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MLT immunology > Unit 6 > Flashcards

Unit 6 Flashcards

1
Q

What are viruses?

A

Submicroscopic pathogens whose size is measured in nanometers

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2
Q

Describe the basic structure of a virus

A
  • A core of DNA or RNA packaged into a protein coat ( capsid)
  • in some viruses, the capsid is surrounded by an outer envelope of glycolipids and proteins derived from the host-cell membrane
  • obligate, intracellular
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3
Q

What are the steps of the basic virus lifecycle?

A

① attachment of the virus to a receptor on the host cell surface
② penetration of virus into host cell through endocytosis
③ degradation of the viral capsid and subsequent release of viral nucleic acid.
④ transcription to produce additional viral nucleic acid
⑤ translation of viral nuclei acid to produce viral proteins
⑥ assembly of the viral components to produce intact virions
⑦ budding off the host-cell membrane or host-cell lysis results
⑧ release of viral progeny

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4
Q

What are the defenses types against a virus?

A
  • Innate defenses
  • humoral antibody responses
  • cell-mediated immunity
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5
Q

Describe innate defenses against viruses

A
  • First line of protection (initial barriers)
  • skin and mucous membrane barriers
  • recognition of PAMPs on virus-infected host cells
  • interferons alpha and beta
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6
Q

What occurs if the initial barrier of innate defense does not work?

A

Other innate defenses are activated when cells of the innate immunity recognize PAMPs on surface or within virus infected host cells

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7
Q

What are other innate defenses against viruses?

A
  • viral cells are stimulated to produce IFN-alpha and IFN- beta after recognizing viral RNA by TLRs
  • IFNs inhibit viral replication by inducing transcription of several genes that code for proteins with antiviral activity
  • they also enhance activity of NK cells
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8
Q

How do NK cells fight against viruses?

A
  • Bind to virus-infected cells and release proteins such as a perforin and granzymes, causing cells to die and release viruses and are now accessible to antibody molecules
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9
Q

What plays a key role in preventing the spread of viral infection through neutralization?

A

Antibodies

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10
Q

Describe antibodies role in preventing the spread of viral infection through neutralization

A

-Involves production of antibodies that are specific for a component of the virus that binds to a receptor on the host-cell membrane
- when these neutralizing antibodies bind to the virus, they prevent it from attaching to and penetrating the host cell. IgA plays large role in this.
- IgG and IgM can bind to viruses in blood stream and inhibit dissemination of infection
- IgG and IgM activate complement
- IgG also promote phagocytosis of viruses and promote destruction of viruses through ADCC
- IgM also viral particles by agglutinating them

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11
Q

What does intracellular viruses require?

A

Cell-mediated immunity

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12
Q

What cells have key roles in cell mediated immunity?

A

-Th1 cells
- cytotoxic T cells

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13
Q

Describe Th1 cells actions that occur in cell mediated immunity

A
  • Produce IFN-gamma, which induces an antiviral ‘ state within the virus-infected cells
  • produce IL-2, which assistsin development of effector cytotoxic T cells
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14
Q

Describe cytotoxic T cells actions that occur in cell mediated immunity

A
  • CD8 + cytotoxic T cells become programmed to expand in number and attack the virus infected cells
  • CD8 is a co-receptor of t-cell receptor on cytotoxic T cells that must bind to viral antigen complexed with MHC class I on infected cell surfaces
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15
Q

What occurs after cytotoxic T cells bind to viral antigen complexed with MHC class I?

A
  • Stimutate granules in the cytotoxic T cells to release perforin and granzymes entering the pores
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16
Q

What are perforins?

A
  • protein that produces pores in the membrane of the infected host cell
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17
Q

What are granzymes?

A
  • Protease that enter cells through pores created by perforin.
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18
Q

What occurs once granzymes enter the viral infected cell?

A
  • Activate apoptosis in the host cell, interrupting the viral-replication cycle and resulting in release of assembled infectious virions
  • The free virions can then be bound by antibodies
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19
Q

Describe humoral antibody responses

A
  • Antibodies attack free virus particles
  • viral neutralization, opsonization, C’ fixation, and ADCC
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20
Q

What are viral escape mechanisms? And examples?

A

① mutations results in production of new viral antigens (influenza viruses undergo frequent genetic changes)
② viruses block action of immune system components (HSV can bind C3b)
③ suppression of the immune response (CMV reduces MHC I
④ immune function altered (EBV stimulates polyclonal B-cell activation)
⑤ latent state is established (VZV remains latent in nerve cells)

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21
Q

What laboratory test are ran to detect a viral infection?

A
  • Serological tests
    -distinguish between current and past infection
    -antibody titers used to monitor course of infection
    -assess immune status
  • molecular
    -detect active infection
    -quantitative tests→ guide antiviral therapy
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22
Q

How are current and past infections detected?

A
  • IgM (+) and IgG (+/-) → current or recent infection. (congenital)
  • IgM (-) and IgG (+) → past infection
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23
Q

What does the presence of virus-specific IgG indicate?

A

Immunity to virus

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24
Q

What is the hepatitis virus?

A
  • Hepatitis is the inflammation of the liver
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25
Q

What is hepatitis caused by?

A
  • radiation ‘
  • chemical toxins
  • secondly to other disease
  • cirrhosis (alcoholism)
  • drugs
  • hypothermia
  • bacteria
  • fungi
  • parasites
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26
Q

What types of hepatitis are transmitted by fecal-oral route?

A

Hep A (HAV)
Hep E (HEV)

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27
Q

What types of hepatitis are transmitted through parenteral route?

A

Hep B (HBV)
Hep D (HDV)
Hep C (HCV)

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28
Q

What are indicators of Hepatitis ?

A
  • flu-like symptoms early on
  • pain in upper right quadrant of abdomen
  • hepatomegaly and liver tenderness with profession
  • jaundice
  • dark urine
  • light feces
  • elevated bilimbin and liver enzymes (ALT)
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29
Q

Describe hepatitis A

A
  • nonenveloped, single strand RNA virus
  • belongs to hepatovinis genus of picornarviridaefamily
  • acute hepatitis in majority of adults
  • infections in children are usually asymptomatic
  • formalin-activated vaccine
  • HAV immune globulin may be recommended for unimmunized persons exposed to virus
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30
Q

How is hepatitis A transmitted?

A
  • Fecal-oral route
  • close person-to-person
  • ingestion of contaminated food or water
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31
Q

What is the treatment for hepatitis A?

A

-supportive → bedrest, nutritional support, and medication for fever, nausea, and diarrhea

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32
Q

What is critical for establishing a diagnosis of hepatitis A?

A
  • Serological tests antibody
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33
Q

what is acute infectionS or immunity to HAV indicated by?

A

(+) IgM anti-HAV → acute infection
(+) total anti- HAV along with (-) IgM anti-HAV

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34
Q

What sheds from the feces of someone with hepatitis A?

