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HDID - Virology > Lecture 81_82: Hepatitis > Flashcards

Lecture 81_82: Hepatitis Flashcards

1
Q

Hepatitis – General:
what is it?
Acute vs Chronic
Cirrhosis vs Decompensated Cirrhosis ?

Symptoms of acute hepatitis ?
labs?

A

Hepatitis – inflammation of the liver which can lead to dysfunction over time

Acute – more symptomatic; can progress to chronic if virus is not cleared

Chronic – usually asymptomatic until onset of cirrhosis

Cirrhosis – scarring of the liver; but not necessarily dysfunction

Decompensated cirrhosis – enough scarring of normal tissue; significant hepatic dysfunction. Requires liver transplant

Symptoms; Jaundince, Icterus, 
Labs to check: ATLs, AST 
Bilirubin 
Prothrombin Time 
INR
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2
Q

Hepatitis B

  • what viral family?
  • virion is aka?
  • describe the nucleic acid content
A

Viral Family; HepaDNAvirus
Virion is aka Dane Particle

Nucleic Acid – partially ds DNA; incompletely circular

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3
Q

Describe the structure of HBV

What are some important antigens ?

What are spheres and filaments

What is E antigen

A
  • Smallest DNA virus
  • Enveloped – surface antigens comprise the viral component of the lipoprotein coat

Partially dsDNA
Surrounded by HB Core antigen

Spheres and filaments – 22nm secretions from the virus with DNA material; circulate in the blood

E Antigen – not well characterized functuon; indicator of transmissibility in high viral loads

Important Antigens-
Surface antigen
Core antigen
E Antigen

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4
Q

Describe the Lifecylce of HBV?
what is unique about DNA replication?
What is unique about the genome?
how is this overcome ?

A

Enters host cell and is uncoated
DNA is “incompletely closed” and enters the nucleus
Host polymerases make the DNA —> cccDNA

cccDNA is supercoiled and fully dsDNA
Persists in the host nucleus indefinitely

cccDNA is transcribed and translated, leading to virion assembly.

DNA replication goes through RNA intermediate and therefore requires Reverse Trasncriptase

Therefore can use RT inhibitors as treatment

The genome – smallest DNA viruses; uses overlapping reading frames

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5
Q

HBV Epi and Transmission

A

1 million with chronic HBV in the US
2/3s unaware
400 million people world wide with chronic HBV
Highest burden in west africa

transmission: Low infectious dose
- Sexually transmitted
- Parenteral – eg IVDU; stable on fomites for 7 days
- Perinatal – 70-90% of transmission is mother to child

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6
Q

pathogenesis and progression of EBV:

A

Pathogenesis –
Host immune responses mediates the tissue damage
Most Damage is done by CTLs
Adative and immune response necessary to clear the virus

Chronic infection can cause immune dysregulation

In general:
The better the immune response to an acute infection, the more symptomatic, and the more likely the virus will be cleared

Therefore:
90% Children infected (such as perinatal): Asymptomatic, but do not clear the virus and develop disease

Only 5% of adults do not clear the disease
95% are symptomatic to acute infection; clear infection

25% of chronic infections lead to cirrhosis
25% of these will have decompensated cirrhosis

(HBV is the 6th most common cause for liver transplant)

5-10% of chronic HBV infections —> Hepatocellular carcinoma

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7
Q

Describe the patterns of diagnositc HBV markers for an acute HBV infection which resolves ?

what is the window period?

whats a marker for acute HBV infection?

what about the HBV DNA ?

A

HBV Surface Antigen – first to appear

Anti-core IgM and IgG — next to appera

Surface antigen begins to be cleared;
Window period passes before Anti-surface antigen begins to appear and persist

Anti core IgM will dissappear but anti-core IgG will persist
Therefore IgM anti-core is good marker for acute HBV infection

HBV DNA – marker for replication and moves in parallel with the HBV surface antigen

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8
Q

Describe the patters of diagnositic HBV markers for chronic HBV Infection ?

A

HBV Surface Antigen and HBV DNA – never cleared and persist

HBV Surface Antibody – Never develops; no immune response was mounted

Viral Load will remain positive

Core IgG will be positive for life

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9
Q

Treatment of HBV –

who to treat? what are the treatments?

Prevention

A

Who to treat? __ based on viral burden and ALT levels

Treatments:
Entecavir — guanosine analog
Tenofovir – adenosine analog

Prevention:
HBV Vaccine – all children in the US – course of 3 injections
Uses surface antigen
vaccinated persons will not have IgG -core antigen

HBV IG – temporary passive protection; given to children born to infected mothers; unvaccinated persons exposed to blood or body fluids. VERY EXPENSIVE

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10
Q 
Hepatitis D Virus -- 
whats unique about this virus? 
antigens?
Genome? 
co infection vs superinfection

when add to ddx?

Diagnosis ?

