death

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Hepatitis B: Pathogenesis

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HBV carried in liver Mechanism of liver damage unknown Damage most likely results from immune response Virus replicates via reverse transcriptase Viral DNA transported to host nucleus Host mRNA makes RNA copy RNA copy transcribed by viral reverse transcriptase New DNA copy is genome for new virus New viruses bud from host cell

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Hepatitis B: Incubation period

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60-90 days on average (range 45-180 days) infectious weeks before getting ill and for variable period after acute infection chronic carriers remain infectious

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Hepatitis B: Symptoms

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Nausea Loss of appetite Vomiting Fatigue Fever Dark urine Pale stool Jaundice Stomach pain Side pain A person may have all, some or none of these

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Hepatitis B: Who is at risk?

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Anyone can get it In the USA, 200,000 people get Hep B every year 5,000 people die every year of Hep B If you have had other kinds of Hepatitis, you can still get Hep B

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Hepatitis B: Who is at highest risk?

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Injection drug users Sex partners of those with Hep B Sex with more than one partner Men who have sex with men Living with someone with chronic Hep B Contact with blood Transfusions, travel, dialysis

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Hepatitis B: How do you get it?

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Direct contact with blood or body fluids of an infected person sharing injection equipment sex baby from infected mother during childbirth Hepatitis B is not spread by food, water or casual contact

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Hepatitis B: Who is a carrier of Hep B virus?

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Some people with Hep B never fully recover from the infection (chronic infection) They still carry the virus and can infect others for the rest of their lives There are about 1 million carriers of Hep B in the USA

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Hepatitis B: Diagnosis and Treatment

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Blood test There is no cure Interferon/Ribaviron

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Hepatitis B: What about Hep B and pregnancy?

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A woman with Hep B can give it to her baby at birth Babies with Hep B can get very sick, can develop chronic infection and spread Hep B, can get cirrhosis or liver cancer Pregnant women should be tested for Hep B Babies should get Hep B vaccine at birth

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Hepatitis B: Who should get Hepatitis B vaccine?

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All babies, at birth All children 11-12 who have not had vaccine People at risk MSM Multiple sex partners Injection drug users People with jobs where exposure to blood might happen

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Hepatitis C: Pathogenesis

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Few details known Infection transmitted via contact with infected blood Incubation period average 6 weeks Over 80% develop chronic infections Virus infects the liver Incites inflammatory and immune responses Cell-mediated immunopathology Disease comes and goes Individuals have times of near normalcy 10% to 20% will develop cirrhosis or liver cancer

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Hepatitis C: Incubation period

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6-7 weeks on average (range 2-6months) infectious one or more weeks before getting ill chronic carriers remain infectious

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Hepatitis C: Symptoms

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Nausea Loss of appetite Vomiting Fatigue Fever Dark urine Pale stool Jaundice Stomach pain Side pain 3 out of 4 persons have no symptoms and can infect others without knowing it

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Hepatitis C: Who is at risk?

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About 35,000 people get Hep C every year down from 180,000 in the 1980s About 3.9 million people in the USA are infected with Hep C. It can cause liver failure, cirrhosis, liver cancer Responsible for 8,000 to 10,000 deaths/year.

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Hepatitis C: Who is at highest risk?

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Injection drug users Estimated that over 75% of injectors nationwide have Hep C In Seattle/King County, 86%

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Hepatitis C: How do you get it?

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Shared injection equipment (60% of new infections) Blood transfusion before May, 1992 (now only 1 in 100,000 chance of transmission) Blood transfer (HCW, tattoo, piercing ...) Sex? (HCV in semen and vf but only 1.5% rate of transmission for long-term partners) Mother to child (<5%) 10-20% of infections have no identifiable risk factors

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Hepatitis C: Diagnosis

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There is a blood test that screens for Hep C antibodies (ELISA or RIBA) Antibodies usually develop within 3 months HIV+ persons may not develop detectable antibodies There is a PCR test (detects parts of actual virus) for Hep C but it is not yet FDA approved If infected, liver enzyme tests or a liver biopsy can check liver function

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Hepatitis C: What happens when you have Hepatitis C ?

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85% of people develop chronic infection (infected for the rest of their life) Rapid progression, slow progression, no progression HCV subtype Alcohol consumption (alcoholics 3 times more likely to develop cirrhosis after 20 years) age (older at time of infection more rapid) gender (men faster progression than women)

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Hepatitis C: Long term pathogenesis

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Over time progressive liver damage may occur 20 -30 % of those infected will develop cirrhosis over 10 - 30 years Of those with cirrhosis 25-30% (5% of overall) will develop end-stage liver disease or liver cancer Many live without symptoms for decades Others experience mild symptoms --intermittent fatigue, nausea, and muscle aches

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Hepatitis C: Treatment

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Interferon/Ribaviron (suggest 40% "cure" rate) Peginterferon Alfa-2a (still in studies - not yet FDA approved)

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Hepatitis C: What should a person do who has Hep C?