A

HAV antigens

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35
Q

What are hepatitis A antibodies must commonly detected by?

A

EIAs
Chemiluminescent microparticle immunoassays

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36
Q

When is IgM anti-HAV detectable in a patient with hepatitis A?

A

Onset of clinical symptoms and declines to undetectable levels by 6 months

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37
Q

Describe tests for total HAV antibodies

A
  • Detect IgM but predominantly IgG, which persists for life
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38
Q

Although IgM anti-HAV is primary marker to detect acute hepatitis. What do you have to look out for?

A

False-negative results due to early phase of infection

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39
Q

What is the most common format of these molecular methods of HAV?

A

-RT-PCR
- used to test samples of food or water suspected of transmitting virus

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40
Q

Describe hepatitis E

A
  • nonenveloped, single stranded RNA virus with four genotypes
  • HEV-1 and HEV-2 are transmitted primarily through ingestion of faces- contaminated drinking water
  • HEV-3 and HEV-4 are transmitted mainly by consumption of infected pork
    -most asymptomatic or self-limiting infections
  • can detect HEV RNA in blood or stool during acute infection
    -belong to hepevirus, in the family hepeviridae
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41
Q

What indicates an acute infection of Hep E?

A

IgM anti-HEV

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42
Q

What indicates past exposures of Hep E?

A

IgG anti-HEV

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43
Q

What does diagnosis of HEV rely on?

A
  • Serology to detect antibodies to the virus (EIAs)
  • molecular methods to HEV nucicic acids
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44
Q

What is used to detect later stages, past exposures, and identify seroprevalence of the infection in Hep E?

A

Immunoassays for IgG anti-HEV

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45
Q

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

A

qPCR, quantization of HEV nucleic acid

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46
Q

What testing can be done for immunocompromised patients that are suspected of having Hep E?

A
  • molecular testing for HEV RNA (qPCR)
  • LAMP
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47
Q

When does HEV RNA become undetectable in blood?

A

3 weeks after symptoms onset

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48
Q

When does RNA HEV become undetectable in stools?

A

5 weeks after onset of systems

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49
Q

How long is the incubation period for Hep A?

A

Average of 28 days

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50
Q

Describe hepatitis B

A
  • DNA virus with 8 genotypes (A-H)
  • belongs to hepadnaviridae family
  • acute infection → symptoms increase with age
  • chronic infection → 6 months or more, occurs in 90% of infected infants and 10% of infected adults
  • preventable with immunization
  • hepatitis B immune globulin (HBIG) may be given to unimmunized persons exposed to HBV
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51
Q

What does chronic hepatitis B increase the risk of?

A

Liver cirrhosis
Hepatocellular carcinoma

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52
Q

Describe hepatitis B surface antigen (HBsAg)

A
  • First HBV marker to appear (2-10 weeks after exposure
  • protein on outer envelope of virus
  • excess circulates in virus-like particles in blood
  • marker for active HBV infection
  • component of hepatitis B vaccine
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53
Q

Describe hepatitis B antigen (HBeg)

A
  • Protein in core of HBV
  • marker of active viral replication
  • indicates high degree of infectivity
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54
Q

What are serological markers of HBV antigens?

A

HBsAg
HBeg

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55
Q

What are the antibodies markers for HBV?

A

Anti-HBc
Anti-HBe
Anti-HBs

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56
Q

Describe anti-HBc of HBV

A
  • Directed against hep B core antigen
  • IgM anti-HBc indicates current/recent infection
  • “core window”
    -total anti-HBc consists mainly of IgG and can indicate a current or past - infection
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57
Q

What is core window?

A
  • Period when neither HBsAg nor HBsAb can be detected in the serum of the patient only the anti-HBc
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58
Q

Describe anti-HBe of HBV

A
  • Directed against HBeAg
    -indicates recovery from hepatitis B
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59
Q

Describe anti-HBs of HBV

A
  • Directed against HBsAg
  • indicates immunity to hepatitis B.
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60
Q

How is HBV transmitted?

A

Transmitted through parenteral or perinatal routes:
- sexual contact
- IV drug use
- during birth process

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61
Q

What is the incubation period of HBV

A

30-180 days

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62
Q

Describe recovery of adults with HBV

A
  • most recovery within 6 months
  • 1% develop fulminant liver disease with hepatic necrosis
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63
Q

Describe chronic hepatitis B

A
  • Majority of infants, 10% of adults, one-third children
  • most likely in immunocompromised patients
  • results in liver inflammation and damage
  • can be treated with anti-viral drugs
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64
Q

Describe structure of the HBV

A
  • Nucleocapsid core surrounded by outer envelope of lipoprotein
  • core of virus contains circular partially double- stranded DNA
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65
Q

How are serological markers of HBV used?

A
  • Differential diagnosis of HBV
  • monitoring course of infection
  • assessing immunity to virus
  • screening blood productsfor infectivity
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66
Q

Why is HBsAg important marker of HBV?

A
  • Indicator of active infection
  • monitoring course of infection and progression
  • screening of donor blood
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67
Q

How are serological markers for hepatitis B most commonly detected? Describe

A
  • Commercial immunoassays (EIAs and CLIA) ‘’
  • typically automated
  • excellent specificity and sensitivity
  • false-negatives and false-positives occur
  • positive results should be verified by repeat testing followed by confirmation with additional assay ( HBsAg neutralization test or molecular methods that detect HBV DNA
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68
Q

What is the method of choice to quantify HBV DNA

A

qPCR

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69
Q

What are molecular methods used to detect HBV DNA?

A
  • PCR
  • qPCR
  • branched DNA signal amplification
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70
Q

What is considered a successful treatment for HBV?

A

1- log10 reduction in HBV DNA levels

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71
Q

Describe hepatitis D

A
  • RNA virus that requires presence of HBV with 3 genotypes
  • superinfection of chronic HBV carriers → chronic liver disease with accelerated progression to cirrhosis and liver failure
  • co-infection with HBV → usually results in acute, self-limited hepatitis
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72
Q

In HDV, what is the marker for active viral replication?

A

HDV RNA

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73
Q

What do co-infection of HDV look like?

A

Positive for anti-HDV and IgM anti-HBc

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74
Q

What do chronic cases of HDV results look like?

A

Positive for anti-HDV and IgG anti-HBc

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75
Q

How is HDV transmitted?

A

Through parents evil or perinatal routes

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76
Q

What marker appearance would make cause to test for HDV?

A

-HBsAg
- involves detection of HDV antibodies and HDV RNA

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77
Q

What testing is used to distinguish HBV and HDV from an acute infection or superinfection?

A

Serology testing

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78
Q

What does the presence of IgG anti-HDV indicate?

A
  • Acute, chronic or past infection
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79
Q

What ave molecular methods used to detect HDV RNA?

