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Exam3Lec1HepatitisViruses Flashcards

1
Q

What is hepatitis?

A

inflammation of the liver
nausea, vomiting, poor appetite, jaundice, dark urine

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2
Q

What is fulminant hepatitis?

A

This is the worst case; build up of toxins in the body

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3
Q

What does chronic hepatitis lead to?

A

leads to cirrhosis (“dying of your liver”, hepatocellular carcinoma

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4
Q

Which type of hepatitis virus has a fecal-oral route of transmission, no chronic infection, and can lead to diseases, specifically acute hepatitis and jaundice?

A

Hep A and Hep E

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5
Q

Which type of hepatitis virus has a blood/bodily fluids of transmission, has chronic infection, and can lead to diseases, specifically cirrhosis and HCC?

A

Hep B, C, D

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6
Q

True or False Organ getting infected by different virus can cause different diseases on that organ

A

True

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7
Q

Hepatitis A virus is is what family and provide details

A

Picornavirus(Hepatovirus) Family

1 serotype and 4 gentoypes
–1 inactivated vaccine (travelers)
–passive immunization effective (<2 weeks post exposure)
Non enveloped, (+ss) ss RNA genome

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8
Q

What is the importance in giving passive immunization <2 weeks post exposure for hep A?

A

Hep A has a short incubation of about 2 weeks, so it needs to be given less than 2 weeks after exposure to prevent Hep A from escaping GI tract to cause systemic spread

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9
Q

What is the acute infection of hep A?

A

incubation time 15-45 days

usually mild disease lasting up to 2 weeks, NO chronic disease (once you get Hep A, you build immunity)

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10
Q

What is the transmission of hep A?

A

close contact, contaminated food/water

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11
Q

What are the symptoms of the hep A virus?

A

Sudden onset of symptoms:
nausea, anorexia, fever, malaise, pain (URQ), jaundice, elevated AST/ALT, dark urine, clay colored stool, enlarges/tender liver

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12
Q

For Hep A, is there a high prevalence of jaundice?

A

No, jaundice occurs <50%, and is more frequent in children and young adults

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13
Q

What is the prevention/therapy for Hep A?

A
  1. immune serum globulin to household contacts of infected for prophylaxis
  2. inactivated virus vaccine
  3. Supportive therapy: good nutrition, avoid hepatotoxic substances (alcohol, bed rest)

overall, once you have Hep A, there is no antiviral to hepA

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14
Q

True or False Hep A is very common in the US

A

FALSE

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15
Q

Hepatitis E is in what family and provide details

A

Calci/Hepevirus (Orthohepevirus) Family

1 serotype & 4 genotypes
-KNOW THIS: Genotypes 1 and 2 most common (In Africa and Asia)

Non enveloped (+)ss RNA genome

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16
Q

What is the acute infection of Hep E?

A

incubation time: 2-6 weeks
95% infections are asympotomatic

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17
Q

How is Hep E transmitted?

A

contaminated food/water

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18
Q

Mortality/morbidity is higher in _____ countries. And has higher fatality in ____

A

developing, pregnant women

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19
Q

Does Hep E lead to chronic infection?

A

NO, once you get inf, you recover, then you have immunity to these viruses (same goes for Hep A)

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20
Q

Hep C is apart of which family, provide details

A

Flaviviridae Family

6 genotypes
-1 and 4 have poor prognosis( not severe)
Enveloped, iscosahedral, (+) ss RNA

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21
Q

Hep C is the only one that has its own genus within a family, what is it?

A

Hepacivirus

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22
Q

How is Hep C transmitted, the acute infection, and persistant infection?

A

transmitted by blood

acute inf: incubation time 6-7 weeks

persistant infection leads to chronic hepatitis (this means that you have a decrease in initial amt of virus you are making in the body but you can reach a set point where you see low lvls of virus)

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23
Q

For Hep C, you have acute then persistant inf, then chronic infection.Why?

A

you don’t develop great immunity to Hep C because you have 6 genotypes and there are differences in disease prevention.

24
Q

There was high prevelance of Hep C from 1950-1959. Why?

A

This was the baby boomer generation and there was a lot of IV drug use occuring. As the generations are getting older, we should see decrease in Hep C.

