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MLT Semester #1 > 1050 Unit 6 > Flashcards

1050 Unit 6 Flashcards

1
Q

What are viruses?

A

Submicroscopic pathogens that can cause many human diseases

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2
Q

Describe structure of a virus

A
  • core of DNA or RNA packaged into protein coat or capsid
  • rely on host cell for replication and survival
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3
Q

What are basic steps of virus life cycle?

A

① attachment of the virus to receptor on host on surface
② penetration or entry of the virus in the host through endocytosis or other mechanisms
③degradation of the viral nucleic acid
④transcription to produce additional viral nucleic acid
⑤ translation of viral nucleic acid to produce Viral proteins
⑥ assembly of the viral components to produce intact virons
⑦ budding off the host, cell membrane or host cell lysis results in…
⑧ release of viral progeny

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4
Q

What provides the first line of defense against viral pathogens?

A

“Barrier”
- skin and mucous membrane

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5
Q

What are two non specific defenses against viruses?

A
  • Type I IFN
    -NK cells
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6
Q

What are virus infected cells stimulated to produce ?

A

IFN alpha and beta following recognition of viral RNA by foll-like receptors

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7
Q

What is the function of IFNs pertaining to viruses?

A

Inhibit viral replication by inducing transcription of several genes that code for proteins w/ antiviral activity

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8
Q

What do IFN alpha and beta enhance, explain?

A

Enhance activities of NK cells which binds to virus infected cells and release cytotoxic proteins such as perforin and granzymes

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9
Q

What happens when cytotoxic proteins are released? (Perforin and granzymes)

A
  • Cause cells to die and release virus
  • these are now accessible to antibody molecules
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10
Q

What occurs when innate defenses do not work?

A

Specific humoral and cell-mediated defenses
Are activated

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11
Q

What are virus specific antibodies produced by? What do they do?

A
  • B-cells
  • plasma cells
  • attack free virus particles in several ways
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12
Q

What plays a key role in preventing viral infection through neutralization? And how?

A

Antibodies → involves production of antibodies that are specific for a component of the virus that binds to a receptor on host cell membrane

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13
Q

What happens when neutralizing antibodies bind to virus?

A

They prevent if from attaching to and penetrating the host cell

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14
Q

How does Secretory IgA play an important role in neutralization?

A

They neutralize viruses in mucosal surfaces in the respiratory and digestive tract. (Usually entry way of pathogens)

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15
Q

What are the Roles of IgM and IgG?

A

① bind to viruses in the blood stream and inhibit dissemination of infection
② activate complement
-IgG → promote phagocytosis of virus through their ospinozing activity and promote destruction of viruses through antibody - dependent cellular cytotoxity
- lgM →inactivate viral particles by agglutinating them

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16
Q

When can antibodies not attack a virus?

A

When the virus has already penetrated host

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17
Q

What is required to eliminate intracellular virus?

A

Cell mediated immunity

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18
Q

What cells play a key role in elimination of intracellular virus?

A
  • Th1 cells
    -CTLS (cytotoxic T lymphocytes)
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19
Q

What does Th1 produce and what is the function of this component?

A

-IFN-g→ induces an anti- viral state in infected cells
-IL -2→ assists in development of effector CTLs

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20
Q

What do CD8 and CTLs do

A

Programmed to expand in number and attack the virus-infected cells

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21
Q

How does CD8 + CTLS recognize the viral infected host?

A
  • The T cell receptor (TLR) on CTL must bind to a viral antigen complexed with class I MHC on surface of infected cell
    -CD8 is a co-receptor here
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22
Q

When molecular interaction stimulate granules in the CTL, what is released and what is its role?

A

Perforin→ produces pores in the membrane of the infected host cell and granzymes enter the pores

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23
Q

What happens when granzymes enter the pores of an Infected host cell?

A

Activates apoptosis in the host cell, interrupting the viral replication cycle and resulting in release of assembled infectious virons

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24
Q

What can free virons can be bound by?

A

Antibodies

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25
Q

Describe the CTL response

A

-powerful
- involves series of cell divisions that can produce up to 50,000 times the original number of cells in a period of 1 to 3 weeks

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26
Q

What are the 5 ways that viruses can “escape” the host cell defense?

A

①mutations result in production of new viral
→ influenza viruses undergo frequent genetic changes
②viruses block action of immune response
→ HSV can bind C3b
③ suppression of the immune response
→CMV reduces MHC I expression
④ immune function altered
→ ebb stimulates polyclonal b-cell activation
⑤ latent state is established
→VZV remains latent in nerve cells

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27
Q

When viruses rapidly divide agents undergo genetic mutations, what do these mutations result in?

A
  • Production of new viral antigens which are not recognized by initial immune response to virus
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28
Q

How do CMV and HIV suppress adaptive immune system?

A

Reducing expression of class I MHC molecules on the surface of virus-infected cells. Making them recognized by CTLs

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29
Q

How does rubeola suppress adaptive immune response?

A

Cause decreased expression of class II MHC, resulting in reduced Th cell activity

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30
Q

Describe epstein-barr virus (EBV)

A
  • Cause polyclonal activation in B lymphocytes
  • inhibit immune responses by producing a protein that can suppress Th1 cells because of its similarity to IL-10
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31
Q

What does HIV suppress?

A

Function of CD4 Th cells

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32
Q

Describe serological testing of viral infection

A

-monitors course of infection
- detects past infection
- assessing immune status

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33
Q

Describe molecular testing in viral infection

A
  • Enhanced our ability to detect active infection
  • essential in guiding anti viral therapy
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34
Q

What does the presence of virus-specific IgM antibodies in patient serum indicate?

A

Current or recent Infection

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35
Q

What does the presence of viral-specific IgG antibodies in patient serum indicate?

A
  • Current or past infection
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36
Q

What does virus specific IgM antibody in newborn indicate?

A

Congenital infection because IgM is actively made during fatal life

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37
Q

What does virus-specific IgG antibodies in newborns indicate?

A

Nothing, IgG antibodies in infants serum are mainly maternal antibodies that have crossed the placenta

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38
Q

What is the family and type of hepatitis A?

A
  • RNA
    -picornaviridae
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39
Q

What is the family and type of hepatitis B?

A
  • DNA
    -hepadnaviridae
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40
Q

What is the family and type of hepatitis C?

A
  • RNA
  • flaviviridae
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41
Q

What is the family and type of hepatitis D?

A
  • RNA genus
    -deltavirus
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42
Q

What is the family and type of hepatitis E?

A
  • RNA
    -hepeviridae
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43
Q

How is hepatitis A transmitted?

A
  • Fecal-oral
  • direct contact w/ infected individual
    -blood transfusion (rare)
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44
Q

How is hepatitis B transmitted?

A
  • Perinatal (mom to baby)
  • sexual (semen and vaginal secretion)
  • parenteral ( blood contact, IV drugs, tattoo)
  • saliva
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45
Q

How is hepatitis C transmitted?

A
  • Parental
  • sexually
    -perinatal
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46
Q

How is hepatitis D transmitted?

A
  • Most parenteral
  • sexually
  • perinatal
    -HBV infection required
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47
Q

How is hepatitis E transmitted?

A
  • Fecal-oral
    -blood transfusion
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48
Q

Which class of hepatitis does not progress to a chronic stage?

A

Hepatitis A

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49
Q

What are complications of hepatitis A?

