Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
97 Cards in this Set
- Front
- Back
What family of virus:
1. HAV 2. HBV 3. HCV 4. HDV 5. HEV 6. HGV |
1. picornavirus
2. hepadna 3. flavi 4. delta 5. calici 6. flavi |
|
which two hepatitis viruses are flaviviruses?
|
HCV and HGV
|
|
Are all hepatitits viruses ssRNA?
|
No, HBV is dsDNA virus
All others ss (+) RNA except HDV (-) |
|
Which hepatitis viruses are transmitted via the fecal-oral route?
|
HEV and HAV
(“Eating off your Ass” gives you Hep E and A) |
|
Which hepatitis viruses are transmitted percutaneous/blood, sexually and perinatally?
|
Hep BCDG (A may also be sexually transmitted)
“Blood, Cuts, Drugs, Going-to-be-a-baby (in utero)” |
|
which hepatitis viruses have a carrier state?
|
Hep BCD (G likely)
“Blood, Cuts, Drugs, and likely Going-to-be-a-baby (in utero)” |
|
which hepatitis virus is most commonly in adults rather than kids?
|
HCV
|
|
What’s the prognosis for hepatitis forms A-G?
|
A. excellent
B. variable C. variable D. acute=good, chronic =poor E. good G. ?? |
|
which forms of hepatitis commonly lead to a chronic state?
|
HBV in infants (80-95%; only 1-10% in adults)
HCD (70-80% chronicity rate) and HDV (70-80% in superinfection of HBV) |
|
What causes hepatitis?
|
caused by multiple agents
hepatitis viruses cause the majority of cases. |
|
Which viruses can cause hepatitis?
|
hepatitis viruses A-G--which target the liver
Epstein Barr virus yellow fever virus cytomegalovirus, which target the liver and other organs. |
|
What are very common causes of Hepatitis?
|
Hepatitis A and C viruses --very different viruses and cause very different types of hepatic disease.
|
|
What kind of virus is Hepatitis A?
|
member of the Picornaviridae family, Heparnavirus genus.
|
|
What kind of virus is Hepatitis C?
|
member of the Flaviviridae family
originally called “non-A, non-B hepatitis virus” (NANB) when serologic tests ruled out HAV and HBV as the causative agents of cases of hepatitis. |
|
What kind, genus and family of virus is Hep A?
|
hepatovirus,
Heparnavirus genus Picornaviridae family. |
|
Structure of Hep A virus?
|
1. Non-enveloped (naked) with a single-stranded, (+)-sense RNA genome.
2. Virions are icosahedral and even more stable than other picornaviruses; resistant to inactivation by heat, detergent, low pH, and desiccation. |
|
What kind of genome does Hep A have?
|
Non-enveloped w/ ss (+)sense RNA
|
|
How do Hep A viruses replicate?
|
1. Replicates like other picornaviruses.
a. Binds receptor on liver cells and a few other cell types. 2. Is NOT cytolytic, released by exocytosis. |
|
What kind of disease does hep A most commonly cause?
|
~40% of acute hepatitis cases caused by HAV.
|
|
How is Hep A transmitted?
|
fecal-oral route and spreads quickly.
|
|
How fast does Hep A spread?
|
Spreads quickly b/c:
a. most infected people are contagious before symptoms appear. b. 90% of children and 25-50% of adults have inapparent, but productive infections. c. virus is released into stool at high concentrations. |
|
How tough is hep A Virus?
|
it can survive in fresh and salt water for many months.
|
|
What causes hep A outbreaks?
|
.HAV outbreaks usually due to a “common source” like contaminated water or raw shellfish, or infected individuals. Infected food handlers, daycare workers, children have the potential to infect many other people.
|
|
Who gets HAV most frequently?
|
Children (schools, camps)
|
|
Where and when is HAV found?
|
Worldwide, all year-long.
|
|
Why is HAV rarely spread via blood?
|
viremia is low and No chronic infections w/ HAV
|
|
Can HAV cause chronic hepatitis?
|
NO
|
|
How does HAV infect?
|
Ingested,
then probably replicates in the GI tract (oropharynx or epithelial lining of the intestines), then enters the bloodstream |
|
Where does HAV replicate?
|
parenchymal cells of liver--hepatocytes and Kupffer cells.
|
|
Before jaundice or Ab detection, where can HAV be found?
|
released from cells into bile and then into stool.
shed in high concentration into stool ~10 days before jaundice or antibody can be detected. |
|
When HAV replicates in liver cells what happens to the cell?
|
Replication is NOT cytopathic, immune response to HAV is thought to result in immunopathogenesis.
