Lecture 6 Flashcards

1
Q

Diff between chronic and latent?

A

Chronić: continous virusreplication at reduced levels
-virion are continually detected

Latent: persistence of viral genome without active virus replication

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2
Q

What is hep A?
Causative agent?
Transmission?
Prevention?
Incubation?

A

Acute
Naked SRNA picornavirus HAV

Fecal oral

Inactivated virus

3-5 weeks

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3
Q

What is hep B?
Type of virus?
Transmission?
Vaccine?
What is detected during the chronic HBV infection?

A

Chronic infections — causes up to 80 liver cancers

Enveloped dsDNA hepadnvirus

Semen, blood

Subunits vaccine

HBsAg —- surface antigen

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4
Q

What does virus/ V-ab lead to?

A

Tissue injury, defective particles can contribute to pathogenisis

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5
Q

What is the Hep B surface antigen?

What isthe surface antibody, what does it indicate ?

What isthe core antibody and what does it mean?

What is the antibody that interacts with the core antibody?

A

HBsAG— detected during acute or chronic, means that the person is infectious

Anti-HB——recovering and immunity for HBV OR successfully vaccinated
-those who are chronic fail to develop this

Anti-HBc—— onset of acute hep B and persists for life, indicated previous or ongoing infection
-for only acute infections

IgM antibody to core antibody , which means that there is an acute infection

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6
Q

What is present if immune due to hep B vaccination OR due to natural infection?

What is present in acutely infected vs chronic?

A

Vaccination: only pos for anti-HB’s—protective

Natural: has both anti-HB’s and anti HBc’s

Acute: is pos for
HBsAg
Anti Hbc
IgM and anti HBc

Chronic: pos for
HBsAg
Anti-HBc

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7
Q

What does chronic HBV activate?
What can chronic HBV lead to?

A

Process similar to wound healing leads to depositions of extracellular matrix
Liver injury, inflammation

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8
Q

What is sufficient to confer protective immunity?
What inhibitors are effective?

A

Antibodies to HBsAg
-recombination vaccine of this has reduced carcinoma rate as

-non nucleoside RT inhibitors against HEPB RT activity

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9
Q

What is hepc?
What kind of virus?
How is it passed?
Symptoms?
Vaccine?

A

Chronić infection— high persistence

Enveloped sRNA flavivrus HCV

Blood

Acute symptoms 2-6 weeks after exposure
Most develop chronic infections + have no symptoms

No vaccine

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10
Q

What fuels increase in HEP c and B?

A

Being fueled by opis and heronin use

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11
Q

What is herpes simplex virus type 1?
What type at site of infection?
When does it go into latency?
What can it cause?

A

Acute phase

Goes latent into trigeminal nerve cells
So no circulating or virus replication, not a lot of gene expression

HSV1 cause oral lesions and HSV2 cause genital lesions

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12
Q

How did lab scientist learn that mononucleosis is an EBV acute phase disease?

A

Lab tech studied EBV and came back seropositive after mononucleosis sick leave

Examined data of the person at the start and end of college carrier and found a strong correlation between EBV seroconversion and reports of mono

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13
Q

What is Burkett lymphoma result from?
What is EBV linked to?

A

—Chromosomal translocations—- those that fuse Ig loci with myć oncogene

  • inappropriate activation of Ig recombination

Some cases of nasopharyngeal cancer

Bad for immunicopromised people

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14
Q

What is chicken pox and shingles an example of?

A

Chicken pox: VZV acute virus phase

Shingles: VZV reactivation

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15
Q

What are types of herpes viruses?

A

HSV 1 and HSV2

Varicella zoster virus (VZV)

Epstein Barr virus (EBV)

Cytomelagovirus (CMV)

KSHV

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16
Q

What is ms?
What is the correlation with EBV?
What does EBV encode but doesn’t recognize?

A

Autoimmune demylelination syndrome causing neurological disease

Antibodies against EBNA1 can cross reaction with GlialCAM (central NS protein for adhesion)

Thymidine kinase—— does not recognize & phosphorylate ganicolovir & acycylovir

17
Q

What is the few EBV protein that is expressed in latency?

18
Q

How do persistent viruses avoid adaptive immune recognition?

A

Makes fake MHC 1 protein that cant display the antigen

Cyctoxic T cell or NK cannot recognize it because the antigen is not displayed and MHC1 is present— so it survives

19
Q

What happens during the acute, chronic, and latent phase of HIV?

A

Acute: flue symptoms with a high viral load— stimulate IFN response

Chronic: Asymptomatic, viral load is low
-CD4 T cells are high and try to kill
-antiretroviral can suppress HIV to undectable levels

Latent: AIDS—-> persistence when replication is prevented