A

-low risk of fulminate
- liver disease

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50
Q

What are complications of hepatitis B?

A
  • 10%-90% develop chronic hepatitis with increased risk for liver cirrhosis and hepatocellular carcinoma
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51
Q

What are complications of hepatitis C?

A
  • 85% develop chronic infection with increased risk of cirrhosis, hepatocellular carcinoma or autoimmune manifestations
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52
Q

What are complications of hepatitis D?

A
  • Increased risk of developing fulminate hepatitis, cirrhosis, or hepatocellular carcinoma
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53
Q

What are complications of hepatitis E?

A
  • Fulminate liver failure in pregnant women
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54
Q

What are the markers for hepatitis A?

A

-IgM anti-HAV
- total anti-HAV
-HAV RNA

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55
Q

What are markers for hepatitis B?

A

-HBsAg
-HBeAg
-IgM anti-HBc
-total anti-HBc
- anti-HBe
-anti-HBs
-HBV DNA

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56
Q

What are the markers for hepatitis C?

A
  • Anti-HCV
    -HCV RNA
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57
Q

What are the markers for hepatitis D?

A

-IgM-anti-HDV
-IgG-anti-HDV
-HDV RNA

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58
Q

What are the markers for hepatitis E?

A

-IgM anti-HEV
-IgG anti-HEV
-HEV RNA

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59
Q

What does the IgM anti-HAV indicate?

A
  • Acute hepatitis A
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60
Q

What does total anti-HAV indicate?

A

Immunity to hepatitis A

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61
Q

What does theHAV RNA marker indicate?

A

Detection of HAV in clinical, food, or water samples

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62
Q

What does the HBsAg marker indicate?

A

_Active hepatitis B infection

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63
Q

What does the HbeAg marker indicate?

A

Active hepatitis B infection with high degree of infectivity

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64
Q

What does the IgM anti-HBc marker indicate?

A

Current or recent acute hepatitis B

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65
Q

What does the total anti-HBc marker indicate?

A

Current or past hepatitis B infection

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66
Q

What does the anti-HBe marker indicate?

A

Recovery from hepatitis B

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67
Q

What does the anti-HBs marker indicate?

A

Immunity to hepatitis B

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68
Q

What does the HBV DNA marker indicate?

A

-acute, atypical, or occult hepatitis B
-viral load made used to monitor effectiveness of therapy
- used to determine HCV genotype.

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69
Q

What does the anti-HCV marker indicate?

A

-current or past hepatitis C infection

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70
Q

What does the HCV RNA marker indicate?

A

-current hepatitis C infection
- viral load may be used to monitor effectiveness of therapy
-used to determine HCV genotype

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71
Q

What does the IgM- anti-HDV marker indicate?

A

Acute or chronic hepatitis D

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72
Q

What does the IgG- anti-HDV marker indicate?

A

Recovery from hepatitis D or chronic hepatitis D

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73
Q

What does the HDV RNA marker indicate?

A

Active HDV infection
-viral load may be used to monitor effectiveness of therapy

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74
Q

What does the IgM anti-HEV marker indicate?

A

Current hepatitis E infection

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75
Q

What does the IgG anti-HEV marker indicate?

A

Current or past hepatitis E infection

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76
Q

What does the HEV RNA marker indicate?

A

Current hepatitis E infection

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77
Q

What is the general meaning of hepatitis?

A

Inflammation of liver

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78
Q

What happens if hepatitis progresses?

A

Can lead to…
- liver enlargement and tenderness
- jaundice
- dark urine
-light feces
.

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79
Q

What is typical by found in the initial laboratory testing?

A
  • Elevations in bilimban and in liver enzymes
  • most notably alanine Aminotransferase (ALT)
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80
Q

Describe genotypes of hepatitis A

A

-two genotypes
- both can be detected with same serological assays

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81
Q

What is the incubation period for hepatitis A?

A
  • Average of 28 days
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82
Q

Describe symptoms of hepatitis A

A
  • Flu-like symptoms
  • children are asymptomatic
    -typically resolves itself in 2 months
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83
Q

Describe treatment of hepatitis A

A

Mainly supportive
- bed rest
- nutritional support
- medication for fever, nausea, and diaherra
- rare → hepatic necrosis and death (mainly in patients with other ailments of liver)

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84
Q

Describe HAV antigens

A
  • Shed in feces of infected individuals during incubation period and early acute stage
  • usually decline to low levels shortly after symptoms appear
  • not clinically useful indicator of disease
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85
Q

Describe testing of hepatitis A

A
  • Serological testing is critical for diagnosis
  • most commonly detected by EIAs and CLIAs
  • routinely diagnosed in symptomatic patients by demonstrating IgM-anti-HAV (declines in 6 months)
    -total HAV antibodies also detect IgM but predominately IgG and persists for life
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86
Q

What is the primary marker of hepatitis A in acute phase?

A

IgM anti-HAV but can cause false negatives results during early phase of infection

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87
Q

Describe molecular testing of hepatitis A

A

-most common format of these methods is reverse-transcriptase polymerase chain reaction RT-PCR
- can also be used to test food or water suspected of transmitting disease

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88
Q

How do you prevent infection in unimmunized that has been exposed to hepatitis A

A
  • Administer prophylactic of hepatitis A vaccine or injections of immune globulin
  • must be administered within 2 weeks of exposure
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89
Q

Describe genotypes of hepatitis E

A

-4 genotypes
- 1 and 2 are primarily associated with consumption of fecal matter in water
→ common in Africa, Asia, the Middle East, and Mexico
→ outbreaks are common after natural disasters
- 3 and 4 are primarily associated with consumption of infected pork
→ Europe, North America, china, Taiwan, and Japan
→ primary hosts are pigs, deer and wild boars or direct contact with infected animal
- have symptoms that make genotypes undistinguishable

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90
Q

Which hepatitis virus is “silent”?

A

Hepatitis E

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91
Q

What is the incubation period for hepatitis E?

A

2 to 10 weeks

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92
Q

What is the recovery period for hepatitis E?

A

4 to k weeks

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93
Q

What are severe consequences of hepatitis E?

A

_ Neurological syndromes
- renal injury
- pancreatitis
- hematological abnormalities

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94
Q

Describe chronic stage of hepatitis E

A

-HEV3 can result in chronic infection in immune compromised individuals
- can progress to liver fibrosis, cirrhosis, and liver failure

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95
Q

What measures are taken to prevent infection ot hepatitis E

A
  • Provision of clean drinking water
    -improvement of sanitation conditions
  • avoidance of undercooked meat, especially pork (HEV3)
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96
Q

Describe testing of hepatitis E

A
  • Diagnosis relies on to detect antibodies to the virus and molecular methods to detect HEV nucleiC acid
  • identified by sensitive EIAs that use recombinant and synthetic HEV antigens
  • rapid immunochromatographic assays have also been developed.
  • antibody test can detect all four genotypes
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97
Q

Acute infection of hepatitis E is indicated how?

A
  • Presence of IgM anti-HEV
  • remains elevated for 8 weeks
  • becomes undetectable at 32 weeks
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98
Q

When do HEV- specific IgG bodies peak?

A

About 4 weeks after symptoms develop and persist for several years

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99
Q

When is molecular testing for HEV RNA recommended for patients with hepatitis E?