A
  • RT-PCR assays
  • also provides quantitative results that can be use to monitor the response of patients to antiviral therapy
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80
Q

Describe hepatitis C

A
  • enveloped, single-strandedRNA virus with 7 genotypes
  • belongs to flaviviridae family and genus hepacivirus
  • most infections are asymptomatic at first but develop into chronic liver disease
  • genotyping is used to determine best therapy
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81
Q

How is HCV transmitted?

A
  • Exposure to contaminated blood, sexual contact, and perinatal exposure
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82
Q

What is detection of anti-HCV IgG used for?

A
  • Screening and diagnosis of HCV
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83
Q

What is qualitative HCV RNA used for?

A

Confirmation

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84
Q

What are quantitative molecular tests used for?

A

Monitor viral load during antiviral therapy

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85
Q

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

A

HCV

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86
Q

What is the HCV genotype that is most prominent
In the United States?

A

Genotype 1

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87
Q

Why is it difficult to create a vaccine for HCV?

A
  • The variability of HCV
  • its ability to undergo rapid mutations within its hosts
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88
Q

What is the incubation period of HCV?

A

2 weeks - 6 months (7 weeks average)

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89
Q

What does chronic HCV lead to?

A
  • Cirrhosis of liver ‘’
  • increased visit of hepatocellular- carcinoma
  • rheumatoid conditions
  • glomerulonephritis
  • vasculitis
  • neuropathy
  • dermatological systems
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90
Q

What is the standard treatment for HCV?

A
  • A combination of pegylated IFN-alpha and ribavirin
  • very effective in genotype 2 and 3
  • only effective for 50% of genotypes
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91
Q

What is anti-HCV IgG most commonly detected by?

A
  • EIAs and CLIAs that use recombinant and synthetic antigens
  • rapid immunoblot is alternative
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92
Q

When do antibodies become detectable in HCV?

A

8-10 weeks after exposure and remain positive for a life time

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93
Q

What could cause a false positive result in serological testing of HCV?

A
  • Because of cross-reactivity in persons with other viral infections or autoimmune disorders
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94
Q

What test is recommended for HCV RNA confirmation?

A
  • Nucleic acid testing
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95
Q

What do qualititative tests distinguish between in HCV?

A
  • Presence or absence of HCV RNA
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96
Q

What are qualitative molecular assays used for in HCV?

A
  • To confirm infection in HCV antibody positive patients
  • detect infection in antibody negative patients ho are suspected of having HCV
  • screen blood and organ donors for HCV
  • detect perinatal infections in babies
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97
Q

What are types of quantitative molecular assays for HCV

A
  • RT-PCR
  • qPCR
  • bDNA application
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98
Q

What are quantitative molecular assays for HCV used for?

A
  • Monitor amount of HCV RNA, or viral load, carried by patients before, during and after antiviral therapy in chronic patients
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99
Q

What is the goal of antiviral therapy of HCV?

A

When patient continuously tests negative for HCV RNA 12 or 24 weeks after therapy is completed

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100
Q

Describe genotyping of HCV

A
  • To determine exact genotype and subtype of vines responsible for infection
  • ran on all HCV positive patient before antiviral therapy
  • important to identify genotype because they vary in their responses to different antiviral drugs
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101
Q

What can genotyping of HCV be performed by?

A
  • PCR amplification and sequencing of target gene
  • PCR followed by identification of the target gene with genotype-specific probes
  • qPCR
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102
Q

What is the reference method of genotyping for HCV? Why?

A
  • PCR/direct sequencing (Sanger sequencing)
  • because it provides precise information abort genomic variability of the virus during course of infection
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103
Q

Describe herpes vinises

A
  • Large, complex DNA viruses that are surrounded by a protein capsid, an amorphous tegument, and an outer envelope
  • herpesviridae family → includes 8 viruses
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104
Q

Describe epstein-barr virus (EBV)

A

-DNA herpes virus most commonly transmitted by intimate contact with salivary secretions
- begins in oropharyux in B cells and epithelial cells and spreads through lymphoreticular system

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105
Q

What are diseases caused by Epstein-Barr virus?

A

Infectious mono
Lymphoproliferative disorders
Certain Malignancies ( burkitt lymphoma)

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106
Q

How can epstein-barr virus be transmitted?

A
  • Salivary secretions ( most frequent)
  • blood transfusions
  • bone marrow
  • solid- organ transplant
  • sexual contact
  • perinatal exposure
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107
Q

What cells are infected in the oropharynx in a patient with EBV?

A

Epithelial cells
B cells

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108
Q

How does EBV enter the B cells?

A

By binding to surface CD21

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109
Q

What are early antigens (EAs) of EBV?

A
  • antigen produced during the initial stages of viral replication in the lyric cycle
  • can be classified into two groups (based on location): EA-D and EA-R
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110
Q

Describe EA-D

A

In EBV, Early antigens that have a diffuse distribution in nucleus and cytoplasm

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111
Q

Describe EA-R

A

In EBV, early antigens restricted to cytoplasm only

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112
Q

Describe latent antigens of EBV

A
  • Appear during the period of the lyric cycle following viral DNA synthesis
  • includes the viral capsid antigens in the protein capsid and the membrane capsid in viral envelope
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113
Q

What antigens appear during the latent stage of EBV?

A
  • EBV nuclear antigen (EBNA) proteins
  • EBNA-1
  • EBNA-2
  • EBNA-3
  • EBNA-4
  • EBNA-5
  • EBNA-6
  • LMP-1
  • LMP-2A
  • LMP-2B
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114
Q

What are classic symptoms of IM?

A
  • Fever
  • lymphadenopathy
  • sore throat
  • fatigue
  • lasts 2-4 weeks
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115
Q

What are laboratory findings of IM?

A
  • Absolute lymphocytosis
  • 20% or more atypical lymphocytes
  • heterophile antibodies→ IgM antibodies
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116
Q

Describe treatment of IM

A

Mainly directed at alleviating symptoms

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117
Q

What are heterophile antibodies?

A
  • Antibodies that are capable of reacting with similar antigens from two or more unrelated species
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118
Q

What procedures can be performed for detection of IM heterophil antibodies?

A
  • Monospot (rapid slide agglutination)
  • paul-bunnell test
  • rapid agglutination tests
  • immunochromatographicassays using purified bovine RBC extract as antigen
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119
Q

When can false positives occur in IM testing?

A
  • Lymphoma
  • viral hepatitis
  • malaria
  • autoimmune disease
  • errors in interpretation
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120
Q

What can AID in diagnosis of IM?

A

-Testing for EBV-specific antibodies
- helpful is patients that test negative for heterophil antibodies or determine past exposure.
- detected by IFAs, blot techniques, ELISA, CLIA or flow cytometric microbead immunoassays

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121
Q

What is the gold standard of EBV serology methods?

A
  • IFAs
  • labs prefer to use EIAs or CLIA tests because the are automated and easier to interpret
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122
Q

What is the most useful marker for acute IM?

A

IgM antibody to the VCA

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123
Q

What results typically indicate primary IM infection?

