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ID > WK 11- Blood Borne Viruses > Flashcards

WK 11- Blood Borne Viruses Flashcards

1
Q

What are the 3 enzymes that HIV contains

A

reverse transcriptase, integrase and protease

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2
Q

What is the viral structure of HIV

A

2 x ssRNA and 3 enzymes

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3
Q

What is the most common type of HIV

A

HIV-1

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4
Q

What are the 4 major groups of HIV-1

A

M (major) group, O (outlier) group & 2 new groups (N & P)

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5
Q

Where are rates of HIV highest

A
  • present in all countries of the world but rates are highest in Sub-Saharan Africa and South Africa
  • Infections in women are increasing
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6
Q

How is HIV transmitted

A

-sexual (MSM), blood or blood products (transfusions, IVDU), vertical (mother to baby- if you treat the mother with antivirals during pregnancy you can reduce viraemia and prevent transmission to baby), oral transmission

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7
Q

What are the 3 clinical stages of HIV

A
  • Acute infection
  • Clinical latency
  • AIDS
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8
Q

What symptoms are associated with acute infection

A

flu-like symptoms that are non-specific- 2-4 wks post exposure
→ fever, lymphadenopathy, headache, rash

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9
Q

What symptoms are associated with clinical latency

A

flu-like symptoms disappear and person may not have symptoms, but as T cells decline they may get lymphadenopathy and chronic diarrhoea – but mainly asymptomatic and last 3-20 years
→ fever, weight loss, GIT disturbances, muscle pains

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10
Q

What symptoms are found in AIDS

A

T cells are completely depleted and there will be systemic symptoms and viral induced cancers (Kaposi’s sarcoma)
→ prolonged fevers, night sweats, unexplained weight loss

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11
Q

How is HIV diagnosed in the lab

A
  • Screening with HIV Ag/Ab combination test (Automated EIA)

- Positive screening are referred for confirmation testing by looking for p24 Ag and then performing western blot

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12
Q

How can a western blot detect HIV

A
  • Have filter paper with viral proteins attached (gp120, reverse transcriptase, gp41, p24→ depending on what stage of illness the pt is at determines the antigens that will be detected)–> add pt serum, if there is Ab in the patient serum the Ab will bind and cause a colour change
  • the more colour changes (lines)-> the more progressed the infection
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13
Q

What is HIV-genotyping

A

once HIV genome is integrated into human genome it produces pro-viral DNA→ pro-viral DNA is able to be detected in the patients lymphocytes→ allows you to test babies and determine vertical transmission

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14
Q

What is the tx for HIV

A

-HAART = Highly Active Anti-Retroviral Therapy
-Combination of at least 3 drugs that suppress HIV
replication & decreased risk of developing resistance

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15
Q

What drugs are used for HIV tx

A
  • NRTI (nucleoside reverse transciptase inhibitor)
  • integrase inhibitor
  • protease inhibitor
  • NNRTI (non-nucleoside reverse transcriptase inhibitor)
  • fusion inibitors
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16
Q

How can HIV be prevented and controlled

A

-Education
-Safe sex, needle exchange
-Antiviral treatment of pregnant HIV +ve
women
-PREP→ pre-exposure prophylaxis
-No vaccine yet→ due to rapid mutation

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17
Q

What is the viral structure of HTLV

A
  • RNA retrovirus

- Genome: 2 copies linear +ve sense ssRNA

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18
Q

What is the difference between HIV and HTLV

A

HIV-1 was originally known as HTLV-3 but now HTLV3 causes lymphocytosis, and HIV causes lymphopaenia

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19
Q

What cell does HTLV1 infect and what is the result

A

predominantly infects

CD4+ve T-lymphocytes-> causes lymphocytosis

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20
Q

How is HTLV-1 transmitted

A

-HTLV enters body inside infected CD4+ve T lymphocytes in blood or semen, as well as
vertically via breast milk and possibly transplacentally
-Intrauterine & peripartum transmission

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21
Q

What are the 3 categories of symptoms of HTLV1

A

Malignant, Inflammatory, Infective

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22
Q

What are the malignant symptoms of HTLV1

A

-Acute T-cell leukaemia/lymphoma (rapidly fatal), Chronic T-cell leukaemia/lymphoma, Cutaneous T-cell lymphoma

