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Vilo > HBV > Flashcards

HBV Flashcards

1
Q

What is hepatitis?

A

inflammation of liver parenchyma, death of hepatocytes

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2
Q

Name the virusfamilies Hepatitis A, B, C, D and E belong to. Which can not lead to a chronic hepatitis?

A

A: Picornaviridae (no chronic hepatitis)
B:Hepadnaviridae
C:Flaviviridae
D:virusoid
E:Hepeviridae (no chronic hepatitis

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3
Q

What is cirrhosis?

A

connective tissue replaces hepatocytes

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4
Q

Describe the pathology of hepatitis

A

chronic carriers because viruses are not cytolytic –> not the virus kills the hepatocytes but the immune system

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5
Q

What does the clinical course of HBV infection look like?

A

actute hepatitis leading to either:
1.death
2.cure
3.persistent infection/chronic hepatitis –> cirrhosis or cancer

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6
Q

What does the immune reaction against HBV look like?

A

-severely delayed (after month) because liver is immunoprivileged organ, non-cytopathic virus, vast amount of antigen

-immune pathology because: cytotoxic Tcell response, NK cells, cytokines, extrahepatic disease manifestation by immune complexes (arteritis, vasculitis)

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7
Q

What are the problems of HBsAg Tests? What is the consequence?

A

-HBV genotypes react differently
-suboptimal sensitivty (no high titers in early phase of infection)
-HBsAg is highly variable under immune pressure/selection

–> wrong negative results

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8
Q

What is the major structural antigen on surface of HBV?

A

Small HBs Protein (SHB)

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9
Q

How can HBV infection be treated? What is the problem?

A

-pegylated Interferon gamma
-RT inhibitors

BUT: resistance

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10
Q

What does the genome of HBV look like?

A

overlapping ORFs–> super condensed genome, ORFs are modular and all regulatory elements overlap with ORFs

-partially dsDNA: complete - strand which is longer than 1 copy and an incomplete + strand with a gap
-ciruclar but not covalentyl closed –> relaxed circular RC-DNA
-5’end of + strand covalently linked to viral RNA with cap
-5’end of - strand DNA with covalently linked P-Protein

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11
Q

How many Poly A signals are in the genome of HBV? what is the consequence?

A

Only one Poly A signal –> all mRNAs have the same sequence at the end

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12
Q

what is the consequence of overlapping ORF in HBV?

A

each nucleotide change in envelope may at the same time lead to amino acid change in the pol-protein and vice versa

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13
Q

describe the replication cycle of HBV

A

1.enter via receptors
2.genome release at nuclear pore
3.cccDNA gets transcribed
4.sgRNA and pgRNA translation
5.formation of immature nucleocapsid with RNA
6.RT step (protein P) to form mature nucleocapsid with DNA
7. either virion assembly and release or repeat of step 2 etc

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14
Q

what does the HBV DNA look like when it enters host nucleus?

A

super coiled (cccDNA) to prevent escape from nucleus)

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15
Q

What are the transcripts and gene products of HBV?

A

-6 mRNAs als transcribed by cellular pol II in nucleus: 2 genomic RNAs and 4 subgenomic RNAs:
-subgenomic RNAs for surface proteins: LMS
-each RNA has cap and tail with identical polyA tail/3’end
-usually only first cistron translated except for p (is encoded in second cistron of pregenomic mRNA)

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16
Q

What is the function of protein P and what is special about its translation in HBV?

A

Protein P has reverse transcriptase activity

is encoded in the second cistron of pregenomic (pg) mRNA (no separate mRNA for P)

17
Q

what is required for the RT step in HBV?

A

-immature capsid
-pg RNA
-core
-P-protein

18
Q

how is the specific packaging of pgRNA into the immature nucleocapsid ensured in HBV?

A

-no packaging of pgRNA without p-protein
-no packaging without intact 5’ end
-fusion of pgRNA 5’ end to heterologoues RNA is packaging signal
-RNA stem loop epsilon at 5’end of pgRNA serves as packaging signal recognized by P-protein

19
Q

where does the reverse transcription take place in HBV?

A

in the immature capsid: viral RNA to partially dsDNA

20
Q

how does the reverse transcription of pgRNA work in HBV?

A

-5’base of - DNA covalently bopund to tyrosine in TP domain of P-protein -> this serves as protein-priming
-first template switch to 3’DR1
- minus DNA synthesis and degradation of pgRNA which served as a template
-plus DNA synthesis as side product where 5’end fragment serves as primer
-2nd template switch: Elongation of plus DNA tp 5’end of minus DNA
-3rd template switch

21
Q

what is the driving force of template switching in HBV DNA synthesis?

A

thermodynamics of strand interaction

22
Q

What is the receptor for HBV infection?

A

NTCP

23
Q

How can HBV infection be prevented? When is it effective?

A

entry inhibitors derived from large envelope protein –> effective when a HBV-positive person gets a liver transplantation

24
Q

What is HDV?

A

-is a satellite virus which needs HBV capsid proteins for packaging
-coding for 1 ORF but no capsid proteins
-rolling circle apmplification
-cellular RNA PolII is involved in genome replication

Vilo (12 decks)

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