A

-Presence of lgM anti-VCA and anti-EA-D
- absence of anti-EBNA

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124
Q

What type of tests are best to detect EBV in immunocompromised patients:

A

Molecular tests

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125
Q

How is cytomegalovirus transmitted?

A
  • DNA herpes virus is transmitted through oral secretions, genital secretions, congenitally, or by transfusion/ transplantation
126
Q

Describe cytomegalovirus (CMV)

A
  • Healthy individuals may be asymptomatic or develop a mononucleosis- like syndrome
    -in immunocompromised persons, CMV can disseminate to lungs, liver, GI tract, CNS, and eyes and cause life-threatening infections
  • may cause congenital defects and decreased survival in infants
127
Q

What are types of testing for CMV?

A
  • Direct virus detection
  • serology
128
Q

Describe direct virus detection of CMV

A
  • viral culture
    -sample placed with a cell type that the virus being tested for can infect
    -if the cells show changes, known as cytopathic effects, then the culture is positive
  • ID of CMV antigens
  • molecular tests for CMV DNA
129
Q

Describe serology methods for CMV

A
  • used to screen blood and organ donors; pregnant women
  • presence of IgG anti-CMV indicates infection
  • low avidity antibodies indicate recent infection
  • most beneficial in determining past exposures
  • usually semi- or fully automated EIAs
130
Q

What is the most common cause of congenital infections

131
Q

What indicates CMV?

A
  • Characteristic cytopatic effects (CPEs) that produce enlarged, rounded, refractile cells
132
Q

Describe the CMV antigenemia assay

A
  • Uses immunocytochemical or immunofluorescent staining to detect the CMV lower-matrix protein pp65 in infected leukocytes from peripheral blood or cerebral spinal fluid
  • 2-4 hours to perform
133
Q

What is the most widely used molecular test for CMV? Why?

A
  • RT-PCR
  • sensitive, simple to perform and provide quantitative results
134
Q

Describe VZV

A
  • DNA herpes virus
  • cause of: varicella (chickenpox) and herpes zoster ( shingles)
  • preventable by vaccine
135
Q

How is VZV transmitted?

A
  • By inhalation of infected respiratory secretions or aerosols from skin lesions
136
Q

Describe varicella

A
  • Highly contagious illness
  • blister-like rash
  • intense itching
  • fever
137
Q

What are the activities of VZV in the primary infection?

A
  • Thought to travel from the skin lesions and the blood to sensory neurons, where it deposits its DNA and establishes a lifelong latent state in the dorsal root, autonomic and cranial ganglia
138
Q

Describe herpes zoster

A
  • Painful vesicular rash caused by the vines moves down the sensory nerve to the dermatome supplied by that nerve
  • most common complication being postherpetic neuralgia
    -life threatening complications: herpes ophthalmicus which leads to blindness, pneumonia, and visceral involvement
139
Q

What is the definitive diagnosis of VZV?

A
  • identifying VZV (or one of its products) in sick lesions, vesicular fluids or tissue
  • used for atypical cases
140
Q

What is the method of choice to detect VZV DNA?

141
Q

How is serology testing useful with VZV?

A
  • Determines immunity to VZV in health-care workers, pregnant women, and organ transplant candidates
142
Q

What cells can be detected in VZV patients?

A
  • Tzanck cells
143
Q

When is quantitative PCR useful with VZV?

A
  • Monitoring response of immunocompromised patients to antiviral drugs
144
Q

What type of specimens are PCRs van on for VZV?

A
  • Scab
  • Skin swabs
  • vesicular fluid
  • throat swabs
  • cerebrospinal fluid
  • blood
  • saliva
    -tissues
145
Q

Why is testing for VZV IgM not done?

A

① IgM antibodies to VZV may not be detectable until the convalescent stage of illness
② they cannot distinguish between primary and reactivated infection
③ may not be free of IgG antibodies when semi’s processed for testing

146
Q

Describe serology testing for VZV

A
  • most of them detect total VZV antibody, which consists primarily of IgG
  • most reliable and sensitive method → FAMA (reference method)
    -most commonly used → ELISA
147
Q

Describe FAMA

A
  • Fluorescent antibody to membrane antigen
  • detects antibody to the envelope glycoproteins of the virus
  • requires live, virus-infected cells
  • not suitable for large scale testing
148
Q

Why can a false positive be caused by using ELISA to detect VZV?

A
  • The method can detect low-levels of antibodies that do not confer long-term protection to varicella
149
Q

Describe rubella virus

A
  • Enveloped, single-stranded RNA virus
  • Cause of German measles
  • can be prevented with immunization
  • genus rubivirus and belongs to family Togaviridae
  • 12-23 day incubation period
  • after incubation, virus replicates in upper respiratory tract and cervical lymph nodes, then travels through blood stream
150
Q

How is the rubella virus transmitted?

A
  • Respiratory droplets
  • across the placenta
151
Q

What can rubella virus cause?

A
  • deafness
  • eye defects
  • cardiac abnormalties
  • mental retardation
  • motor disabilities
  • miscarriage
  • stillbirth in infants born to infected mothers
152
Q

What are symptoms of rubella virus?

A
  • Erythematous (macropapular rash). Appears first on the face, then spreads to the trunk and extremities
  • low grade fever
  • malaise
  • swollen glands
  • upper respiratory infection lasting 1-5 days
  • 50% infected with Rubella are asymptomatic
  • arthritis
153
Q

What population has severe consequence with the rubella virus? Why ?

A
  • Pregnant women, especially in first trimester
  • may cause miscarriage, stillbirth, or congenital rubella syndrome
154
Q

What can occur if infants are born with congenital rubella syndrome (CRS)

A
  • Many abnormalties
    -Deafness
    -eye defects (cataracts and glaucoma)
    -cardiac abnormalties
    -mental retardation
    -liver and spleen damage
    -motor disabilities
155
Q

What type of methods are ran for rubella virus?

A
  • Serology
  • viral culture
  • molecular methods
156
Q

Describe serology testing of rubella virus

A
  • Presence of IgG is used to screen for immunity
  • congenital infection is indicated by rubella- specific IgM or fourfold rise in IgG
  • low avidity antibodies indicate recent infection
157
Q

Describe viral culture of the rubella virus?

A
  • Diagnosis can be obtained this way
  • viral growth is slow
  • may not produce characteristic CPE
158
Q

If CPE is absent in the viral culture of rubella, what should be done next?

A

Viral nucleic acid can be identified by RT-PCR or viral proteins can be detected with IFA or EIA

159
Q

What is the most widely used test for rubella virus?

A
  • Molecular methods → RT-PCR
  • used to detect rubella RNA
160
Q

What clinical samples can be tested with RT-PCR for rubella?

A
  • Chorionic villi
  • placenta
  • amniotic fluid
  • fetal blood
  • lens tissue
  • products of conception
  • pharyngeal swab
  • spinal fluid
  • brain tissue
161
Q

What are the most common methods used to confirm Rubella?

