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Drug Action IV > Virus part 2 (Patho) - Block 3 > Flashcards

Virus part 2 (Patho) - Block 3 Flashcards

1
Q

Describe the structure of HIV?

A

Retrovirus Class VI: enveloped, spherical, diploid, + single stranded RNA virus with a DNA intermediate
* Contains 2 copies of + sense RNA

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2
Q

What are structural genes of HIV?

A

Gag: encodes for nucleocapsid and matrix
Pol: encodes reverse transcriptase, integrase, and protease for viral replication
Env: encodes structural proteins gp120 and gp41 (viral attachment)

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3
Q

What is the importance for acessory (regulatory) genes?

A

Support transport of viral mRNA, manipulate host cell cycle, and block host intracellular immune defenses

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4
Q

Describe activity of HIV?

A
  1. RNA is transcribed into complementary DNA by reverse transcriptase
  2. Copy (provirus) inserts in the host-cell’s DNA and is replicated along host DNA
  3. Can remain latent until activation signal
  4. Active transcription of the provirus leads to new virions -> buddinding becoming lytic
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5
Q

What is a viral trophism?

A

Specificity of a virus for host tissue due to surface receptors on host cells that can support viral replication

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6
Q

What are HIV’s methods of attachment?

A

Viral spike proteins gp120 and gp41 attach to CD4 and a co-receptor (CXCR4 or CCR5)
* CCR5: macrophages, DCs, effector T cells
* CXCR4: naive and memory T cells

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7
Q

What are the preferred target for HIV?

A

T cells

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8
Q

How does HIV replicate?

A
  1. HIV gp120 binds to CD4 and then CXCR4 or CCR5
  2. HIV gp41 causes fusion with target membrane
  3. Nucleocapsid containing viral genome and enzymes enters the cell
  4. Viral genome and enzymes are released -> removal of core proteins
  5. Viral reverse transcriptase catalyzs reverse transcription of ssRNA forming RNA-cDNA hybrids
  6. Orginal RNA template is partially degraded by ribonuclease H -> synthesis of second DNA strand to yield HIV dsDNA
  7. The viral dsDNA is translocated to nucleus and integrated into host chromosomal DNA by the viral integrase enzyme
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9
Q

Describe the HIV life cycle?

A
  1. Transcription factors stimulate transcription of proviral DNA into genomic ssRNA and mRNA
  2. Viral RNA is exported to cytoplasm
  3. Host cell ribosomes catalyze synthesis of viral precursor proteins
  4. Viral protease cleaves precursors into viral proteins
  5. HIV ssRNA and proteins assemble beneat the host cell membrane where gp41 and gp120 are inserted
  6. The membrane buds out forming the viral envelope
  7. Released viral particles complete maturation, remaining precursor proteins are cleaved by viral protease in viral particles
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10
Q

What are the benefits of HIV combo inhibition?

A
  1. Delay drug resistance by slowing HIV replication
  2. Reduces viral load and transmission
  3. Delays the onset of AIDS
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11
Q

HIV portal of entry?

A
  • Infects DC and T cells in Mucosal epithelia of the vagina and rectum
  • DC and T cells are concentrated on the foreskin
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12
Q

How does HIV progress upon transmission?

A
  1. Can directly infect the resting memory CD4+ T cells in vaginal mucosal epithelium
  2. Langerhans take up virus and carry it to draining lymph nodes infecting other T cells
  3. Infected T cells leave lymph nodes and travel lymphatically to blood stream -> viremia
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13
Q

What cells does HIV infect and kill?

A

CD4 helper T cells along with macrophages and DCs

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14
Q

What components can sustain infection?

A
  1. Enlarged LN in 2 areas for 3 months
  2. Integration into host DNA escaping immune response
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15
Q

How does HIV evade the immune system?

A
  1. Downregulates MHC class 1 molecules to protect against cytotoxic T cell
  2. Forms syncytia allowing cell to cell spread
  3. Increased mutations of the env gene lead to changes in the proteins that make up the capsid and spike proteins (surface antigens)
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16
Q

How is HIV maintained through latency?

A

Laten HIV can go undetected allowing clonal expansion of latently infected CD4 T cells not targeted by ART

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17
Q

What is a barrier for an HIV cure?