Antibody, complement, ADCC contribute to lysis of infected cells and liver damage (icterus). |
|
What’s icterus?
|
liver damage signified by yellow discoloration of skin and mucous membranes (jaundice)
|
|
What causes liver damage w/ HAV?
|
Immune system response to the virus
Specifically: Ab, complement, ADCC cause lysis of infected cells |
|
How many serotypes does HAV have?
|
1
|
|
what kind of protection does an individual have after HAV infection?
|
lifelong due to IgG antibodies induced by infection provide lifelong protection against
re-infection (only 1 serotype) |
|
does HAV produce chronic infections?
does HAV cause immune complex-related syndromes, like rash or arthralgia? |
no
no |
|
How is severity of HAV infection in kids vs adults?
|
milder in children than in adults and usually asymptomatic.
|
|
Time course of HAV infection?
|
incubation period is 3-4 weeks followed by initial Sx
virus shed in stool 2 wks before Sx appear, stop before Sx appear symptoms abrupt 15-50 days after exposure Sx intensify 4-6 d before icteric phase |
|
What are the Initial symptoms of HAV infection?
|
fever, fatique, nausea, loss of appetite, abdominal pain.
|
|
When do Sx of HAV infection occur?
|
Symptoms occur abruptly 15-50 days after exposure and intensify for 4-6 days before icteric phase.
|
|
What are the Symptoms of HAV infection?
|
similar to those of other hepatitis virus which cause liver damage due to immunopathogenesis:
dark urine pale feces elevated liver enzymes. |
|
When is HAV shed in stool? When does it stop?
|
up to 2 weeks before symptoms appear
stops before symptoms disappear. |
|
Prognosis for HAV infection?
|
Complete recovery occurs in 99% of cases.
Fulminant hepatitis occurs in 1-3 persons per 1000 infected with HAV and is associated with 80% mortality rate. |
|
How common is fulminant hepatitis due to HAV?
|
1-3 : 1000 infected w/ HAV
80% mortality |
|
How is HAV infection diagnosed?
|
a. time course of clinical symptoms,
b. identification of known infected source, c. specific serologic tests. |
|
What are some specific serological tests to diagnose HAV?
|
Detection of anti-HAV IgM indicates acute HAV infection
detection of anti-HAV IgG indicates a previous HAV infection (or vaccination) and immunity to re-infection. |
|
What does anti-HAV IgM indicate?
|
Acute HAV infection
|
|
What does anti-HAV IgG indicate?
|
Previous HAV infection or vaccination
Immune to reinfection |
|
How is HAV infection prevented after exposure?
|
80-90% effectiveness by prophylaxis with immune serum globulin (passive immunization) given before or early after exposure (<2 weeks).
|
|
What kind of vaccine is given to prevent HAV?
|
A killed (inactivated) HAV vaccine is available
|
|
Who is the killed HAV vaccine recommended for?
|
a. people living in or traveling to areas where HAV is endemic,
b. children 2-18 years old, c. men who have sex with men. |
|
How is HAV vaccine given?
|
2 doses: an initial dose and a booster 6-12 months later.
|
|
What are some ways to prevent spread of HAV?
|
good hygiene
avoid potentially contaminated food and water. |
|
What kind of virus and family is HCV?
|
member of Hepaciviridae group
Flaviviridae family. |
|
Structure of HCV?
|
Enveloped w/ icosahedral capsid and single-stranded, (+)-sense RNA genome.
|
|
What kind of genome does HCV have?
|
ssRNA, (+) sense
(same as HAV) |
|
How does HCV replicate?
|
1. not very well understood.
2. in the cytoplasm. 3. Viral genome translated into a single polyprotein , then cleaved by viral protease into individual viral proteins. 4. Virions bud from ER (release mechanism unclear) |
|
What’s the reservoir for HCV?
|
Humans
|
|
How is HCV transmitted?
|
primarily through blood.
(most prevalent blood-borne pathogen in U.S.--4.9 million people are infected; 200 million worldwide) Most cases via contaminated needles (i.v. drug use). |
|
How are blood donations screened for HCV?
|
Screen for HCV and HCV antibodies.
|
|
What are some ways HCV transmission can occur w/ blood donations?
|
i. contaminated, pooled immune globulin
ii. organ donations iii. factors VIII or IX given to hemophiliacs. |
|
Who is infected w/ HCV?
|
Almost all HIV-infected individuals who were or are i.v. drug users are infected with HCV.
|
|
What’s the problem w/ chronic HCV in the population?
|
High incidence of chronic asymptomatic infections results in frequent transmission to others.
|
|
Where does HCV replicate?
|
Hepatocytes (NOT cytopathic.)
Many infections become chronic (persistent). |
|
How is HCV infection controlled?
|
Hepatocytes are killed by immune attack by CTLs.
|
|
Which hepatitis virus infection causes increased frequency of hepatocellular carcinoma?