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Get regular medical care--tell doctor about ALL drugs (including herbs)!!! Have a healthy diet (no iron supplements, reduce salt intake, no large doses of vitamin A) Get needed rest No alcohol or Tylenol, cut back on other drug use Avoid chemical fumes and other environmental toxins Get vaccinated for A and B!!! Do not share injection equipment. Do not donate blood or plasma, organs or sperm Do not share toothbrushes, razors Cover areas of open skin Use safer sex?

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Hepatitis C and HIV

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30 - 40% of HIV+ people in US also infected with Hep C More rapid progression of Hep C (twice as fast) Little to no affect on HIV progression (still inconclusive) Complications of medication regimens Increases risk of perinatal transmission

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Unique Features of Herpesviruses

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• Herpesviruses have large, enveloped icosadeltahedral capsids containing double-stranded DNA genomes. • Herpesviruses encode many proteins that manipulate the host cell and immune response. • Herpesviruses encode enzymes (DNA polymerase) that promote viral DNA replication and are good targets for antiviral drugs. • DNA replication and capsid assembly occurs in the nucleus. • Virus is released by exocytosis, cell lysis, and through cell-cell bridges. • Herpesviruses can cause lytic, persistent, latent, and (for Epstein-Barr virus) immortalizing infections. • Herpesviruses are ubiquitous. • Cell-mediated immunity is required for control.

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Disease Mechanisms for Herpes Simplex Viruses

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• Disease is initiated by direct contact and depends on infected tissue (e.g., oral, genital, brain). • Virus causes direct cytopathologic effects. • Virus avoids antibody by cell-to-cell spread and syncytia. • Virus establishes latency in neurons (hides from immune response). • Virus is reactivated from latency by stress or immune suppression. • Cell-mediated immunity is required for resolution, with limited role for antibody. • Cell-mediated immunopathologic effects contribute to symptoms.

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Epidemiology of Herpes Simplex Virus (HSV): Disease/Viral Factors

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• Virus causes lifelong infection • Recurrent disease is a source of contagion • Virus may cause asymptomatic shedding

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Epidemiology of Herpes Simplex Virus (HSV): Transmission

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• Virus is transmitted in saliva, in vaginal secretions, and by contact with lesion fluid (mixing and matching of mucous membranes) • Virus is transmitted orally and sexually and by placement into eyes and breaks in skin • HSV-1 is generally transmitted orally; HSV-2 is generally transmitted sexually

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Epidemiology of Herpes Simplex Virus (HSV): Who Is at Risk?

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• Children and sexually active people are at risk for classic presentations of HSV-1 and HSV-2, respectively • Physicians, nurses, dentists, and others in contact with oral and genital secretions are at risk for infections of fingers (herpetic whitlow) • Immunocompromised people and neonates are at risk for disseminated, life-threatening disease

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Epidemiology of Herpes Simplex Virus (HSV): Modes of Control

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• Antiviral drugs are available • No vaccine is available • Health care workers should wear gloves to prevent herpetic whitlow • People with active genital lesions should refrain from intercourse until lesions are completely reepithelialized

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Disease Mechanisms of Varicella-Zoster Virus (VZV)

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• Initial replication is in the respiratory tract. • VZV infects epithelial cells, fibroblasts, T cells, and neurons. • VZV can form syncytia and spread directly from cell to cell. • Virus is spread by viremia to skin and causes lesions in successive crops. • VZV can escape antibody clearance, and cell-mediated immune response is essential to control infection. Disseminated, life-threatening disease can occur in immunocompromised people. • Virus establishes latent infection of neurons, usually dorsal root and cranial nerve ganglia. • Herpes zoster is a recurrent disease; it results from virus replication along the entire dermatome. • Herpes zoster may result from depression of cell-mediated immunity and other mechanisms of viral activation.

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Epidemiology of Varicella-Zoster Virus: Disease/Viral Factors

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• Virus causes lifelong infection. • Recurrent disease is a source of contagion.

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Epidemiology of Varicella-Zoster Virus: Transmission

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• Virus is transmitted mainly by respiratory droplets but also by direct contact.

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Epidemiology of Varicella-Zoster Virus: Who Is at Risk?

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• Children (ages 5 to 9) experience mild classic disease. • Teens and adults are at risk for more severe disease with potential pneumonia. • Immunocompromised people and newborns are at risk for life-threatening pneumonia, encephalitis, and progressive disseminated varicella. • Elderly and immunocompromised people are at risk for recurrent disease (herpes zoster [shingles]).