A

-in immunecompromised person because they often yield a false negative

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100
Q

What is the gold standard for diagnosis of acute HEV infection?

A

Quantitation of HEV nucleic acid can be performed by qPCR

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101
Q

What testing is used to detect acute hepatitis E in a resource-limited settings?

A

-loop-mediated isothermal amplification assay (LAMP)
- can be performed on blood or stool samples
- no expensive equipment

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102
Q

When does HEV RNA become undetectable?

A

-blood → 3 weeks after symptom onset
-stool→ 5 weeks after symptom onset
-therefore, a negative result forHEV RNA does not exclude possibility of recent infection

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103
Q

What is the major cause of morbidity and mortality throughout the world?

A

Hepatitis B

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104
Q

Where is hepatitis B prevalent?

A
  • Far east
  • parts of Middle East
  • sub Saharan Africa
  • Amazon areas
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105
Q

What measures have been taken to prevent hepatitis B infection?

A
  • Screening for blood donors
    -treating plasma-derived products to inactivate hepatitis B
  • implementing affection infection control measure
  • immunizations
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106
Q

Describe the vaccine for hepatitis B

A
  • Consists of recombinant hepatitis B surface antigen (HBsAg) produced from genetically engineered beast or mammalian cells
  • can also be administered to those who have been exposed along with hepatitis B immune globulin (HBIG)
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107
Q

What is hepatitis B immune globulin (HBIG )?

A

-preparation derived from donor plasma with high concentrations of antibodies to HBV that provides temporary protection

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108
Q

What is the incubation period for hepatitis B?

A

30 to 180 days

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109
Q

Describe symptoms of hepatitis B

A

-90% of newborns are asymptomatic
-acute hepatitis symptoms observed in 10% in ages 1-5
- 1/3 and adults adolescents
- last several weeks to several months
- 1% develop fulminant liver disease with hepatic necrosis

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110
Q

When do most HBV infected people recover?

A

6 mouths and develop immunity

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111
Q

Describe chronic infection of hepatitis B

A

-virus persists in the body for 6 month or more
-occurs in majority of infected Infants
- 1/3 of infected children
- 10% of infected adults
- more likely to develop in people who cere immune compromised and who have HIV
-results in inflammation and damage to liver and makespatient at high risk (for developing cirrhosis or hepatocellular carcinoma

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112
Q

What is the treatment for a chronic infection of hepatitis B?

A
  • Antiviral drugs to reduce liver inflammation and the risk of developing liver complications
    -therapies consist of nucleoside analogues that inhibit the polymerase Enzyme needed for viral replication and IFN alpha (which enhances the immure response against the vines)
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113
Q

Describe genotypes for hepatitis B?

A

_8 genotypes
-A-H are named
- identified by nucleotide sequence differences in their genomes
- can be identified by same serological assays

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114
Q

Describe structure of intact HBV viron

A
  • 42 nm sphere
  • has nucleu capsid core surrounded by an outer envelope of lipoprotein
  • core contains circular partially stranded DNA
    → a DNA dependent DNA polymeraseenzyme
    → two proteins
    →→hepatitis is core antigen
    →→hepatitis Be antigen (HBeAg)
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115
Q

Describe the protein Found on the outer envelope of hepatitis B

A
  • Hepatitis B surface antigen (HBsAg)
  • produced in excess and is found in noninfectious spherical and tabular particles that lack viral DNA and circulate freely in the blood
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116
Q

How are serological markers used in reference to hepatitis b?

A
  • Differential diagnosis of HIV infection
  • monitoring course of infection in patients
  • assessing immunity to virus
  • screening blood productsfor infectivity
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117
Q

What is the first marker to appear in hepatitis B?

A

-HBsAg →protein on outer envelope of virus
-active infection
-detectable at 2-10 weeks after exposure
-levels peak at acute stage.
- serum becomes undetectable at 4 to 6 mouth after the onset of symptoms in acute infection
-remains elevated for 6 months or more in chronic infection

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118
Q

When will HBeAg appear in hepatitis B?

A
  • Protein in core of HBV
  • Appears shortly after HBsAg
  • disappears right before HBsAg
    -marker is present during periods of active replication of the virus and indicates a high degree of infectivity.
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119
Q

Why is the hepatitis B core antigen not detectable in serum?

A

The viral envelope masks it

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120
Q

Once host develops immune response, what marker/ antibody would appear first in hepatitis B

A

-IgM anti-HBc
- appears 1 to 2 weeks after ,HBsAg during acute infection and persists in high titer for 4 to 6 months, then gradually declines
-useful in detecting infection when HBsAg is undetectable
- used in addition to HBsAg for screening donor blood

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121
Q

Describe IgG antibodies to the core antigen in hepatitis B

A

-produced before lgM anti-HBc disappears and persists for a lifetime

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122
Q

When does anti-HBs appear in hepatitis B?-

A
  • Appears during recovery period of acute infection
  • a few weeks after HBsAg disappears
  • antibody persist for years and provide protection
  • not produced during chronic infection
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123
Q

Describe serological testing of hepatitis B

A
  • Most commonly detected by EIAs and CLIAs
  • typically automated
  • excellent specificity and sensitivity
  • false positives and false negatives can occur
  • positive results should be repeated with same sample and confirmed with assay such as HBsAg neutralization test or molecular test that detects HBV DNA
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124
Q

Describe molecular testing of hepatitis B

A
  • Detect HBV DNA in serum or plasma
  • based on target amplification by traditional or qPCR or branched DNA signal amplification
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125
Q

When can HBV DNA be detected in serum?

A
  • 21 days before HBsAg
  • can be used to detect early acute infection
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126
Q

Besides detecting early infection, what else is HBV DNA used for?

A
  • Evaluate effectiveness of antiviral therapy in patients w/ chronic hepatitis B
  • success til treatment is indicated by a 1-log(v10) reduction in HBV DNA levels by 6 months
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127
Q

What does hepatitis D consist of?

A
  • Circular RNA genome and a single structural protein called hepatitis delta antigen within its core
  • surrounded by viral envelope that is of HBV origin and contains the HBsAg
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128
Q

Describe genotypes of hepatitis D

A

-3 genotypes
-1 is most common (world wide)
- 2 is in Japan and Taiwan
-3 South America

129
Q

Where is hepatitis D highly prevalent?

A

Mediterranean Europe, Middle East, amazon basin, central Africa and parts of Asia

130
Q

What are two ways a hepatitis D infection can occurs

A

①HDV transmitted simultaneously as a co-infection with HBV
② can be contracted as a superinfection of individuals who are already chronic HIV carriers

131
Q

What do 70% of people with a superinfection develop ?

A

_ Develop chronic liver disease with accelerated progression to cirrhosis and liver failure

132
Q

Describe treatment of a chronic infection of hepatitis D

A

_ Combination of IFN alpha and antiviral drugs

133
Q

Describe GENERAL testing for hepatitis D

A

-testing for HDV should be performed in all patients HBsAg positive
- involves detection of HDV antibodies or HDV RNA
-antibodies detected by immunoassays employing hepatitis D antigen

134
Q

Describe presence of IgM anti-HDV

A

-appearance may be delayed
-may persist for only short period of time
- may be missed
- can persist in chronic infection

135
Q

Describe serological testing in hepatitis D

A

-used to help distinguish HBV and HDV co-infections from HBV and HDV superinfections.
- co-infection→positive for IgM anti-HBC
- superinfections → positive for IgG anti-HBc

136
Q

Describe molecular testing for hepatitis D

A
  • Detect HDV RNA (present in all hepatitis D)
    → routinely used to confirm a positive HDV antibody screening
    → serum HDV RNA is performed by sensitive real time PCR (RT-PCR) assays
  • assays also provide quantitative results that can be used to monitor the response of patients to antiviral therapy
137
Q

What is the most common blood borne infection in the United States?