A
  • Serology tests (rapid and cost effective)
  • detect rubella antibodies
  • ELISA → most widely used
  • hemagglutination inhibition (HI)
  • latex agglutination
  • immunoassays
162
Q

Describe ELISA testing of rubella

A
  • Specific solid phase capture ELISAs can be used to detect IgM rubella antibodies
163
Q

What assays can simultaneously detect measles, mumps, rubella, and varicella?

A
  • Automated chemiluminescence assays
  • multiplex bead immunoassay
164
Q

How is a primary rubella infection indicated?

A
  • Presence of rubella-specific IgM antibodies
    OR
  • four-fold or greater rise in rubella specific IgG antibody titers collected at least 10-14 days apart
165
Q

What are the causes for false-negative and false positives in rubella?

A

False negative → if sample is obtained too early
False-positive → individuals with parvovirus infections, enterovirusinfections, heterophil antibodies or rheumatoid factor

166
Q

Describe test ran to confirm positive IgM results of rubella

A
  • EIA → measures avidity of rubella IgG antibodies, which helps distinguish between recent and past infections
  • low antibody avidity → recent infection
    -high antibody avidity→ past infections
167
Q

Describe Laboratory testing of congenital rubella infection

A
  • Begins with serological evaluation of the ‘ mothers antibodies and measurement of rubella-specific IgM antibodies in fetal blood, cord blood, or neonatal seruml
  • any positive IgM results should be confirmed by viral culture, RT-PCR amplification, or demonstration of persistentLY nigh taters of rubella IgG antibodies after 3- 6 months of age
168
Q

Describe rubeola

A
  • RNA virus single-stranded RNA virus
  • genus morbillivirus in the paramyxoviridae family ‘
  • after initial infection of the epithelial cells in upper respiratory tract,rubeola virus is disseminated through the blood to multiple sitesin body, such as the skin, lymph nodes and liver
  • preventable by immunization
  • diagnosis is usually based on clinical presentation and confirmed by serology
169
Q

How is rubeola transmitted?

A

Through respiratory droplets

170
Q

What does rubeola cause?

A
  • Measles
  • subacute sclerosing panencephalitis (SSPE)
171
Q

What is the incubation period for rubeola?

A

10-12 days

172
Q

What are the symptoms of rubeola?

A
  • Fever
  • cover
  • runny nose
  • conjunctivitis
  • Koplik spots appear on mucous membrane of inner cheeks or lips
173
Q

What is a the rubeolla virus characterized by?

A

Erythematous (maculopopular eruption) that begins at hairline, then spreadsto the face and neck and gradually moves down to trunk, arms, hands, legs, and feet

174
Q

What complications can measles result in?

A
  • Diarrhea
  • otitis media
  • croup
  • bronchitis
  • pneumonia
  • encephalitis
175
Q

What is SSPE associated with ?

A

Extremely nigh titers of rubeola antibodies

176
Q

What is the preferred method to detecting IgM antibodies in rubeola?

A
  • IgM capture ELISA method
  • 3-4 days after symptoms
177
Q

What is the preferred method of detect IgG antibodies of rubeola?

A
  • ELISA
  • detectable 7-10 days after symptoms and persist for life
  • IgG antibodies indicate immunity
178
Q

When are molecular methods used to detect rubeola RNA?

A
  • In which serological tests are inconclusive or inconsistent
  • can be used to genotype the virus
179
Q

What is the preferred molecular method for detecting rubeola?

180
Q

Describe mumps virus

A
  • Single stranded RNA vines
  • paramyxoviridae family, genus ribulavirus
  • most common clinical manifestation is parotitis
  • replicates initially in nasopharynx and regional lymph nodes
  • preventable by immunization
  • diagnosis is usually based on clinical presentation
  • confirmation is done by culture or RT-PCR
181
Q

How is mumps transmitted?

A

Respiratory droplets, saliva, fomites

182
Q

What are fomites?

A

Inanimate objects or substances that can transmit infectious organisms

183
Q

What is the incubation period of the mumps virus?

A

14-18 days

184
Q

How does the mumps virus function?

A
  • Virus spreads from blood to various tissues:
    -meningesof brain
    -salivary glands
    -pancreas
    -testes
    -ovaries
  • produces inflammation at site
185
Q

What is parotitis?

A
  • Inflammation of the parotid glands
  • occurs in 30.40% of patients with mumps
186
Q

What is the gold standard for detecting the mumps virus

187
Q

What are the preferred specimens for a culture of mumps?

A

Buccal swab
Saliva from buccal cavity

188
Q

What is the primary diagnostic test for mumps? Why?

A
  • RT-PCR
  • because it is more sensitive than serology
189
Q

Describe serological testing of mumps

A
  • Provides simple means of confirming mumps ‘ ‘ diagnosis but has some important limitations
  • EIAs and IFA mostly only measure IgG mumps virus antibodies
  • most commonly used → ELISA
  • use of solid-phase IgM capture assays reduces incidence of false positivesbecause of rheumatoid factor C
190
Q

What is a current or recent infection of mumps indicated by?

A
  • Presence of mumps-specific IgM antibody in a single serum sample or by at least a four-fold rise in specific IgG antibody between two specimens collected during the acute and convalescent phases of illness
191
Q

Describe human t-cell lymphoytropic virus type I and type II (HTLV-I & HTLV-2)

A
  • Closely related retroviruses that preferentially infect T-lymphocates ( usually CD4+)
  • serological tests for antibodies to HTLV-I/II are used to diagnose infections and screen blood donors.
  • have RNA as their nucleic acid and enzyme reverse transcriptase
  • was 3 structural genes: gag, pol, and env and region called pX
    -ELISA or CLIA are used to screen
    -western blot or LIA are used for confirmation of positive results
192
Q

What does HTLV-I cause?

A

-adult T-cell leukemia/lymphoma (ATLL) and HAM/TSP

193
Q

How are HTLV types I and II transmitted?

A
  • Mainly blood borne
  • sexual contact
  • perinatal (especially breastfeeding)
194
Q

What is “gag?”

A

Codes for viral core proteins

195
Q

What is “pol?”

A

Codes for viral enzymes

196
Q

What is “env?”

A

Encodes proteins in viral envelope

197
Q

What is “pX?”

A

Encodes several regulatory proteins, including tax and Rex

198
Q

What is reverse transcriptase function of HTLV?

A

To transcribe the viral RNA into DNA

199
Q

What are the 4 subtypes of ATLL? What are they characterized by?

A
  • acute
  • T-cell non-Hodskin’s lymphoma
  • chronic
  • smoldering
  • a monoclonal proliferation of matureT cells that express the surface markers CD3, CD4, and CD25
200
Q

How is HAM/TSP characterized?

A
  • Slowly progressive weakness and stillnessof legs
  • back pain
  • urinary incontinence
201
Q

What has been associated with HTLV-I?