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Epidemiology of Varicella-Zoster Virus: Modes of Control

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• Antiviral drugs are available. • Immunity may wane in the elderly population. • Varicella-zoster immunoglobulin is available for immunocompromised people and staff exposed to virus, as well as newborns of mothers showing symptoms within 5 days of birth. • Live vaccine (Oka strain) is available for children.

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Disease Mechanisms of Epstein-Barr Virus

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• Virus in saliva initiates infection of oral epithelia and spreads to B cells in lymphatic tissue. • There is productive infection of epithelial and B cells. • Virus promotes growth of B cells (immortalizes). • T cells kill and limit B-cell outgrowth. T cells are required for controlling infection. Antibody role is limited. • EBV establishes latency in memory B cells and is reactivated when the B cell is activated. • T-cell response (lymphocytosis) contributes to symptoms of infectious mononucleosis. • There is causative association with lymphoma in immunosuppressed people and African children living in malarial regions (African Burkitt lymphoma) and with nasopharyngeal carcinoma in China.

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Epidemiology of Epstein-Barr Virus: Disease/Viral Factors

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• Virus causes lifelong infection. • Recurrent disease is cause of contagion. • Virus may cause asymptomatic shedding.

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Epidemiology of Epstein-Barr Virus: Transmission

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• Transmission occurs via saliva, close oral contact ("kissing disease"), or sharing of items such as toothbrushes and cups.

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Epidemiology of Epstein-Barr Virus: Who Is at Risk?

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• Children experience asymptomatic disease or mild symptoms. • Teenagers and adults are at risk for infectious mononucleosis. • Immunocompromised people are at highest risk for life-threatening neoplastic disease.

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Diagnosis of Epstein-Barr Virus

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1. Symptoms a. Mild headache, fatigue, fever b. Triad: lymphadenopathy, splenomegaly, exudative pharyngitis c. Other: hepatitis, ampicillin-induced rash 2. Complete blood cell count a. Hyperplasia b. Atypical lymphocytes (Downey cells) (T cells) 3. Heterophile antibody (transient) 4. EBV-antigen specific antibody

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Disease Mechanisms of Cytomegalovirus (CMV):

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• CMV is acquired from blood, tissue, and most body secretions. • CMV causes productive infection of epithelial and other cells. • CMV establishes latency in T cells, macrophages, and other cells. • Cell-mediated immunity is required for resolution and contributes to symptoms; role of antibody is limited. • Suppression of cell-mediated immunity allows recurrence and severe presentation. • CMV generally causes subclinical infection.

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Epidemiology of Cytomegalovirus Infection: Disease/Viral Factors

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• Virus causes lifelong infection • Recurrent disease is source of contagion • Virus may cause asymptomatic shedding

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Epidemiology of Cytomegalovirus Infection: Transmission

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• Transmission occurs via blood, organ transplants, and all secretions (urine, saliva, semen, cervical secretions, breast milk, and tears) • Virus is transmitted orally and sexually, in blood transfusions, in tissue transplants, in utero, at birth, and by nursing

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Epidemiology of Cytomegalovirus Infection: Who Is at Risk?

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• Babies • Babies of mothers who experience seroconversion during term are at high risk for congenital defects • Sexually active people • Blood and organ recipients • Burn victims • Immunocompromised people: symptomatic and recurrent disease

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Epidemiology of Cytomegalovirus Infection: Modes of Control

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• Antiviral drugs are available for patients with acquired immune deficiency syndrome. • Screening potential blood and organ donors for cytomegalovirus reduces transmission of virus.

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HAV=

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~unenveloped-naked ssRNA virus ~food-borne/ fecal oral ~green onions, lettuce, spinach, raw dish

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HAV main symptoms

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~Jaundice ~clay-like feces ~pale stools

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HAV- route in body

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intestines--> liver--> bile--> stool Ingestion--> 10 day incubation--> increased feces viral load (contagious)--> symptoms by 3-6 weeks

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our antibodies vs HAV

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we can quickly make antibodies (2 types) to destroy HAV antibodies can also be used for Tx

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HBV transmission

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through sex or blood

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HBV similar to HIV?

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~uses reverse transcriptase ~you can live with it for a long time

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what is the main immunogenic factor in HBV?

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as budding, release the protein (HBsAg)-on surface of virion is released as well

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What is Hep D? and what is its relationship to Hep B?

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Hep D= delta agent its a small co-virus w/ Hep B and produces the most severe chronic form

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what type of virus is HCV?

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ssRNA

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