A

Hepatitis C

138
Q

What is the leading cause of chronic liver infection In the U.S.?

A

Hepatitis C

139
Q

What are some characteristics of HCV?

A
  • Enveloped
  • single stranded
140
Q

Describe genotypes of hepatitis C

A

-7 genotypes
-1-7 names
-numerous subtypes for each
-1 most common
-1-3 predominant in North America, Europe and Japan
- 3-6 south and Southeast Asia
-4,5, and 7 parts of Africa
-important to know what typeto determine most effective treatment

141
Q

Why is it difficult to design a vaccine for hepatitis C?

A

-the variability of HCV
- ability to undergo rapid mutations within host

142
Q

What is the incubation period of hepatitis C?

A

7 weeks (2 weeks to 6 month range

143
Q

Describe symptoms of hepatitis C

A
  • Symptoms of acute hepatitis
  • 80% asymptomatic which leads to chronic infection
    -70% of patients develop chronic infection
  • 50% of these individuals develop cirrhosis (occurs slowly over 25-30 years )
  • increased risk of hepatocellular carcinoma
144
Q

What may develop when a patient has a chronic infection of hepatitis C

A
  • Cirrhosis
  • hepatocellular carcinoma
  • glomerulonephritis
    -vasculitis
  • other autoimmune manifestations
  • neuropathy
    -ophthalmological symptoms
  • dermatological symptoms
145
Q

Describe treatment of of hepatitis C

A
  • Clearance may occur or spontaneously
  • may require antiviral drugs
  • standard treatment involve A combination of pegylated IFN alpha and ribavirin
    →this treatment most success in genotype 2 and 3
    → was numerous side effects
  • direct-acting antiviral drugs (DAAs) and host-targeted agents (HTA) that inhibit specific steps of viral replication cycle
146
Q

Describe serological testing of hepatitis C

A

-anti-HCV IgG is most commonly detected by sensitive EIAs or CLIAs that use recombinant and synthetic antigens
- antigens developed from conserved domains of capsid core protein and nonstructural proteins NS3, NS4, and NS5
-rapid immunoblot assay can be used for POCT
- positive results must be confirmed
→ CDC recommends nucleic acid test for HCV RNA confirmation
→→ if NAT is non reactive this suggests past HCV infection or false positive test

147
Q

When do HCV antibodies become detectable?

A

8-10 weeks
Can remain positive for a lifetime

148
Q

What could cause a false positive in hepatitis C testing?

A
  • Cross reactivity in personswith other viral infections or autoimmune disorder
  • to distinguish between a true positive and a false positive, HCV antibody testing can be repeated with different assays from initial tests.
149
Q

Describe molecular testing of qualitative assays for hepatitis C

A
  • Assays for HCV RNA can be qualitative or quantitative
  • qualitative distinguish between presence or absence of HCV RNA in a clinical sample
    → used to confirm infection in HCV antibody positive patients
    → detect -infectionin antibody patients
    → screen blood and organ donors
    → detect perinatal infections
  • qualitative RT-PCR and transcription mediated amplification (TMA) are available
    → become positive within 1-3 weeks after infection
150
Q

Describe molecular testing of quantitative assays for hepatitis C

A
  • Performed by RT-PCR, qPCR, or bDNA amplification
  • used to monitor the amount of HCV RNA or the “viral load” before, during, and after antiviral therapy
    → goal is to achieve a sustained virological response (SVR)
    →→ patient test negative continuously for 12 or 24 weeks after therapy
151
Q

Describe genotyping testing in hepatitis C

A

-to determine genotype and subset
- performed by PCR amplification and sequencing of the target gene
- reference method because it provides precise information regarding genomic variability of virus in patients during course of disease

152
Q

Describe structure of herpes virus

A
  • Large complex DNA viruses that are surrounded by a protein capsid, an amorphous tegument, and outer envelope
153
Q

What are the 8 types of herpes?

A

①HSV-1
②HSV-2
③VZV
④EBV
⑤CMV
⑥HHV-6
⑦HHV-7
⑧HHV-8

154
Q

What are some diseases caused de EBV

A

-mononucleosis (IM)
-lymphoproliferative disorders
- several malignancies

155
Q

How can EBV be transmitted?

A
  • Mostly through intimate contact with salivary secretion
  • blood transfusion
  • bone marrow and organ transplants
  • sexual contact
  • perinatal exposure
156
Q

Describe EBV infection rate

A

-in poor sanitation, lower socioeconomic groups → early childhood
- industrialize nation wl higher hygiene standards → adolescents or adults
- 100 % of population has had it by .age 40

157
Q

What are the steps in an Initial infection of EBV?

A

‘① occurs.in orophanynx where the virus infects epithelial cells and B lymphocytes
② EBV binds to beta1 interns on surface of epithelial cells, which take up the virus by endocytosis
③ inside epithelial cells, EBV enters a lytic cycle until acute infection is resolved
④ virons spread to adjacent structures, including the salivary glands and tonsils
⑤EBV infects B lymphocytes and spread through lymphoreticular system
⑥EBV enters B cells by binding to surface CD21
⑦ virus infected B cells become polycionally activated, proliferating and secreting antibodies
→EBV - specific antibodies, heterophile antibodies and autoantibodies

158
Q

What are characteristics of the lytic cycle of EBV

A

_ Rival replication
- lysis of host cells
- and release of infections viron

159
Q

What cells keep the initial infection of EBV in check?

A
  • NK cells
  • specific CTLs
160
Q

Describe latent state of EBV

A
  • EBV can persist in the body indefinitely in small percentage of memory bars
    -EBV nucleiC acid exists as episomal DNA outside of chromosomes in this case viral replication does not occur
161
Q

What does periodic reactivation of EBV results in?

A
  • Re-entry of the virus into the lytic cycle, with viral shedding into saliva and genital secretions
162
Q

Describe antigens that are in the early stages of EBV

A
  • Produced during the initial stages of viral replication
    -known as early antigens
  • these antigens are further classified into two groups
    Based on location
    →EA-D: has diffuse distribution in nucleus and cytoplasm
    →EA-R: restricted to cytoplasm only
163
Q

Describe antigens in late stage of EBV

A

_ - Appear during the period of the lytic cycle following viral DNA synthesis
- they include viral capsid antigens (VCAs) in proton capsid and membrane antigens in envelope

164
Q

What antigens are present in the latent stage of EBV

A

-EBV nuclear antigens
→EBNA-1 through EBNA-6
-latent membrane proteins
→LMP-1, LMP-2A, LMP-2B

165
Q

Describe symptoms in EBV

A

-infants and young children are generally asymptomatic or mild
- primary infection in adults and adolescents commonly results in IM
→ more than half of patients with IM with three classic symptoms:sever, lymphadenopathy and sore throat (last 2 to 4 weeks)
- fatigue, myalgias, and need for sleep persists for months

166
Q

What are characteristics of laboratory findings in patient with IM?