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23
Q

What are the inflammatory symptoms of HTLV1

A 
-HTLV-Associated Myelopathy (“HAM” or
“Tropical Spastic Paralysis”)
-Uveitis
-Arthropathy
-Sjogren’s syndrome
-Polymyositis
-Thyroiditis
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24
Q

What are the infective symptom of HTLV1

A
  • Strongyloidiasis
  • Crusted scabies
  • Bronchiectasis
  • Infective dermatitis
  • TB, leprosy
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25
Q

How is HTLV1 diagnosed

A
  • PCR is used to determine whether the Ag are mothers or babies→ used in vertical transmission as not always sure whether the Ag is due to infected mother or foetus
  • Detection of HTLV-specific Ab by serology
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26
Q

How is HTLV-1 prevented

A
  • No specific treatment
  • Breastfeeding considerations
  • Screening of donated blood products
  • Barrier protection to prevent sexual spread
  • IVDU avoid needle sharing
27
Q

What family does HBV belong to

A

Hepadnaviridae

-partially ds circular DNA

28
Q

What are the 3 important viral antigens

A

HB surface Ag (HBsAg, viral envelope protein)

  • HB core Ag (HBcAg)
  • HBeAg
29
Q

What is the epidemiology of HBV

A

endemic in the asia-pacific area→ risk groups include indigenous Australians, IVDU, high risk sexual activity, those born overseas in endemic areas

30
Q

How is HBV transmitted

A

Transmission:
-Parenteral & mucosal (esp. sexual) exposure
to infected blood or body fluids (saliva, semen,
vaginal secretions, breast milk)
-Transmission to foetus during pregnancy & at
delivery→ every pregnant woman is screened for HBV so normally under control before birth
-IVDU
-Needle-stick injuries
-Reuse of needles
-Child to child transmission (biting, etc)
-Sharing of personal items (razors, toothbrushes,
nail clippers, etc)

31
Q

Where does HBV replicate

A

replicates in hepatocytes in the liver

32
Q

What is the pathogenesis of HBV

A

HBV travels to liver via bloodstream →Mechanisms by which HBV infects
hepatocytes not yet well understood
-Virus infects healthy liver cells & triggers immune
response that destroys the damage and destruction of the hepatocytes
→Hepatitis B is an immune mediated disease, as
opposed to HIV which destroys immune cells

33
Q

What is acute infection of HBV

A

HBV infection considered acute during 1st 6

months following infection

34
Q

What is a chronic infection of HBV

A

If HBsAg persists >6months the infection is considered
chronic (patient has been unable to clear the virus after 6 months→ failed to mount an immune response)
-Chronic infection can be life-long

35
Q

What are the symptoms of acute HBV

A
  • many cases are asymptomatic and can transmit unknowingly – common in children
  • Symptoms common in adult infection:
  • Loss of appetite
  • Nausea & vomiting
  • Tiredness
  • Abdominal pain
  • Muscle & joint pain
  • Jaundice (usually occurs ~12wks post infection)
  • Small % cases develop fulminant hepatitis
36
Q

What are the symptoms of a chronic HBV infection

A
  • again most cases are unaware and can be asymptomatic but can present with:
  • Tiredness, depression, irritability
  • RUQ pain
  • Nausea & vomiting
  • Loss of appetite
  • Joint aches & pains
37
Q

What is the course of a disease if an infant is infected with HBV

A

-Infants rarely experience symptoms of acute

infection, h/w 90% will develop chronic HepB (happens in endemic regions)

38
Q

What is the course of a disease if a child is infected with HBV

A

Rarely experience symptoms of acute

infection, h/w 30% will develop chronic HepB

39
Q

What is the course of a disease if an adult is infected with HBV

A

-Adults and adolescents commonly experience

symptoms of acute infection, h/w <5% will develop chronic HepB

40
Q

Why do adults get symptoms of HBV but do not get chronic infection

A

Thought to be a result of a matured immune system-> this is why babies get chronic infection (unable to clear the infection) but do not get any symptoms (as HBV is immune mediated)