A

Infected resting memory T cells

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18
Q

How can we diagnose HIV?

A
  1. NAAT detects vRNA and proviral DNA in blood
  2. Immunoassays:
    * Detect HIV-1/2 antibodies in blood and saliva
    * Detect presence of HIV-1 p24 capsid antigen in blood
    * Detect IgM and IgG and p24 antigens
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19
Q

False positive immunoassay results come from?

A
  1. Cross reactivity
  2. Multiple transfusion
  3. Flu vaccine
  4. Autoimmune dx
  5. Improper sample handling
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20
Q

False negative immunoassay results come from?

A
  1. Recent infection
  2. Immunosuppressants
  3. B-cell dysfunction
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21
Q

How do you measure viral load?

A

NAAT

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22
Q

Distinguish the phases of HIV infection (untreated)?

A

Day 0: normal range of CD4+ T cells 500-1500 cells/uL
Stage 1: Acute phase
* Asymptomatic and Symptoms typically begin 2-8 wks. post-exposure
* Viremia: viral load in blood is high
* Viral set point: viral load when CD4+ T cell numbers rebound

Seroconversion: development of antibodies against HIV (e.g. CTL response)
Stage 2: Asymptomatic phase (no outward sx)
Stage 3: AIDs, CD4+ T cells <200 cells/uL, severe immune suppression -> death

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23
Q

How does the body respond to HIV?

A
  1. MHC class I molecules present viral peptides to CD8+ T cells
  2. CTL’s kill infected CD4+ T cells
  3. Anti-HIV antibodies can prevent virions from binding to host cells and induce an NK cell response
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24
Q

What are examples of AIDS-defining conditions?

A

Opportunistic infections and cancer

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25
Q

What is the structure of HSV?

A

Enveloped linear dsDNA viruses

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26
Q

Where are HSV latenet infections located?

A

Nerve ganglia

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27
Q

Describe the growth of HSV?

A

Virions are released by exocytosis, lysis, and spread through syncytia

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28
Q

Where does rapid lytic growth of HSV located?

A

Mucoepithelial cells

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29
Q

What are the groups of HSV? How are they identified?

A

HSV1: cold sores
HSV2: Genital herpes, STD
Varicella zoster: chicken pox and shingles

Identified with NAAT and antibody screening (Zoster)

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30
Q

How is HSV1 transmitted?

A

Saliva containing virions or direct contact with lesions and vertical transmission

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31
Q

Cytopathology of HSV1?

A

Syncytia and necrosis of epithelial cells, cell morphology changes -> vesicular lesion

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32
Q

Where are HSV1 latent infection located?

A

Trigeminal ganglia

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33
Q

Presentations of HSV1?

A
  1. Pustular ulcerative lesions
  2. Ophthalmic herpes
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34
Q

Transmission of HSV2?

A

Direct contact with genital secretions (sexual and vertical)

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35
Q

What is the cytopathology of HSV2?

A

Multinucleate giant cell formation, necrosis, inclusion bodies in neural cells

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36
Q

Where is HSV2 latent infection located?

A

Sacral S2-3 or lumbar ganglia

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37
Q

Presentation of HSV2?

A

Local painful nonsuppurative vesicular lesions

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38
Q

Describe the activity of HSV1?

A
  1. Virus penetrates the epithelial barrier and releases the capsid into the cytoplasm
  2. Capsid moves to nucleus to release DNA and undergo replication
  3. Moves to trigeminal ganglion by innervating neuron and remains latent
  4. DNA converts into nonintegrated circular DNA molecule in the ganglion
  5. Reactivated -> travels through sensory neurons to epidermis -> recurrent infection
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39
Q

Location of latent infection of VZV?

A

Sensory ganglia

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40
Q

Transmission of varicella?

A

Respiratory or ocular routes and direct contact with skin

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41
Q

What is the difference between varicella and zoster?

A

Varicella: chickenpox
Zoster: skingles

42
Q

Describe the activity of VZV?

A
  1. Replication occurs in URT in Tcells -> blood and lymph
  2. Infected T cells then invade other tissues -> secondary viremia -> blister like lesions
  3. Acute itchy eruptions that develop vesicles on skin due to secondary viremia
  4. Virions enter the termini of sensory neuron and move to dorsal root ganglia causing a latent infection
  5. Recurrent varicella infection causes severe pain and dermatomal blister-like rash
43
Q

What is the tissue trophism of hepatitis virus?