A
  • Absolute lymphocytosis of greater than 50% of the total leukaustes and atleast 20% atypical lymphocytes
  • a typical lymphocytes are predominantly activated cytotoxic T calls that are responding to the viral infection
167
Q

What is a heterophile antibody

A
  • Antibody capable of reacting with similar antigens from two or more unrelated species
    -IM association →IgM antibodies are produced because polyclonal B cell activation and capable of reacting with horse RBC, sheep RBC, and bovine RBC
  • produced in 40% of patient with IM in the first week
    -by 3rd week, 80 to 90% of patients
  • disappear by 3rd month after onset of symptoms
168
Q

Describe testing for ,detection of heterophile antibodies

A

-monospot→rapid slide agglutination method
→ serum premixed with guinea pig ,kidney antigen still capable of agglutinating horse RBC
→ No longer used
- rapid agglutination tests or immunochromeographic assess using purified bovine RBC extract as antigen

169
Q

What causes false positives testing for IM?

A
  • Lymphoma
  • viral hepatitis
    -malaria
  • autoimmune disease
  • error in interpretation
170
Q

What can help to diagnose IM when patients test negative for heterophile antigens?

A

-testing for EBV specific antibodies
- by indirect immunofluorence assays (IFAs)
- using EBV- infected cans, blot techniques, encyme-linked immune sorbet assay (ELISA) or CLIA using recombinant or synthetic EBV proteins or flow cytometric microbead immunoassays
- all have high sensitivity but IFAhas the higher level of specificity (gold standard of serological methods)

171
Q

Describe markers found in IM

A
  • Most useful →IgM anti-VCA for acute infection
    → appears at onset and disappears by 3 months
    -IgG anti-VCA
    → present at onset of symptoms but persist for life
    → indicates past infection
    -EA-D antibodies present in acute infection
  • positive for anti-EA-D and IgM anti-VCA and absence of anti-EBNA indicates primary acute infection
172
Q

Describe chronic active EBV infection

A
  • Severe, life threatening symptoms rAssociated with IM
  • symptoms persist or recur for 6 or more months
    -EBV can integrate its DNA into the genome of cells it infects and transform them into cancer cells
  • can cause lymphoproliferative disorders in the immunOcompromised
    → results from inability of immunosuppressed patients to control EBV infection, leading to massive polyclonal expansion of EBV infected B cells and illness with high mortality rate
173
Q

How can EBV malignancy be diagnosed?

A
  • Serological method→ test for EBV antibodies
    -molecular method → to detect EBV DNA
174
Q

Describe molecular testing in EBV

A
  • May be more reliable than serological methods in immunocomprosmised patients
  • quantitative PCR is useful in monitoring viral load in transplant patients, high EBV viral load indicates need to decrease immunosuppressive treatment and administer antiviral therapy
175
Q

How is CMV transmitted?

A
  • Close, prolonged contact with infections body secretions
  • solid organ transplant
  • perinatal exposure
  • isolated in saliva, urine, stool, vaginal and cervical secretions, semen, breast milk, and blood
176
Q

Describe an acute infection of CMV

A
  • Asymptomatic in healthy individuals
  • some people experience IM- like symptoms (fatigue, myalgia and fever)
177
Q

Describe more severe CMV disease

A
  • Immunocompromised patients
  • mostly involves gastrointestinal tract, CNS, and hematological abnormalities
178
Q

What cells does the CMV virus persist in a latent state?

A
  • Monocytes
  • dendritic cells
  • myeloid progenitor cells
  • peripheral blood leukocytes
  • may be reactivated later in life.
179
Q

What are clinical consequences for immunocompromised patients infected with CMV

A
  • More serious, especially inorgan-transplant recipients and patients with HIV/AIDS
  • infections resulting from reactivation of CMV in recipient or transmission from donor
180
Q

CMV infections of a previously unexposed recipient is associated with what? Explain it.

A
  • With increased risk for allograft failure or graft-versus-host disease (GVHD)
  • poses risk for variety of syndromes such as fever and leukemia, hepatitis, pneumonia, GI complications, CNS dysfunction and retinitis
181
Q

CMV remains a major opportunistic pathogen in what kind of patients

A
  • With low CD4 t-cell counts
182
Q

What are ways to prevent or treat CMV?

A
  • Serological testingperformed to identify CMV positive donors
    -is CMV infection has been established in a transplant patient, immunosuppressive treatment shoudbe reduced to lowest dose possible
    -variety of antiviral drugs used to treat CMV infection
183
Q

What is the most common cause of congenital infections?

A

CMV

184
Q

What virus has significantly higher risks in pregnancy?

A
  • CMV
  • transmission can occur through placenta, by passage of infected birth canal or by postnatal contact w/ breast milk
185
Q

CMV Symptoms of infant?

A
  • Platelet dysfunction
  • CNS involvement
  • 10% of asymptomatic infants develop sensorineural hearing loss
186
Q

Describe testing for immunocompromised and neonates for CMV

A
  • Assays for direct detection of virus such as viral culture, identification of CMV antigens and molecular tests forCMV DNA are necessary to detect current CMV infection
187
Q

What type of testing is best for detecting past exposures to CMV

A

Serological

188
Q

Describe isolation of virus in culture of CMV

A
  • Isolation of virus in culture is traditional method of direct viral detection
    → human fibroblast cell lines are inoculated w/ CMV- infected specimens, most commonly urine, respiratory secretionsor anti coagulant whole blood
    → presence of virus is indicated by characteristic cytopathic effects (CPEs) that produce enlarged rounded refractile cells
    → limited because CPEs do not appear for a few days to several weeks
  • centrifugation enhanced method
    → reduced time of detection
    → infected cells grown on coverslips sin shell vial
    → incubated w/ fluorescent-labeled monoclonal antibodies
189
Q

What are testing methods of direct identification of CMV serological testing?

A
  • Isolation of virus in culture
  • CMV antigenemia assay
190
Q

Describe CMV antigenemia testing

A

-uses immunocytochemical or immunofluroscent staining to detect CMV protein, pp65, in infected leukocytes from peripheral blood or cerebral spinal fluid
- can be completed in 2-4 hours

191
Q

Describe molecular testing in CMV

A
  • Detect CMV DNA or mRNA
    -RT-PCR most widely used method because sensitive, simple to perform, and can provide quantitative results
  • identification of CMV/ CMV DNA in amniotic fluid at 20th week is gold standard for confirming fetal infection
  • quantitative PCR is used to monitor effectiveness of antiviral treatment in immunocompromised host
192
Q

How do you detect past and possible future (risks) infections of CMV

A
  • Serological → EIAs
  • assay for CMV IgG are most useful at documenting past infection and determine if individual is at higher risk for future infections
  • low-avidity IgG antibodies indicate recent infection
  • high avidity IgG antibodies past exposure
193
Q

Why are assays for IgM CMV limited?

A

-potential for false-negative results in newborn and immunocompromised
- potential for false positives in presence of rheumatoid factor
- cannot indicate primary infection because it persists up to 18 months

194
Q

What two distinct diseases are caused by VZV

A
  • Chick pox
  • shingles (herpes zoster)
195
Q

How is VZV transmitted?