41
Q

What is HBsAg

A
  • Indicator of current infection

- Can be detected in acute & chronic HBV

42
Q

What is HBsAb

A

-Indicator of immunity (prior infection or

vaccination)

43
Q

What is HBeAg

A
  • Indicator of virus replication & infectivity

- Presence indicates individual is highly infectious

44
Q

What is HBeAb

A

-Indicator of recovery from infection

45
Q

What is HBcIgM

A

-Indicator of recent infection

46
Q

What is HBcTotal Ab

A

-Indicator of past infection
-Test may be performed if patient does not
seroconvert after vaccination

47
Q

What is HBV DNA

A

May be used to clarify the stage of infection,
especially if LFTs are abnormal and if the HBsAg
and/or the HBeAg are detected
-Can be used for monitoring response to treatment

48
Q

What other tests can be done to diagnose HBV

A

-LFTs: ALT (alanine aminotransferase) – released into blood when liver cells injured
-Liver biopsy: Not often used now
-AFP (alpha- foetoprotein): blood test to detect liver cancer, AFP is a tumour marker (i.e. An embryonic protein produced by
cancer cells)
-Coagulation profile: Will be deranged in hepatitis (no clotting factors will be produced)

49
Q

What is the tx of HBV

A

-Number of antiviral agents available
→ no ‘cure’= aim is to reduce replication and transmission to other contacts and pt deterioration
-Australia use Tenofovir, IFN
-mainly only consider tx if liver damage has occurred

50
Q

How is HBV prevented

A
  • Vaccination→ Safe & effective, part of routine childhood vaccination schedule-> given at birth
  • Plus recommended for other at-risk groups
  • Avoid transmission risk
  • HBIG (immunogloblulin) within 72hrs post exposure→ prevent acquiring HBV from needlestick
51
Q

What family does Hep C belong to

A
  • flavivirus (most are mosquito borne)

- Ss +ve sense RNA genome

52
Q

What are the main strains of hep C in aus

A

3a, 1a, 1b

53
Q

How is HCV transmitted

A

majority are due to IVDU

  • other means= Non sterile tattooing/body piercing
  • Non sterile medical procedures/vaccinations
  • Needle stick injuries
  • Household exposure
  • Other blood to blood contact→ source of HCV infection unknown in some cases
54
Q

What is the pathogenesis of HCV

A

-Direct invasion of hepatocytes
-Molecular mechanisms not fully understood
-HCV induces a strong early innate response but
seems to be resistant to the antiviral effects of this response, resulting in chronic infection in up to 80% cases

55
Q

What complications can arise from HCV

A

Over the course of 10-20yrs of chronic
infection extensive scarring of the liver occurs
(fibrosis & cirrhosis) & in some cases hepatocellular cancer develops→ most people develop chronic infection

56
Q

What are the factors that suggest someone will develop cirrhosis/liver cancer from HCV

A

male, alcohol intake, HBV/HIV co infection, obesity, age at time of infection (fastr disease if infected over 40)→ all increase the risk of developing cirrhosis or liver cancer

57
Q

What tests are done to screen for HCV

A

Screening test: EIA for HCV Ab

  • 2nd EIA for confirmation
  • HCV Ag test if required
58
Q

What lab diagnostic tests are available for HCV

A

HCV PCR

  • Qualitative or quantitative (“viral load”)
  • Useful for monitoring of treatment
  • HCV genotyping: can be useful guide for duration of therapy
59
Q

What family does HDV belong to

A

Deltavirus→ ssRNA

60
Q

Why is HDV a ‘defunct’ virus

A

Lacks polymerase→ needs concurrent HBV infection

61
Q

What diseases does hep D cause

A
  • acute and chronic hepatitis

- Co-infections (if concurrent HBV infection) or super infections (someone who is a carrier of HBV)

62
Q

What is the pathogenesis HDV

A

Dissemination via blood to liver – replicates in
hepatocytes→Hepatocytes are the only susceptible cells
-Highly pathogenic virus

63
Q

What lab Dx are available for HDV

A

Lab diagnosis:

  • look for HBV first→ if they don’t have HBV they will not have HDV
  • Serology for Ab and HDAg
  • PCR for HDV RNA

ID (13 decks)

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