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Prions and Retroviruses > Prions and Retroviruses > Flashcards

Prions and Retroviruses Flashcards

1
Q

what are Prions?

A
  • conformational alteration of a normal CNS protein from a helix to a beta pleated sheet
  • progressive degenerative CNS diseases are proteins without any nucleic acids at all
  • formerly termed ‘slow viruses’ -but they are NOT VIRUSES
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2
Q

how do you get prion viruses?

A

diseases inherited and others acquired (infectious)

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3
Q

The basic mechanism of pathology?

A

proteins (MEANS THEYRE TOUGH) of abnormal conformation (prions) which act as templates for other body proteins (prion proteins) to adapt the abnormal conformations
= this causes proteins

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4
Q

How are prions like proteins?

A

PRIONS are NOT ALIVE - therefore you cannot kill them
- being that prions are proteins - (they’re tough) and these agents are extremely resistant to all forms of inactivation except incineration

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5
Q

PrPc vs PrPsc

A

PrPc - a normal surface component of neurons and glial cells (a helix) and is highly conserved between species
PrPsc - infectious form (beta pleated sheet) = prion
PrPsc - is very resistant to inactivation

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6
Q

What do Prions cause?

A 
1- Creutzfeld-Jacob Disease 
2- Scrapie (sheep and goats)
3- Kuru (spasticity and ataxia, kuru means to be afraid) KURU IS NOT EXTINCT
4- Fatal Familial Insomnia
5- Gerstmann-Straussler-Scheinker Syndrome (in humans and in animals - INHERITED)
6- Bovine Spongiform Encelopathy
7- Ungulate spongiform encephalopathy
8- Transmissible mink encephalopathy
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7
Q

Creutsfeld-Jacob Disease

A

a progressive, fatal disease of the CNS - similar to Kuru - that is seen most frequently in teh 6th and 7th decades

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8
Q

Initial signs of CJD?

A

changes in cerebral functions are thought to be initially psychiatric but are followed by dementia, spasticity, seizures and death after 1-5 years

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9
Q

Variants?

A
  • There is an inherited variant but the disease has been transmitted by human growth hormone and organ transplants, including corneas
  • recently, a new variant in younger patients was described in britain which was ascribed to consumption of beef from cattle with mad cow disease
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10
Q

Causes rules on beef consumption?

A

new rules on the food use of CNS tissues and the elimination of infected hers have brought variant CJD under control!

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11
Q

Retroviruses

A

enveloped, ss RNA viruses taht encode reverse transcriptase (an RNA-dependent DNA polymerase) that copies the genome into dsDNA that can be integrated into the DNA of the host cell (provirus)s

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12
Q

Two main groups of Retroviruses?

A

1 - Oncoviruses

2 - Lentiviruses - prototype lentivirus is visnavirus in sheep

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13
Q

Oncoviruses

A

do not kill the viruses they infect, they just continue to produce virus particles infedinitely

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14
Q

Oncoviruses transform the infected cells by what 3 mechanisms? (step one)

A

1 - encoding for an oncogene (not described in humans)

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15
Q

Oncoviruses transform the infected cells by what 3 mechanisms? (step two)

A

2- insertional mutagenesis (disruption of growth regulator genes by the random insertion of the provirus (not known

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16
Q

Oncoviruses transform the infected cells by what 3 mechanisms? (step three)

A

3- Activation of host cell growth regulator gene expression by viral protein

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17
Q

Oncoviruses: HTVL 1 vs 2

A

HTVL 1 - associated with adult T-cell leukemia, a rare malignancy found in Japan, Africa and the Caribbean and with tropical spastic paraparesis
HTVL 2 - associated with hairy cell leukemia - Appear to be transmitted by sexual and arenteral routes, although the long incubation period (10-20 years) makes epidemiological investigation difficult.

18
Q

How was lentivirus discovered ?

A

In 1981 epidemiologists noted an increase in the number requests for pentamidine to treat PCP, Pneumoniae due to pneumocystis jerovecii (81 cases in children) a previously rare opportunistic pathogen
- cases then noted in San Fran and New York
Analysis showed that these cases were occurring mainly in young homosexual makes who had helper T cells and were susceptible to a number of infections

18
Q

Lentiviruses

A

the prototype virus of this type is visnavirus in sheep

19
Q

Why were young homosexual males an unusual profile?

A

It was usually cancer chemo patients or old people

20
Q

How was AIDS coined as what this was?

A

Almost all previously described immune deficiency diseases were conenital

21
Q

Who discovered AIDS?

A

The virus responsible was isolated first I’m France by Luc montagnier and then second by Robert Gallo in the US and was renamed HIV

22
Q

What did further analysis of HIV show?

A

That the virus is comparatively new and probably originated as a mutant simian virus in central
Africa

23
Q

Where were the first HIV cases found?

A 
As early as 1939
In Germany (now Poland)
24
Q

What were AIDS cases related to?

A
  • heterosexual activity, IV drug abuse, hemophilia, transfusion and vertical transmission

NO EVIDENCE THAT CASUAL CONTACT CAN RESULT IN INFECTION

25
Q

HIV-1A

A

Mainly spreads heterosexually

-

26
Q

HIV 1B

A
  • the predominant Strain in Europe and North America
  • spreads mainly via anal inter purse
  • soon after infection there is a flu-like illness which is associated with seroconversion
27
Q

what happens after 8-10 years?

A

There’s a depletion in CD4 cells resulting in opportunistic infections and also dementia secondary to direct infection of the central nervous system

28
Q

When do you use the term AIDS?

A

When the advanced stage of the disease is reached - CD4 count < 200

29
Q

What about above 200??

A

Above 200 serology Positive for HIV antibiotics = you have HIV infections ***

30
Q

What is the count is over 500?

A

Immunity is normal

31
Q

Immunosuppressive is directly associated with what?

A

Immunosuppression correlates inversely to the CD4

32
Q

Risk to caregivers?

A

From a needle stick - approximately 1/300 (PEP can be given in these cases)

33
Q

How does HIV 2 spread?

A

Heterosexually

34
Q

What was aids originally called?

A

gay related immune deficiency

35
Q

Origins of HIV?

A
  • SIVcpz found in Gabon serologically reacts with HIV-1
  • entered human population through bush meat trade (Cameroon)
  • SIVcpz probably evolved into HIV-1 and HN-O
  • SIVsm 80-90% genetic homology with HIV-2
  • HIV-1 = main cAuse of AIds in North America
36
Q

HIV -like viruses

A
  • occur in cattle, lions, horses, sheep, goats and simians (SIV)
  • mostly benign but cause disease in equines and house cats
  • SIV first isolated from Japanese macaques
  • SIVgm (gm stands for African green monkey) , SIVcpz (chimpanzee)
  • SIVsm (sooty mangeby)
37
Q

Diagnosis of HIV

A

HAART - plus aggressive prophylaxis and treatment of opportunistic infections is not curative but the life span of those infected has improved markedly

38
Q

Biggest risk factor associated with new cases?

A

IV drug abuse

39
Q

Natural history of HIV

A
  • complex interplay between viral replication and immunological defences
  • average time (without therapy) from infection to an AIDS-defining illness is ten years for HIV-1, longer for HIV-2
  • there are nonprogressors, rapid progressives and HIV resistant people
40
Q

Degree of immunosuppression

A

CD4 counts of < 200 = AIDS

Drops less than 50 = DANGEROUS infection / viruses

Prions and Retroviruses (1 decks)

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