A
  • variety of autoimmune and inflammatory disorders
    -uveitis (intraocular inflammationof the eyes)
    -infective dermatitis
    -myositis (inflammation of the muscles)
    -arthropathy (inflammation of the joints)
202
Q

When do HTLV antibodies develop?

A

30-90 days after exposureto the virus and persists for life

203
Q

When is a sample considered positive for HTLV-I performed with western blot?

A

-if visible bands are produced for one of the env proteins (either gp46 or gp62/68) AND one of the gag proteins (either p19, p24,or p53

204
Q

Describe PCR methods for HTLV testing

A
  • detects HTLV type I and II DNA
  • Can be used to monitor the proviral load in patients during therapy
205
Q

Describe toxoplasmosis

A
  • Found in feces of house cats and rodents (other mammals)
206
Q

How is toxoplasmosis transmitted?

A
  • Accidental ingestion of oocyst (fecal contamination of meat, raw milk, etc)
  • transplacental transmission
207
Q

How does on individual prevent congenital toxoplasmosis?

A

-avoid touching mucous membranes of mouth and eyes while handling raw meat
-wash hands and Kitchen surfacesafter coming in contact with raw meat
-not allow flies and cockroaches access to food
-avoid contact (or wear gloves) when handling cat litter boxes or gardening

208
Q

What are signs and symptoms of toxoplasmosis?

A
  • Usually asymptomatic, organism can multiply in any organ of body
  • similar to mono (if symptoms are mono)
  • spontaneous recovery
209
Q

Describe congenitalinfections of toxoplasmosis

A
  • Of most concern ‘
  • result in CNS malformation and mortality of the neonate
  • 75% have no symptoms at birth, disease is dormant, discovered only when neurological problems such as blindness occurs
210
Q

What is the method of choice for a laboratory diagnosis for toxoplasmosis?

211
Q

Describe TORCH testing

A
  • Consists of tests for antibodies to four organisms that cause congenital infections transmitted from mother to fetus
    T → toxoplasmosis
    O→ others
    R→ rubella
    C→ CMV
    H→ herpes simplex virus (HSV)
212
Q

What are the “ others “ of TORCH?

A
  • Syphilis
  • HBV
  • coxsackie virus
  • EBV
  • VZV
  • human parvovirus
213
Q

What viruses affect the respiratory system?

A
  • Adenovirus
  • influenza
  • mumps
  • measles
  • RSV
214
Q

What virus affects the skin?

215
Q

What virus effects the GI tract?

216
Q

What is the role of CTLs in immune responses against viruses?

A

Destroy virus-infected host cells

217
Q

A newborn suspected of having a congenital viral infection should be tested for virus - species antibodies of which class?

218
Q

The serum of an individual who received all doses of the hepatitis B vaccines should contain what?

219
Q

Heterophile antibodies are routinely detected by their reaction with what?

A

Bovine erythrocyte antigens

220
Q

What is the method of choice for detecting VZV infection inimmunocompromised hosts?

A

(Real-time) qPCR

221
Q

Describe human immunodeficiency virus (HIV)

A
  • Causes AIDS (acquired immunodeficiency syndrome)
  • two types: HIV-1 and HIV-2
222
Q

Describe HIV-1 (will be referred to as in this set)

A
  • Cause of most HIV infections worldwide
  • 4 groups → M, O, N, P
  • 9 subtypes in group M→ A, B , C, D, F, G, H, J, K
  • group M is responsible for most cases
  • predominant subtype→ C
  • most prevalent in US→ B
  • belongs to genus lentivirinae of virus family Retroviridae
  • decrease in cell population is a hallmark feature
223
Q

Describe HIV-2

A
  • Originated in west Africa
  • causes fever cases
  • less pathogenic
  • lower transmission rate
224
Q

What are ways HIV can be transmitted?

A
  • Sexual contact involving exchange of body fluids → responsible for majority of cases
  • contact with blood or other body fluids
  • perinatal → before, during and after( breast milk)
225
Q

What body fluids are infective with HIV?

A
  • Blood
  • semen and vaginal secretions
  • synovial, pleural, peritoneal and pericardial
  • CSF
  • breast milk.
226
Q

What are characteristics of HIV

A
  • Retrovirus
  • contains two copies of ssRNA
  • reverse transcriptase transcribes the viral RNA into DNA
  • surrounded by a protein coat (capsid)
  • outer envelope of glycoproteins embedded in a lipid bilayer
227
Q

What is gp120

A

Docking glycoprotein

228
Q

What is gp41?

A

Transmembrane glycoprotein

229
Q

What is p17?

A

Matrix protein

230
Q

What is p24?

231
Q

Why is HIV considered a retrovirus?

A

because it contains RNA as its nucleic acid and a unique enzyme called reverse transcriptase

232
Q

Describe the HIV structure

A
  • spherical particle
  • includes 3 structural genes: gag, pol and env
  • 100-120 nm in diameter
  • contain inner core with two copies of single stranded RNA surrounded by protein coat (capsid) and an outer envelope of glycoproteins embedded in lipid bilayer
  • glycoproteins are knob-like structures that are involved in binding the virus to host cells during infection
233
Q

describe gag of HIV

A
  • codes for p55
  • p55 is a precursor for p6, p9, p17 and, p24
  • all are located in the nucleocapsid of the virus
  • p17 embedded in the internal portion of the envelope (matrix)
  • p6, p9, and p24 located in capsid that surrounds the internal nucleic acids
234
Q

Describe env of HIV

A
  • codes for the glycoproteins gp160, gp120, and gp41 which are all found in the viral envelope
  • gp160 is a precursor protein that is cleaved into gp120 and gp41
    -gp120 forms protruding knob structures on the outer envelope
  • gp41 is a transmembrane glycoprotein that spans the inner and outer membrane and attaches to gp120
    -both gp120 and gp41 are involved in fusion and attachment of HIV to receptors on the host cells.
235
Q

Describe pol of HIV

A
  • codes for enzymes necessary for HIV application
  • located in the core of the virus in association with HIV RNA
  • enzymes: reverse transcriptase (p51), RNAse H (p66), integrase (p31) and protease (p10)
236
Q

describe p66 of pol in HIV

A

enzyme involved in the degradation of the original HIV RNA

237
Q

describe p31 of pol in HIV

A

an enzyme that mediates the integration of viral DNA into the genome of infected host cells.

238
Q

Describe p10 of pol in HIV

A

cleaves precursor proteins into smaller active units used to make the mature virions

239
Q

Briefly Describe replication of HIV

A
  • attachment of HIV to host cell
  • main target: CD4 Th
  • coreceptor required
240
Q

What are the steps of HIV replication?