A
  • Mostly through inhalation of infected respiratory secretions and/or aerosols from skin lesions
    Transplacental transmission to fetus can occur
196
Q

Describe varicella

A
  • Primary infection with VZV
  • highly contagious illness characterized by a blister-like rash with severe itching and fever
  • majority in childhood.
197
Q

What are symptoms of varicella

A
  • vesicular lessons appear on face and trunk and spread to other areas
  • usually mild and self-limiting in healthy children
  • may produce secondary bacterial infection caused by scratching of lesions
  • primary infections tend to be more severe
    -immunocompromised →extensive slanrash, neurological conditions,pneumonia, hepatitis, and nephritis
198
Q

Describe primary infection of VZV

A

-thought to travel from San leasions and blood to sensory neurons where it deposits DNA and lifelong latent state established.

199
Q

Describe shingles

A

-Reactivation resulting in eruption of painful vesicular rash
- rash can persist for week to months
→ more severe in immunocompromised, elderly, and pregnant women
- complications → postnerpatic neuralgia (Extremely painful), herpes ophthalmicus ( causes blindness), pneumonia

200
Q

Describe testing of varicella and herpes zoster

A

-usually based on identify vesicular lesions
- definitive diagnosis based on identifying VZV or its products in skin lesions, vesicular fluids or tissue
- microscopic detection of Tzanck cells (giant, multi-nucleated) in stained smears allow for rapid identification of virus. No longer used
→ can not distinguish between VZV and HSV
-qPCR for VZV DNA is method of choice!
→ also useful in monitoring response in immunocompromised patient to antiviral drugs

201
Q

What can PCR be tested on to detect VZV ?

A
  • Vesicular fluid. Scabs, sweat, San swabs, throat swabs, cerospinal fluid, blood, saliva, and tissues from biopsies/autopsies
202
Q

Why is testing for VZV IgM is not performed routinely?

A

_ May not be .detectable until convalescent stage
- cannot distinguish between primary and reactivated infection
- They may not be free of IgG antibodies when serum is processed for testing

203
Q

How is immunity determined for VZV

A
  • Serology most useful
  • most detect Total VZV antibody which consists primarily of IgG
  • most sensitive and reliable → fluorescent test called fluorescent antibody to membrane antigen (FAMA) that detects antibody to the envelope glycoproteins of the virus
    → requires live virus infected cells and not suitable for large-scale routine testing
  • most common → ELISA (no vival culture needed)
    → false positive can occur because can detect low levers of centibilly that do not confer long ‘ term protection
203
Q

How is immunity determined for VZV

A
  • Serology most useful
  • most detect Total VZV antibody which consists primarily of IgG
  • most sensitive and reliable → fluorescent test called fluorescent antibody to membrane antigen (FAMA) that detects antibody to the envelope glycoproteins of the virus
    → requires live virus infected cells and not suitable for large-scale routine testing
  • most common → ELISA (no vival culture needed)
    → false positive can occur because can detect low levers of centibilly that do not confer long term protection to variety
204
Q

What are characteristics of rubella virus?

A
  • Single-stranded enveloped RNA
  • genus → rubivirus
  • family → togavividae
    -replicates in upper respiratory tract and cervical lymph nodes
205
Q

How is rubella transmitted?

A
  • Respiratory droplets
  • transplacental
206
Q

What virus causes German measles?

A
  • Rubella virus
  • mainly in children but can occur in Unvaccinated adults
207
Q

What is the incubation period for rubella virus?

A

12 to 23 days

208
Q

What are symptoms of rubella vines?

A

-erythematous
-maculopopular rash (resolves in 3 to 5 days)
- low grade fever
- malaise
- swollen glands
-upper respiratory infection
- 50% of infected individuals are asymptomatic

209
Q

Describe treatment of rubella virus

A
  • Usually resolves itself with no complication
  • no specific treatment is available
210
Q

Describe the effect rubella virus has on pregnant

A

-Severe consequences including miscarriage, still birth and congenital rubella syndrome (CRS)
- chance of severe consequences Occurring increases when infection occurs during first trimester
- vaccines are availa to children and infants that will prevent future infections in pregnant women

211
Q

What can occur when an infant is born with CRS?

A
  • May have several abnormalities
  • deafness
  • eye defects → cataracts and glaucoma
  • cardiac abnormalities
  • mental retardation
  • liver and spleen damage
    -motor disability
212
Q

Describe general testing of rubella virus

A
  • Important in German measles because symptoms mimic other viral infection
  • culture of virus
  • demonstration of viral RNA
  • detection of virus-specific antibodies
  • viral nucleic acid can be identified by RT-PCR (MOST COMMON)
    -viral proteins can he detected by IFA or EIA
213
Q

Describe molecular methods in testing for rubella virus

A

-RT-PCR most widely used
- can be used to detect rubella RNA in variety Of clinical samples.

214
Q

Describe serological testing of rubella vines

A
  • Most common means of confirming diagnosis
    -most common today → ELISA
    → used to detect IgM rubella antibodies.
    -used to screen for immunity to rubella (IgG)
  • low avidity antibodies indicate recent infection
215
Q

What can simutaneously detect mumps, measles, varicella and rubella

A
  • Automated chemo luminescence assays
    -multiplex bead immunoassays
216
Q

How is primary rubella infection indicated?

A
  • Either by presence of rubella specific lgM antibodies
    -Or by a four fold or greater rise in rubella - specific IgG antibody titer
  • time of collection is
    Important because IgM antibodies don’t appear until 5 days after onset of rash and IgG may not be detectable for 8 days
217
Q

Explain reasonings for false negative and false positive in rubella

A

False negative → if sample is obtained to early
False positive → IgM antibodies can persist
In low levels for years
False positive → parvovirus infection, enterovirus infection, heterophil antibodies, or rheumatoid factor.

218
Q

Describe characteristics of rubeola vines

A
  • Single stranded RNA vines
  • genus → morbillivirus
  • family → paramyxovividae
  • highly contagious
219
Q

How is rubeola virus transmitted?

A
  • Direct contact with aerosolized droplets from respirators secretions of infected individual
220
Q

What occurs after the initial infection of rubeola virus of epithelial cells of upper respiratory tract?

A
  • Rubeola virus is disseminated through the blood To multiple sites in the body such as the San, lymph nodes and liver
221
Q

What disease does the rubeola virus cause?

A

Measles

222
Q

What is the incubation period for rubeola virus?

A

10 - 12 days

223
Q

What are symptoms of the rubeola virus?

A

During prodromal period
- Fever
- cough
- coryza (runny nose)
- conjunctivitis

After prodromal period
-Koplik spots appear on inner cheek or lips
→ white gray lesions against red background
→ rash after 14 days
-erythematous
- maculopapular eruption beginning on hairline

224
Q

What complications can result from rubeola?

A
  • Diarrhea
  • otitis media
  • croup
    -bronchitis
  • pneumonia
    -encephalitis
  • subacute sclerosing panencephalitis (SSPE)
225
Q

How does rubeola affect pregnancy?

A
  • Higher riskof premature labor
  • spontaneous abortion
  • low birth weight
226
Q

Describe serological testing fo rubeola

A

-most practical and reliable in confirming diagnosis
- indicated by presences of rubeola-specific IgM antibodies or four-fold rise in rubeola specific IgG antibodies
-IgM capture ELISA method
-ELISA also use for detection of IgG antibodies
→ appear a few weeks after IgM appearance
→persist for life
→ indicates immunity to measles

227
Q

What is associated with extremely high titer of rubeola antibodies?