A

Virus that cannot cause harm without HBV infection

single stranded RNA Genome
Only unique antigen is the Delta Antigen

Co-infection: HBV and HDV acquired together
Superfinction: HBV first followed by HDV infection later

Add to DDx when someone with chronic HBV infection all of sudden has changes in the transaminases (ALT)

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11
Q

Hepatitis C Virus
family? genus?
Structure?

unique morphology

A

Flavivirus – Hepacivirus

Enveloped
RNA
Glycoproteins in lioid envelope
Nucleopcapsid with Core antigens

Pleomorphic characteristics — lipo particles in the blood stick to the glycoprotein

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12
Q

Describe the life cycle of HCV?
tropism
whats unique about the translation of the genome

A

infects the Hepatocyte

Viral Entry —> uncoating
processes occur in association with the Endoplasmic Reticulum

Replication of RNA

9.4K Nucleotides are translated into 3000 amino acid long chain. Which is then cleaved by proteases (host and virus)
Proteins form a menbraneous web with the ER

To exit the cell – Hijacks the lipid secretions pathways
budding

The virus never integrates; takes place outside of the nucleus

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13
Q

Targets for Treatment of HCV

A

The nonstructural Protiens –
proteases,
polymerase, and
NS5A (unknown enzymatic activity, but effective target for treatment)

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14
Q

Why is it difficult to ammount a host immune response to HCV?

A

RNA Dependent RNA Polymerase – lacks proof-reading fuction – high mutation rate

Different Genotypes and Subtypes

Viral Proteins – can also inhibit the innate immune response –
eg NS4A – cleaves translated proteins for packaging but acts nonspecifically and cleaves host proteins involved in immune response

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15
Q

Pathogenesis and Progression of HCV

A

Acute infection:
15% mount immune response and clear disease
80% devleop chronic Hepatits

Host CTL Response leads to collateral damage of the liver

20% of chronic cases lead to Cirrhosis
25% of cirrhosis cases become decompensated cirrhosis

HCC is only prevelant in HCV Cirrhosis –
It is thought that the cirrhosis leads to the cancer; not the extra-nuclear HCV RNA

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16
Q

Epi and Trasmission of HCV

what country has the highest rate
what genotype is most prevelent in the US and europe ?
what genotype is easiest to treat clinically?

A

Epi – 185 million cases world wide. 130 million chronic cases
3-5 million cases in the US
Genotype 1 – most difficult to treat

Leading cause for liver transplants
cause of 27% of cirrhosis; 25% of all HCC
Highest in Egypt

Transmission:
60% via IVDU, body piercings
Transfusions - 1 in 10,000
10% unknown

Genotype 2 is easiest to treat

17
Q

HCV
what co-morbiditis are associated with disease progressin?

which features are not associated with disease progression ?

A

Alcoholism
DM, Iron Overlaod

Not associated: Viral load, genotype

18
Q

Diagnosis of HCV

A

○ ELISA Screening Test for HCV Antibodies
§ — 98% sensitivity

If positive, confirm with HCV viral load

19
Q

Treatment of HCV

what metric is used to

goals of therapy

A

treatment based on liver damage – assessed bt histology

Interferon Therapy – prior to 2011
Toxicities and side effects
Not very effective

Direct Acting Anti-virals (protease inhibitors)
Very expensive

		§ Virus does not integrate -- therefore it is curable 
		§ Sustained virological response --- Undectable viral load 3-6 months after therapy

With cure – patients are NOT immune to new infecti

20
Q

what is the appropriate combination therapy treatment for HCV?

A

Sofosbuvir RNA Polymerase Inhibitor (NS5B) + Ledipasvir (NS5A Inhibitor)

NS5A – no enzymatic activity; but associated with replication and assembly

21
Q

Hepatitis A
RNA or DNA ?
What family of virus?
How is transmitted?

whats unique?

A

Picornavirus
SS Linear RNA

fecal-oral transmission – raw oysters and uncooked shellfish

THE VIRUS NEVER BECOMES CHRONIC

22
Q

Hepatitis A -
Pathogenesis
Clinical Features

A

Pathogenesis – virus replicates in hepatocytes; released into bile and stool. Infectious prior to clinical symptoms

Clinical Features: due to mounting immune response
30 day incubation
Sx: fatgue, abd, loss of appetite, nausea, vomiting, diarrhea; jaundice, elevated LFTs, dark urine, light stool;

Adults are more symptomatic
Clears in 2-4 weeks
immune for ever

THE VIRUS NEVER BECOMES CHRONIC

23
Q

Hep A
Treatment
Prevention

A

Supportive –
Lifelong immunity after infection or vaccination

Prevention 
	Hygiene, sanitation 
	Vaccine -- Pre exposure 
			§ 0 month, and booster at 6 months 
		○Who gets the vaccination  --- newborns, travelers, MSM, IDU, Patients with HBV, HCV;

Passive Immunization – immune globulin therapy – pre and post exposure
○ Given to travelrers; exposure risks

24
Q

Hep E

Family –
RNA or DNA ?
Transmission

A

Hepevirus

Single Stranded Linear RNA

Fecal oral transmission –

THIS DISEASE CAN BECOME CHRONIC

25
Q

How is hep E similar to hep A?

how is it different?

A

Different:
Hep E can become chronic disease –but rare
Pregnant women – higher mortality rate

Same:
Replicates
Sheds into stool
infectious prior to symptoms

26
Q

Hep E – epi

Dx

treatment

A

Uncommon in the US

Dx: Serology,

Treatment: Symptomatic

HDID - Virology (16 decks)

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