A
  1. Binding - HIV binds to receptors on surface of CD4 cell
  2. Fusion - HIV envelope and and CD4 cell membrane fuse and allows virus to enter cell
  3. Reverse transcription - inside cell, HIV uses and releases reverse transcriptase, which HIV RNA into HIV DNA. This allows HIV to enter nucleus of CD4 cell
  4. Integration - inside nucleus, HIV releases integrase. Uses integrase to insert its viral DNA into the DNA of the CD4 cell
  5. Replication - HIV uses machinery of CD4 cell to make long chains of HIV proteins. These proteins are building blocks for more HIV
  6. Assembly- new HIV proteins and HIV RNA move to surface of cell and assemble into immature HIV
  7. Budding - immature HIV pushes out of host CD4 cell surface. New HIV release proteases, which break down the long protein chains in immature HIV, forming mature HIV
241
Q

what is T-tropic or X4 strains of HIV?

A

that preferentially infect T-cells

242
Q

what is M-tropic or R5 strains of HIV?

A

can infect T-cells and macrophages

243
Q

what chemokine receptor is required for HIV to enter T-lymphocytes?

244
Q

what chemokine receptor is required for HIV to enter macrophages?

245
Q

when does HIV not virally replicate?

A

during the latent stage

246
Q

what are the type of immune responses for HIV?

A
  • innate
  • humoral antibody production
  • cell-mediated immunity
247
Q

Describe the innate defenses against HIV

A
  • NK cells medicate cytolysis of HIV infected cells
  • dendritic cells stimulate release of cytokines that have antiviral effects
248
Q

Describe humoral antibody production against HIV

A
  • Antibodies are detected by 6 weeks after infection.
  • Antibodies produced later may prevent HIV from infecting host cells and participate in ADCC
249
Q

Describe cell-mediated immunity against HIV

A
  • T cells produce cytokines with antiviral activity
  • CTLs destroy HIV-infected host cells
250
Q

what are the HIV escape mechanisms?

A
  1. genetic mutaions rapidly occur, generating new viral mutants with altered antigens
  2. down regulates expression of MHC-I molecules on infected host cells
  3. can survive as a patent provirus for prolonged periods
  4. As a result, HIV persists and destroys the immune system
  5. CD4 T cells are the prime targets of destruction, resulting in reduced effectiveness of antibody and cell-mediated immune responses
251
Q

How is HIV suspected to kill or render function of CD4 Th cells?

A
  1. loss of plasma-membrane integrity because of viral budding
  2. destruction by HIV-specific CTL
  3. viral induction of apoptosis
252
Q

what is the central role in the immune system for CD4 T cells?

A

regulating the activities of B and T cells

253
Q

what is the acute stage of HIV characterized by?

A
  • rapid bursts of viral replication before the development of HIV-specific immune responses
  • high levels of viremia is found in this stage
  • decrease in CD4 T-cell number
254
Q

what are the symptoms of acute stage of HIV?1

A
  • flu-like symptoms
  • IM-like symptoms
  • many are asymptomatic during this stage
255
Q

describe HIV latent stage

A
  • decrease in viremia
  • increase in CD4 T-cell number
  • symptoms are subtle or absent
256
Q

describe the last stage of HIV

A
  • full blown AIDS
  • characterized by profound immunosuppression with very low numbers of CD4 T cells
  • resurgence of viremia
  • patients demonstrate neurological symptoms
  • appearance of life-threatening opportunistic infections and malignancies
257
Q

what are the symptoms for infants with AIDS?

A
  • failure to thrive
  • persistent oral candidiasis
  • hepatosplenomegaly
  • lymphadenopathy
  • recurrent diarrhea
  • recurrent bacterial infections
258
Q

Describe antiretroviral therapy (ART)

A
  • drugs that block various steps of the HIV replication cycle
    -nucleoside analog reverse transcriptase inhibitors
    -nonnucleoside reverse transcriptase inhibitors
    -protease inhibitors
    -integrase inhibitors
    -fusion inhibitors
    -CCR5 antagonists
    -Post attachment inhibitors
  • are most effective when used in combination
  • has significantly improved morbidity and mortality of HIV-infected persons and has reduced the rate of perinatal transmission
259
Q

what are ways to prevent HIV?

A
  • screening blood/ organ donors for HIV
  • education of the general public on HIV transmission, safety measures
  • precautions for health-care workers
  • vaccine-being researched
260
Q

Describe screening and diagnosis of HIV

A
  • previous algorithm and test methods
  • current algorithm and test methods
261
Q

Describe testing of HIV

A
  • performed on infants
262
Q

Describe previous testing algorithm of HIV

A
  • screen for HIV-1/HIV-2 antibodies by ELISA or rapid EIA
  • confirm positive test results by repeating ELISA, followed by Western Blot
263
Q

Describe the Western Blot test

A
  • also known as immunoblotting
  • tests for a specific protein with a protein mixture
  • is performed after gel-electrophoresis has separated protein
  • uses antibodies to identify specific proteins
  • separated proteins are transferred onto nitrocellulose or nylon membranes and identified by specific antibodies that are tagged by a secondary protein
264
Q

Describe the wester blot interpretations of HIV

A
  • no band: negative
  • positives are harder to interpret
  • CDC says must have antibody against two or three of the following bands:
    -p24
    -gp41
    -gp120/160 (these bands are very close together and is hard to distinguish between the two.
265
Q

Describe the current CDC testing algorithm for HIV

A
  • initial screening: HIV-1/2 antigen/antibody combination immunoassay
  • If positive: run HIV-1/2 differentiation immunoassay
    -HIV-1(+) & HIV-2 (-): HIV-1 antibodies present
    -HIV-1(-) & HIV-2(+): HIV-2 antibodies present
    -HIV-1(+) & HIV-2(+): HIV-1 and HIV-2 antibodies present
  • If both HIV negative, run HIV-1 NAT
    -HIV-1 NAT (+): acute HIV-1 infection
266
Q

what is the principle of the fourth generation HIV-1antibody/HIV-2 antibody/p24 antigen combination immunoassay?

A
  1. incubate patient serum with solid phases onto which HIV-1antigens, HIV-2 antigens and antibody to HIV-1 p24 have been bound
  2. Following incubation, HIV-1 or HIV-2 antibodies in the patient sample will bind to their respective antigens.
  3. HIV-1 p24 antigen in the patient sample will bind to anti-p24 solid phase
  4. Wash, then add conjugate consisting of labeled anti-24 labeled HIV-1/HIV-2 antigens
  5. Following, incubation, wash, and addition of trigger solutions or substrate/stop solution, relative light units or optical absorbance are measured
  6. Confirm positive results with rapid EIA
267
Q

What are some ways the HIV is monitored?

A
  • peripheral blood CD4 T-cell counts
  • Quantitative viral load assays
  • Drug resistance and tropism
268
Q

Why do false-positives occur in the 4th generation HIV-1/2 antibodies and p24 antigen test?

A
  • heat inactivation
  • repeated freezing and thawing
  • presence of heterophil antibodies
  • passive immunoglobulin administration
  • administration of of an experimental HIV vaccine to patient
269
Q

What is seroconversion?

A

the change of a serological test result from antibody negative to antibody positive.