A

SSPE

228
Q

What could cause a false-negative result for rubeola î

A

Samples collected before 72 hours

229
Q

Describe molecular methods used for rubeola?

A
  • Detect rubeola RNA
  • used in situation when serological testing is inconclusive
  • also used to genotype
    -RT-PCR
230
Q

What are characteristics of the mumps virus?

A
  • single stranded RNA virus
  • genus → rubulavirus
    -family→ paramyxovividae
231
Q

Explain transmission of mumps

A
  • respiratory droplets, saliva, and fomites and replicates in nasophangux and lymph nodes
232
Q

What are formites?

A

Inanimate object/substances that can transmit infectious organisms

233
Q

What is the incesation period of the mumps i

A

14 - 18 days

234
Q

Where does the mumps virus spread?

A

-from blood to:
→ meninges of brain
→salivary glands
→ pancreas
→ testes
→ ovaries

235
Q

What are symptoms of the mumps?

A

-inflammations of parotid gland

236
Q

What is treatment for mumps.

A
  • Only medications that alleviate symptoms
  • resolves its self in 7-10 days
237
Q

Describe diagnosis of mumps

A
  • If parotitis is present, No laboratory testing required for diagnosis
238
Q

Describe molecular methods of testing for mumps

A

RT-PCR is recommended for confirmationn

239
Q

Describe serological testing for mumps

A
  • Simple means of confirming diagnosis
  • limitations
    →EIAs and IFAs→ only measure IgG mumps virus antibodies
  • ELISA most commonly used
    → solid-phase IgM capture assays
240
Q

What are characteristics of HTLV-1 and HTLV-2?

A
  • Both have 3 structural genes
    -infect T cells
  • viruses have RNA as their nucleic acid and reverse
    Transcriptase
241
Q

What do HTLVs infect?

A

-the prefer to infect CD4+ T lymphocytes
-CD8+ T cells
- dendritic cells
- macrophagesr

242
Q

What are the 3 structural genes in HTLVs?

A
  • Gag → which code for viral core proteins
    -pol→ codes for rival enzymes
  • env→ encodes proteins in the viral envelope
243
Q

Where is the px region found and what does it do?

A

-HTLVs
- encodes several regulatory proteins,Tax and Rex

244
Q

What is the function of CTLs r

A
  • Effectively, control proliferation or virus-infected cells
245
Q

What does a HTLV-1 infection of CD4+ T cells do?

A
  • Can increase production of inflammatory Cytokines
  • impair production of Th1 cytokines necessary for cell-mediated immunity
    -induce differentiation of T regulatory cells
246
Q

How do Treg cells in HTLVs facilitate viral persistence?

A

Suppressing host’s immune response to the virus

247
Q

How are HTLVs transmitted?

A
  • Blood borne → transfusing or IV drugs
  • sexual contact
  • mother to child→ breast feeding
248
Q

Where are HTLVs prevalent?

A

-HTLV-1 → Japan, Caribbean, south and Central Africa, Middle East, Romania, South America and papua new guinea.
-HTLV-2→ native Indian populations in Americas, a few Pygmy tribes in central Africa and IV abusers in North America and Europe

249
Q

What disease does HTLV-1 cause?

A
  • Adult t-cell leukemia/ lymphoma (ATLL)
    → acute, t-cell non-Hodgkin lymphoma, chronic, and, smoldering
    → characterized by monoclonal proliferation of mature T cells that express the surface markers CD3,CD4, and CD25
  • HTLV- associated myelopathy/tropical spastic para paraparesis ‘(HAM/TSP)
250
Q

What are the symptoms of HAM/TSP?

A
  • Leg stiffness
  • back pain
    -urinary incontinence
  • inflammation of joints, muscle
251
Q

Symptoms for HTLV-2

A

Most people are asymptomatic

252
Q

Describe serological testing for the HTLVs

A

-tests used to detect HTLVs antibodies
-EIA, CLIA, and IFA
-particle agglutination test for confirmation
→ western blot assays most commonly used

253
Q

Describe serological testing

A
  • IgM (+)→ current or recent infection
    -IgG(+) → past infection
254
Q

Describe molecular testing

A
  • Detect active infection
    -Quantitative tests - guide antiviral therapy
255
Q

What is the cause for inflammation of the liver in hepatitis?

A
  • Radiation
  • chemical toxins
  • cirrhosis
  • drugs
  • hypothermia
  • bacteria
  • fungi
    -parasites
256
Q

Describe hepatitis A vaccine

A

Formalin- inactivated HAV

257
Q

Describe “core window”

A

Period when neither hepatitis B surface antigen nor HBeAg can be detected in the serum of patient, only the anti-HBc.

258
Q

Describe rubeola diagnosis

A
  • Based on clinical presentation of confirmed by serology testing.
259
Q

Where is toxoplasmosis vims found?

A

-feces of house cats and rodents

260
Q

How is toxoplasmosis transmitted

A
  • ingestion of oocytes (fecal contaminated of meat, raw milk
  • transplacental
261
Q

How to prevent toxoplasmosis?

A
  • Avoid touching mucous membranes of mouth and eyes while handling raw meat
  • wash hands after touching raw meat
  • keep flies and cockroaches away from soul
  • avoid direct contact when handing cat item box
262
Q

What are symptoms of toxoplasmosis

A
  • Usually asymptomatic
    -if have symptoms, similar to mono
263
Q

Describe treatments for toxoplasmosis

A
  • None, spontaneous recovery
264
Q

Describe congenital infection of toxoplasmosis

A

-most concern
-result in CNS malfunction and mortality of neonate
-75% have no symptoms at birth, disease is dormat,
And only discovered when neurological problems arise (blindness)

265
Q

Describe testing for toxoplasmosis

A
  • EIA
266
Q

Describe torch testing

A
  • Consist of antibodies to four organisms that cause congenital infectious transmitted from mother to fetus
    →toxoplasmosis gondii
  • rubella
    -CMV
    -HSV
    -o is for others → syphilis, hepatiTIS B, coxsackle virus,EBV,VZV, human parvoVIrus
267
Q

Adenovirus is…

A

Respirating

268
Q

Arbovirus is…

A

From SKin-mosquitos, ticks

269
Q

Rotovirus is..

A

Garstointestinal (fecal oral route)

270
Q

Describe HIV-1

A
  • Cause of most HIV infections worldwide
  • four groups: M, O, N, P
  • nine subtypes in group M→A-K
271
Q

How can HIV be transmitted?

A
  • Sexual contact → most common
    -blood
  • perinatal
272
Q

What are characteristics of HIV ?

A

-retro virus
- contains a copies of ssRNA
-reverse transcriptase transcribes the viral RNA into DNA
- surrounded my a protein coat (capsid)
- outer envelope of glycoproteins embedded in a lipid

273
Q

What is the marker for docking glycoprotein?

A

gp120

274
Q

What is the marker for transmembrane glycoprotein?

A

gp41

275
Q

What is the marker for matrix protein?

A

P 17

276
Q

What is the marker for the capsid

A

p24

277
Q

What is the protein product of the gag gene?

A

-p17
-p24
-p9
-p6

278
Q

What are the protein product for the env gene?