25
It is projected that decompensated cirrhosis and HCC is to decrease by 2030, why?
GenZ and later does not have high prevalence and we have new and upcoming HCV drugs to treat
26
Explain Hep C antivirals
Hep C genome is a polyprotein, so protease clips different parts, so we have diff fxns in this big long polyprotein. Antiviral treatment targets specific polyproteins, more specifically those that are nonstructural which are used for replication. Usually these antivirals are given in combination So NS3 (which is NS4A and NS4B ) antivirals are given in combination and targets protease and helicase. NS5A and NS5B are given in combination and that targets RNA replication as well (phosphoprotein RNA relpication assembly and rna-dep polymerase)
27
There is high efficacy of HCV antiviral treatment, what is used to test this effectiveness?
SVR12(%) Sustained Viral Response after 12 weeks. It tests whether or not there is virus in the blood after 12 weeks. It was shown that 8-12 weeks after treatment with drug combinations, there is over 90% efficacy of clearing virus. All 6 genotypes are sensitive to these drug combinations
28
What is the family of Hepatitis B, and provide details:
Hepadnaviridae Family enveloped, icosahedral, circular dsDNA HBV polymerase=reverse transcriptase
29
How is Hep B transmitted?
blood, mucosal contact (sexual, perinatal)
30
What is the pathogenesis of Hep B?
incubation time: 60-90 days low incidence of illness and high incidence of persistance in young children
31
Hep B is both hepatotropic and non-cytopathic, what does this mean?
This means that liver damage occurs and this is due to the host response to viral infection. SO remember, the virus itself does not cause damage to liver cells, its the immune T cell response that causes damage
32
What is chronic active hepatitis in Hep B?
alternating clinical exacerbation and remission (this means that there is damage to liver-it comes back and goes away constantly) immunologic tolerance: chronic active carriers do not make antibodies to HBsAG (this is hep B surface antigen) BUT they will build immunity against core Hep B antigen
33
In this picture, explain why only 10% of babies have resolved infection of HBV (ADD pic)
this is because babies do not have a fully developed immune system
34
In this picture, 90% of babies and 20-50% of people in early childhood develop chronic infection of HBV due to what? ADD PIC
The immune tolerance phase
35
Provide basic details of Hepatitis D virus
satellite of HBV (-) RNA genome envelope derived from HBV
36
Hep D encodes two proteins (RNA editing) what are they and what do they do?
HDAg-S: required for HDV replication HDAg-L: inhibits replication and is required for virion formation ## Footnote concept is similar to early and late genes
37
What are the patterns of infection for Hep D and explain
Coinfection of HBV and HDV: results in BOTH acute type B hep and acute type D hep Superinfection by HDV: affects chronic HBV carriers results in severe acute hep and chronic type D hep ## Footnote In general, for both of these, you need Hep B to be infected with D
38
What are exanthems?
External rashes
39
What are enanthems?
internal rashes
40
What are you forms of enanthems/exanthems?
macular, papular, vesicular, pustualar, or a combination (ex: maculopapular)
41
What are the classical viral exanthems?
-measles: rubeola (1st disease) -rubella: German measles (3rd disease) -parvovirus B19: erythema infectiosum (5th disease) -HHV-6 & HHV-7: roseola infantum (6th disease)
42
What are the non-classical (other) viral exanthems?
-Alphaherpesvirus:HSV-1, HSV-2, VZV -Gammaherpesvirus: HHV-8 (KSHV) -Poxviruses: Variola, monkeypox, molluscum contagiosum
43
What is the family of Rubella and provide details?
linear, (+)ss RNA, icosahedral, enveloped
44
How is rubella transmitted?
respiratory (VERY CONTAGIOUS)
45
What are the symptoms of rubella?
They are typically mild 1. non-specific macular rash of head, neck, and trunk 2. low grade fever 3. sore throat
46
Rubella: What is congenital transplacental infection?
Affects NON-IMMUNE PREGNANT WOMEN the virus reaches the placenta and eventually the fetus. This infection leads to immune tolerance and viral persistance in the fetus because fetus immune system is not fully mature
47
20-30% of mothers infected with congenital transplacental infection during pregnancy deliver babies with serious birth defects, what are they?
cardiac defects, nerve defects, eye defects, mental retardation, anemia.
48
Infants with congentital rubella has a very characteristic rash, what is it?
"blueberry muffin" skin lesions
49
What is the family of Human Herpesvirus 6 (HHV-6 A/B) and provide details
Beta-Herpesvirus Family linear, dsDNA, icosahedral, enveloped
50
HHV-6 is ubiquitous meaning its very widespread. It's two subtypes predominates where in the world?
HHV-6A predominates in sub-Saharan Africa HHV-6B predominates in Europe, Japan, US
51
What is the latency of Human Herpesvirus 6 (HHV-6 A/B)?
Shortly after primary infection latent viral DNA can be detected in monocytes (macrophages) -after primary infection, life-long latent virus is integrated into telomeres
52
HHV6-B(review if this is A too) is the most common cause of what in children?
febrile seizures in children (6-24 months)
53
What is the exanthem of HHV-6B?
exanthem subitum ("sudden rash") aka roseola
54
Diagnosis of HHV-6B is based on clinical observations, how does this look like?
Incubation: 4-6 days Fever: 3-5 days (can go up very quickly, it causes the seizures) macular rash
55
A person can have inherited chromosomally-integrated HHV-6 (ciHHV-6), what does this mean?
About 1% of people inherit the integrated HHV-6 genome from their parents/grandparents.
56
What is the immunity and treatment of HHV-6?
1. Prevention: no vaccine 2. Immunity: cellular immunity -problem: HHV-6A killsT-cells -ciHHV-6 individuals have little immunity against HHV-6 due to tolerance( this means that you have it through germlines so you get immunity b/c body treats as self) 3. Treatment: ganciclovir and derivatives, foscarnet

Microbiology (18 decks)

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