270
Q

What are the two markers used to monitor HIV for disease progression and guide the treatments?

A
  • the peripheral blood CD4 T-cell count (best indicator of immune functions)
  • HIV-1 RNA level (viral load)
271
Q

Describe CD4 T-cell enumeration

A
  • CD4 T-cell numbers are the best indicator of immune function in HIV-infected individuals
  • incubate peripheral blood with fluorescent-labeled anti-CD4; analyze results by flow cytometry
  • in untreated patients, CD4 T-cell number declines progressively, and CD4 T: CD8 T-cell ratio is less than 1:1
  • CD4 T-cell count of less than 200/ul indicates stage 3 HIV
  • A significant decline in CD4 T-cell count over time may indicate a need to change ART or administer prophylactic therapy for certain infections
272
Q

what is the peripheral blood CD4 T-cell count in a healthy individual?

A

450-1500 cells/ul

273
Q

what is the gold standard for enumerating CD4 T cells?

A

immunophenotyping with data analysis by flow cytometry

274
Q

Describe the CDC classification list of HIV

A

0-5
- 0: early infection of patient who tested positive for HIV in initial screening but has a negative or indeterminate confirmatory test
- 1-3: based on peripheral blood CD4 T-cell count or percentage. If this information is missing, classified as unknown

275
Q

Describe quantitative viral load assays

A
  • measure amount of HIV RNA circulating in patient plasma
  • methods: qPCR and bDNA
  • HIV RN detectable about 11 days after infection
  • successful therapy with ART results in the decline in the viral load to an undetectable antigen
  • Patients with persistently increased viral load should undergo drug resistance testing and may need a possible change in ART
276
Q

Why are viral load tests used?

A
  • help predict disease progression
  • monitor patient response to ART
  • guide treatment plan
277
Q

Describe the viral load assays of HIV RNA

A

-based on amplification methods that increase the number of HIV RNA copies
-most common: PCR and bDNA assay

278
Q

what are the 2 PCR methods that have been developed to detect HIV nucleic acid?

A
  • RT-PCR (not usually used)
  • qPCR
279
Q

what is the basic principle of RT-PCR for HIV RNA?

A
  • to amplify a DNA sequence that is complementary to a portion of the HIV RNA genome
280
Q

What are disadvantages of RT-PCR for HIV RNA?

A
  • limited dynamic range
  • highly susceptible to cross-contamination with extraneous nucleic acid
281
Q

what is the basic principle of bDNA assay

A

based on amplifying the detection signal generated in the reaction.
- accomplished by using a solid-phase sandwich hybridization assay that incorporates multiple sets of oligonucleotide probes and hybridization steps that produce a series a branched molecules.

282
Q

what are disadvantages of bDNA?

A
  • requires larger sample volume
  • lacks internal controls
  • lower specificity
283
Q

what are drug resistance testing methods for HIV?

A
  • genotype resistance assays
  • phenotype resistance assays
  • Tropism testing
284
Q

Describe genotype resistance assays of HIV

A
  • performed in clinical laboratory settings
  • HIV reverse transcriptase and protease genes from RNA in patient plasma are amplified by RT-PCR
  • products are sequenced and analyzed with software for mutations
  • Results are reported as: Resistance, Possible resistance, no evidence of resistance
285
Q

Describe phenotype resistance assays of HIV

A
  • Determine ability of HIV from clinical samples to grow in the presence of antiretroviral drugs
  • involve sophisticated technologies only performed by specialized reference laboratories.
286
Q

-Describe tropism testing of HIV

A
  • genotypic or phenotypic assays are performed to determine if the patient has virus that will bind to the CCR5 co-receptor and be responsive to CCR5 antagonists
287
Q

Describe testing of infants younger than 18 months in HIV

A
  • all pregnant women should be tested for HIV
  • Maternal antibodies in infant serum can complicate serological test results
  • molecular methods are used for diagnosis
  • Qualitative HIV-1 DNA PCR using infants peripheral blood mononuclear cells is the preferred method
  • Serological testing at 12-18 months of age may be used to confirm the diagnosis
288
Q

HIV visions bind to host T cells through which receptors?

289
Q

What is typical of the latent stage of HIV infection?

A
  • Proviral DNA is attached to cellular DNA
290
Q

What is the drug zidovudine an example of?

A

Nucleoside analogue reverse-transcriptase inhibitor

291
Q

Why would a false negative result in a test for HIV ?

A

Collection of the test sample before seroconversion

292
Q

What does the conjugate used in 4th- generation immunoassays for HIV consists of labeled?

A
  • HIV-1 and HIV-2- specific antigens plus antibody to p24
293
Q

What is the first detectable antibodyin serum after infection with hepatitis B?

294
Q

What is the difference between HAV and HBV incubation periods?

A
  • HAV→ short
  • HBV→ long
295
Q

How do you interpret these results?
Anti-HAV (IgG)→ negative
Anti-HAV (IgM)→ negative
HBsAg→negative
Anti-HBc→ positive
Anti-HBs→ negative
HBeAg→ negative

A
  • HBV in cove window phase
296
Q

What is the most common cause of congenital infections?

297
Q

What populations does VZV cause severe complications in?

A
  • Immunocompromised patients
  • pregnant women
298
Q

What is the clinical importance of CMV?

A

Life threatening for immunocompromised patients and infants

299
Q

A patient has IgG and IgM antibodies against viral capsid antigens of EBV. What does this patient have

A
  • Current EBV infection
300
Q

What are heterophile antibodies routinely detected bytheir reactionwith this agent?

A

Bovine RBC antigens

301
Q

What does the presence of IgM anti-rubella antibodies in serumfrom an infantborn with a rash?

A

Congenital infection with rubella virus

302
Q

What are the a most commonly used tests to detect mumps virus,?

A

RT-PCR
ELISA

303
Q

What is method of choice for defecting VZV in immunocompromised hosts?

304
Q

Describe Tzack smear

A

Scrap lesion with scalpel but put on slide and stain, then look for giant multinucleated cells

305
Q

What does p24 encode for?

306
Q

How should these results be interpreted HIV?
ELISA: positive
Repeat ELISA: neg
Western blot: no bands

A

Negative for HIV

307
Q

What type of cells can HIV infect?

A
  • primarily lymphocytes
  • monocytes
308
Q

What does the HIV cove consists of?

A

Two identical strands of RNA

309
Q

What is uncaring of genome, making RNA into DNA?

A

Reverse transcriptase

310
Q

Why is HIV called a retrovirus?

A

Can transcribe RNA into DNA

311
Q

A 22-year-old male sees his physician for an annual checkup. He reportedhaving flu-like symptoms including fever, sore throat, and lymphadenopathy several months ago.he has lust about 10 pounds but otherwisefeels fine. HIV testing is recommended and ordered
ELISA→ positive
Western blot→ positive
CD4+ T-cell count is 500/ml
What disease and stage is this ?

A

HIV positive in latency stage 1

MLT immunology (7 decks)

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