A

-gp120
-gp41

279
Q

What are the protein products of pol?

A

-p66
-p51
-p31
-p10

280
Q

What is the protein product for tat gene?

A

p14

281
Q

What is the protein product of the rev gene?

A

p19

282
Q

What is the protein product of nef gene?

A

p27

283
Q

What is protein product of the vpr gene?

A

p15

284
Q

What is the protein product of the vif gene?

A

p23

285
Q

W what is the main target for replication of HIV?

A

CD4 Th

286
Q

Describe steps of replication of HIV

A

① attachment of HIV to host cell to CD4 Th
② coreceptor(chemokines) required → promote fusion of HIV envelope with plasma cell membrane
③ reverse transcriptase converts viral RNA into complementary DNA (cDNA)
④cDNA is integrated into the host genome as a provirus
⑤ viral DNA is transcribed into viral RNA and proteins
⑥viral particles are assembled
⑦intact virons bud out of host cell membrane

287
Q

What other cells can HIV infect?

A
  • Langerhan cells
  • monocytes
  • macrophages
  • microglial brain cells
288
Q

Describe strains of HIV viruses

A

-infect t-cells→ t-tropic or x4
- infect t-cells and macrophages → m-tropic or R5

289
Q

What is importance of CXCR4 chemokines receptor in HIV replication?

A

Required for HIV to enter T lymphocytes

290
Q

W what is the importance of the CCR5 chemokines receptors of HIV replication?

A

Required for entry of HIV into macrophages

291
Q

What are innate defenses for HIV

A
  • Nk cells mediate cytolysis of HIV infected cells
  • dendretic cElls stimulate release of cytolanos that have antiviral effects
292
Q

L how can the initial viral replication of HIV in laboratory?

A
  • Presence of increased levels of p24 antigen and viral RNA in hosts’ bloodstream
293
Q

Describe the humoral antibody production immune response for HIV

A
  • Antibodies are detected by 6 weeks after infection
  • antibodies produced later may prevent HIV from infecting host cells and participate in ADCC
294
Q

Describe cell-mediated immunity immune response of HIV

A
  • T-cells produce cytokines with antiviral activity
    -CTLs destroy HIV - infected host cells
295
Q

What are symptoms of HIV

A
  • Decline in immune system
296
Q

Describe early stage of HIV….

A
  • Rapid burst of viral replication before the development of hiv-specific immune response
  • begins to disseminate to the lymphoid organs
    –flu-like symptoms or IM- like symptoms
  • some develop neurological problems
  • many are asymptomatic
297
Q

) Describe latency stage of HIV

A
  • Decrease in viremia as vines is cleared through circulation
    -symptoms are subtle or absent
    -CD4 will remain stable and then sudden rapid of decline
298
Q

Describe final stage of HIV

A
  • AIDS
  • immunosuppression and low CD4 T cell count
    -resurgence of viremia
  • life threatening infections and malignancies
  • median of 10 years to have full blown AIDS
299
Q

What are symptoms in infants that have HIV

A
  • Failure to thrive
  • persistent oral candidiasis
  • hepatosplenomegaly
    -lymphadenopathy
  • recurrent diaherra
  • recurrent bacterial infections
300
Q

HIV positive patients are broken down into what 5 categories

A

-0 → early HIV infection, positive lab result followed by negative HIV results within 6 months
-1-3 → based on peripheral blood CD4 t cell count
- unknown → information missing

301
Q

Describe treatment of HIV

A
  • ART→ antiretroviral therapy
    -drugs that block various steps of HIV replication cycle
    -nucleoside analog reverse transcriptase inhibitors
  • monnucloside relese reverse transcriptase inhibitors
  • protease inhibitors
  • integrate inhibitor
  • fusion inhibits
    -CCR5 antagonists
  • post attachment inhibitor
302
Q

Describe prevention of HIV

A
  • Screening blood/organ donors
  • educating general public
  • precautions for health care workers
303
Q
  • Describe laboratory testing for HIV
A

-Screening and diagnosis
→ previous/current algorithms and test methods
- monitoring for disease
→CD4 T cell count
→HIV viral load
→ drug resistance testing
- testing infant.

304
Q

Desire previous CDC testing alogrithms

A

’ -screen for HIV-1 and HIV-2 antibodies. By ELISA or rapid EIA
- confin by repeating ELISA, follow by western blot

305
Q

How to interpret western blot testin

A
  • No bands-negative
  • must have antibody against of the three bands
    → p24
    → gp41
    → gp120/160
306
Q

Describe current CDC algorithms for testing

A
  • HIV-1/2 antigen/antibody combination immunoassay →POSITIVE
    → HIV - 1/2 antibody differentiation immunoassay
    → indeterminate results →HIV-1 NAT
307
Q

Steps of HIV - 1/2 antibody/ palantigen combination immunoassay

A

-Incubate patient serum with solid phase with hiv-1/2 antigens and p24 have been bound
-hiv-1/2 antibodies will bind to n antigens
-hik-p24 antigen will bind to anti-p24 on solid phase
- wash and add conjugatewith labeled anti-p24 and labeled hiv 1/2 antigens
- incubate, wash, and add trigger solution
- confirm wi rapid EIA

308
Q

Beside western blot test

A
  • Also known as immunoblotting
  • uses antibodies to identify specific protein
  • performed after gel electrophoresis has separated
    Protein
  • separated proteins transferred onto nitrocellular or nylon membranes
309
Q

What are talk positives of the wester blot

A
  • serum collected to early
  • contaminant of cells used in culture
310
Q

DescribeCD4 T- cell enumeration

A
  • Best indicator of immune function of HIV-infected people
  • incubate peripheral blood with fluorescent- labeled anti-CD4, analyze results by flow cytometry
  • it untreated, CD4/CD8 ratio is less than 1:1
    -CD4 t-cell countof less than 200 microliters indicated AIDS
311
Q

Describe quantitative viral road assays

A
  • Measure amount of HIV RNA circulating in patient plasma
    qPCR
    -bDNA
  • detectable 11 days after interchange
  • therapy with ART
312
Q

What are 3 resistance testing for HIV ?

A
  • Genotype resistance assays
  • phenotype resistance assays
    -tropism testing
313
Q

Describe genotyping resistance assay

A
  • HIV reverse transcriptase and protease genes from RNA are amplified by RT-PCR
  • results reported as
    → resistance
    → possible resistanCE
    → no evidence of resistance
314
Q

Describe phenotype resistance assay

A
  • Determine HIV ability to grow in presence of antiretroviral drugs
    -performed by specialized labs
315
Q

Describe tropism testing

A

,- genotype or phenotypic assays performed to determine it patient has virus that will bind to CCR5 co-receptor and be responsive to CCR5 antagonist

316
Q

Describe testing got children and pregnant women for HIV

A
  • All pregnant women tested
    -maternal antibodies in infant serum can complicate serological test results
  • molecular methods are for diagnosis
  • qualifizatie HIV -I DNA OCR using infant peripheral blood mononuclear calls
  • screolgica testing at 12-18 monTHS of age may be used to confirm diagnosis
317
Q

Describe HIV escape of immune response

A
  • Genetic mutation rapid, generating new viral mutants
  • down regulate expression of MHC-1 molecules on infected cows
    -can survive as latent provirus for prolonged period
    -CD4 trolls are destroyed

MLT Semester #1 (15 decks)

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