Is it a viral oncogene? |
HCV infection due to increased cell division and mutation
not a viral oncogene. |
|
What increases the rate of Hepatocellular carcinoma in HCV infected individuals?
|
alcoholism enhances frequency of HCC in HCV-infected
|
|
Is there a humoral immune response to HCV?
|
Kinda, Ab’s are made, but are not protective.
|
|
How commonly does HCV lead to chronic infection?
|
~70% of patients are chronically infected and continue to produce virus for at least 1 year.
|
|
Can re-infection occur w/ HCV once the virus is cleared?
|
not known if reinfection can occur or whether there is lifelong immunity.
(~70% of pts are chronically infected) |
|
What are 3 types of liver disease caused by HCV?
|
1. Acute hepatitis w/ virus clearance and recovery (~15% cases)
2. Chronic persistent infection w/ disease progression later (~70%) 3. Severe rapid progression to cirrhosis (15% chronic cases) |
|
How often does HCV cause acute hepatitis with virus clearance and recovery?
|
~15% of cases
|
|
What are the symptoms of acute HCV infection?
|
similar, but milder than w/ acute HAV and HBV infections
inflammatory response less intense. Sx: fever, anorexia, nausea, vomiting and jaundice. |
|
What happens most often w/ initial HCV disease?
|
Disease inapparent and leads to chronic persistent disease.
|
|
How often does HCV cause chronic persistent infection with progression to disease later in life?
|
~70% of cases
|
|
what’s the progression like to chronic hepatits w/ HCV?
|
Progress to chronic active hepatitis w/in 10-15 years.
Cirrhosis and liver failure after 20 years = most common indicator for liver transplantation. Hepatocellular carcinoma (HCC) after 30 years in < 5% of cases. |
|
How common is hepatocellular carcinoma in those infected w/ chronic HCV?
|
After ~30 yrs of chronic HCV infection < 5% of cases develop HCC
|
|
How common is severe rapid progression to cirrhosis w/ HCV infection?
|
~15% of chronic cases
|
|
How is HCV diagnosed in the lab?
|
1. detection of anti-HCV antibodies by ELISA.
2. RT-PCR is used to detect HCV genome in serum, blood supply, etc. 3. elevated liver enzymes in chronic infection (detect HCV Ab’s and HCV RNA for at least 6 months) |
|
What do you need to know about detecting HCV Ab’s by ELISA?
|
Seroconversion occurs within 7-31 weeks of infection.
Ab’s not always detectable in viremic or immunocompromised, or individuals on hemodialysis. Detect HCV Ab’s and HCV RNA for >6 mo for chronic infection |
|
How is HCV infection treated?
|
w/ alpha interferon, pegylated interferon (Peg-intron) and ribavirin.
|
|
What do alpha interferon, pegylated interferon (Peg-intron) and ribavirin treatments do for HCV infection?
|
a. reduce viral replication and liver damage, but don’t eliminate carrier state.
b. Associated w/ S/E’s (may limit their use in combo) |
|
how is transfusion-acquired HCV prevented?
|
screening
|
|
How is HCV prevented?
|
NO vaccine
Screen transfusion blood, etc |
|
Can pooled immune serum globulins be given for postexposure prophylaxis?
|
No, they’re ineffective.
|
|
Can HAART (highly active anti-retroviral therapy) be used for HCV infection?
|
HAART may exacerbate hepatitis in patients co-infected with HIV and HCV.
|
|
What does HEV commonly cause?
|
E causes Enteric Dz
Major cause of enterically transmitted hepatitis epidemics in Asia, Africa, India, and Mexico. |
|
What are the symptoms and disease produced by HEV infection?
|
Resembles HAV:
1. Higher mortality rate in pregnant women than with HAV. 2. Does not cause chronic infection. |
|
How is HEV diagnosed?
|
Exclude other hepatitis viruses b/c lab tests not readily available.
|
|
How is HEV treated/prevented?
|
No treatment or vaccine.
|
|
Where was HGV found? What does it cause?
|
Isolated from a patient with post-transfusion hepatitis, but has not been shown to cause hepatitis.
Can cause a chronic infection lasting for decades. |
|
If you get HGV, what’s the prognosis?
|
~60-70% of those infected clear the virus and develop Ab’s
not shown to cause hepatitis can cause chronic infection lasting for decades |
|
How is HGV transmitted?
|
sexual intercourse and blood
|
|
Where is HGV found?
|
in the blood of millions of people worldwide.
U.S—in blood from 2% random blood donors, 15% of HCV-infected individuals, and 35% of HIV-infected individuals. |
|
What kind of interaction does HGV have w/ HIV?
|
May interfere with replication of HIV and increase lifespan of coinfected individuals.
|
|
What virus family does HGV belong to?
|
Member of the Flaviviridae family, like HCV, enveloped, single-stranded, (+)-sense
RNA genome. Also known as GB virus. |
|
What kind of virus/family is HEV?
|
Non-enveloped w/ ss (+)-sense RNA genome
Tentatively classified as member of the Caliciviridae family. |