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Microbiology > Lecture 17 > Flashcards

Lecture 17 Flashcards

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Biology 101 flashcards
1
Q

What three virion enzymes does HIV carry?

A

Reverse transcriptase, Integrase, Protease

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2
Q

What is the structure of HIV?

A

nucleic acid in center, surrounding core protein, matrix protein, envelop, envelop proteins

(retrovirus)

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3
Q

How many regulator genes are in HIV and which two are essential for replication?

A

6 total- tat and rev are essential

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4
Q

What are accessory genes?

A

Genes that are not essential for replication

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5
Q

Steps of replication process

A

attachmet of CD4 molecule, entry, uncoating

reverse transcriptase- RNA genome to proviral DNA

transported to nucleus

integrase unites proviral DNA to host DNA

host cell RNA polymerase transcribes proviral DNA to mRNA

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6
Q

Transmission of HIV

A

primarily through sexual contact

also through blood transfussion /perinatal infection

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7
Q

Pathogenesis of HIV

A

infection occurs in genital mucosa

HIV infects and kills lymphocytes leading to loss of CMI which predisposes to opportunistic infection

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8
Q

What happens to the helper T cells during HIV?

A

HIV kills helper T cells and cytoxic T cells also kill the virus infected helper T cells

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9
Q

What happens when helper T cells are reduced?

A

AIDS is produced

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10
Q

What is the main immune resistance to HIV?

A

cytotoxic T cells which controls the infection for a long time

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11
Q

What does polyclonal activation of B cells result in?

A

high immunoglobulin level which may cause auto immune disease through thrombocytopenia

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12
Q

3 stages of HIV infection

A
  1. acute stage
  2. Latent stage
  3. Late immuno deficiency stage
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13
Q

Describe acute stage of HIV

A

present 2-4 weeks: fever, lethargy, sore throat, generalized lymphadenopathy, rashes on trunk, arms and legs, leukopenia

resolves spontaneously in 2 weeks

Abs appear after 3 -4 weeks

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14
Q

Describe latent stage of HIV

A

set point occurs- new viral production- viral load will reamain constant for a number of years (asymptomatic period), fatigue and weight loss can occur- viruses present in lymph nodes

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15
Q

Describe Late immuno deficiency stage

A

Decline in number of CD4 cells- increase in severity and frequency of opportunistic infections- immuno compromised state

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16
Q

What is the screening test for HIV

A

ELISA- HIV abs present from the serum

envelop Abs rise gradually and stay high in the end

Confirmed by western blot test

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17
Q

Treatment of choice for HIV

A

ziduvidin and lamivudin and indinavir- all together called Highly active anti retroviral therapy

given for lifetime

NNRTI can also be given

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18
Q

Treatment for children with AIDS

A

2 nucleoside inhibitors and 1 non nucleoside inhibitor

treatment is life long

no vaccine available

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19
Q

Common opportunistic infections in AIDS patients

A

Pneumocystic caini, kaposis sarcoma

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20
Q

Viral opportunistic infection in AIDS patients

A

Herp simplex, vzv, CMV

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21
Q

Fungal opportunistic infections in AIDS patients

A

Candida (thrush), crypto, meningitis and histplasma capsulatum

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22
Q

Protozoal opportunistic infections in AIDS patients

A

toxoplasmosis

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23
Q

Bacterial opportunistic infections in AIDS patients

A

tuberculosis

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24
Q

What does integration of viral genome to host cell DNA result in?

A

persistence infection

25
Q

Where does Hepatitis A virus (HAV) replicate?

A

cytoplasm

26
Q

Transmission of HAV?

A

fecal contamination of water

27
Q

Who are the reservoirs of HAV?

A

children most affected, humans are the only reservoir

28
Q

Pathogenesis of HAV

A

liver cells are infected causing cell necrosis- when infection clears, damage is repaired

all viral infections look the same

29
Q

Is HAV common in US?

A

YES- 50-75% of adults have abs

30
Q

Clinical features of HAV?

A

after two weeks of infection, fever, anorexia, nausea, comiting and jaundice- dark colored urine, pale feces

most cases resolve in 2-4 weeks

most infections are asymptomatic

31
Q

Vaccine for HAV?

A

YES- IgG provides life long immunity

32
Q

Treatment for HAV?

A

no antiviral drug- only prevention

33
Q

Prevention of HAV

A

proper sewage disposal, hand washing after defecation

34
Q

Other name for Hep B virus?

A

Dane particle/hepadna virus

35
Q

Describe look of HBV

A

enveloped DNA virus, partially double stranded

36
Q

What does the envelop of HBV virus contain?

A

HBsAG- protein called surface antigen

also known as Australian Ag

37
Q

What is the capsid protein of HBV known as?

A

core Ag - HBcAg

38
Q

Distribution of Hep B virus?

A

world wide distribution

most prevelant in South east Asia- incidence of hepatocellular carcinoma here

39
Q

Pathogenesis of Hep B

A

infects liver cells and causes necrosis

cytoxic T cells kill viral infected liver

40
Q

Is there a chronic carrier stage of Hep B?

A

YES- few DNA integrates to host cell DNA

41
Q

What does Ag-Ab complexes in HBV patients lead to?

A

arthralgia, arthritis, urticaria immune complex glomerulonephritis

42
Q

Percentage of HBV patients that become chronic carriers?

A

5%

43
Q

What will occur in carrier HBV patients?

A

high incidence of hepatocellular carcinoma

44
Q

What happens to patients who recover from HBV?

A

lifelong immunity

HBsAb is responsible for this!

45
Q

Clinical features of HBV patient

A

prevelant for 10-12 weeks- similar symptoms as in other hepatitis virus but more serious jaundice

chronic infection leads to cirrhosis of liver/cancer

46
Q

Treatment of chronic HBV infection

A

Alpha interferon and lamivudine (reverse transcriptase)

47
Q

Prevention of HBV infection

A

vaccine available- vaccine contains HBsAg alone

48
Q

What is available for passive immunity of HBV

A

Hyper immunoglobulin (anti serum) containing HBsAb

49
Q

Who is the reservoir for Hep C (HCV)?

A

Human

50
Q

Transmission of HCV?

A

blood transfussion, IV drug addicts

51
Q

Where is HCV common?

A

US

52
Q

Pathogenesis of HCV?

A

infects hepatocytes- strongly predisposes to hepatocellular carcinoma

alcoholism enhances risk leading to cirrhosis

53
Q

Clinical features of HCV

A

same as in HBV but milder

jaundice features will also be there

arthralgia, vasculitis and purpura occurs due to immune complexes

54
Q

How do you detect HCV?

A

lab diagnosis by ELISA

something that will show increase in liver enzymes

elevated transaminase

55
Q

Treatment of HCV?

A

alpha interferon and ribavirin

pegylated interferon- long acting

56
Q

Is there a vaccine for HCV?

A

NO- hyper immuno globulin

57
Q

What is the arbo virus?

A

arthropod born viruses

58
Q

What does Arbo virus cause?

A

eastern/western equine encephalitis

west nile virus

yellow fever

Microbiology (16 decks)

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