A

Liver inflammation -> jaundice, GI sx, N/v, fatigue, fever

44
Q

mechanisms of liver injury in viral hepatitis:

A
  1. Direct cellular injury due to viral replication
  2. Indirect injury due to immune responses against viral antigens
45
Q

Structure of Hep A?

A
  1. Enterovirus of picornaviridae
  2. Non-enveloped icosahedral nucleocapsid
    • sense ssRNA genome
46
Q

Activity of Hep A?

A
  1. Virus enters in the GIT -> liver by blood
  2. Binds to glycoprotein (HAVCR-1) on hepatic cells
  3. Replication in cytoplasm
  4. Translated as one large polypeptide that is cleaved by a virus-encoded proteases to form capsid proteins and virus enzymes (RNA polymerase)
  5. Virions are assembled and released by exocytosis from hepatocytes and enters the bile where it is released in the stool.
47
Q

Transmission of Hep A?

A

Fecal oral, person-person, sexual transmission

48
Q

Describe the pathogenesis of Hep A?

A
  1. Asymptomatic shedding
  2. Long incubation time
49
Q

Clinical presentation of Hep A?

A

Clay colored stool or dark urine, jaundice, Elevated bilirubin and ALT

50
Q

Labs of Hep A?

A

Anti-HAV IgM antibodies
NAAT

51
Q

What is the cause of cellular damage from Hep A?

A

Cell-mediated immune response to the virus:
1. NK cells and cytotoxic T cells -> damage hepatocytes
2. Inflammation of the liver
3. B cells produce IgG antibodies providing lifelong protection

52
Q

What are dxs that derive from hep B?

A
  1. Chronic hepatitis
  2. Cirrhosis
  3. Hepatocellular carcinoma
53
Q

Structure of HBV?

A

Circular dsDNA hepatotrophic virus
* Enveloped icosahedral virium “Dane particle”

54
Q

What are the components of a dane particle?

A
  1. Surface antigens (HBAg) of glycoproteins L, M, and S (HBsAg)
  2. Core antigens: HBcAg, HBeAg
55
Q

Describe the replication process of hep B?

A
  1. HBV attaches to surface of hepatocytes through HBsAgs and a surface bile acid transporter
  2. Virus uncoats and is delivered to the nucleus as a circular dsDNA genome where it is transcribed into mRNA
  3. mRNA is used to make viral enzymes and capsid proteins and is also used to make dsDNA
  4. Uses viral by RNA-dependent DNA polymerase to undergo reverse transcription to cover RNA into DNA within the cytoplasm
  5. Progeny HBV virions are released by budding and also releases HBsAg as a decoy
55
Q

How is HBV transmitted?

A
  1. Blood
  2. Sexual intercourse
  3. Vertical
56
Q

How does HBV lead to infection?

A
  1. Virus enters the blood and infects hepatocytes
  2. Antibodies against HbsAg are generated to neutralize virus used as diagnostic markers
  3. Cytotoxic T cells recognize viral surface antigens (CMI)
  4. Virus replicates in the liver and enters the blood (viremia)
  5. iver damage is due to inflammation and necrosis, caused by CMI (i.e. indirect damage)
57
Q

Chronically HBV patients serve as ____?

A

Reservoir

58
Q

Presentation of acute HBV infection?

A

Preicteric phase: fever, malaise anorexia, nausea
Acute icteric phase: 1-2 months, dark urine, pale stools, jaundice, dark urine

Tender and enlarged liver

59
Q

What causes lifelong immuntity from HBV?

A
  1. Antibodies against HBsAg
  2. Neutralizes virus before it can infect hepatocytes
60
Q

Hep strain that can be prevented by vaccination?

A

Hep B

61
Q

What is fulminant hepatitis?

A
  1. Extensive liver necrosis
  2. high fever, abdominal pain, renal dysfunction, severe liver impairment, ascites form
  3. COinfection with HepD
62
Q

Asymptomatic carriers HBV?

A

have anti-HbeAg antibodies and little to no virions in the blood

63
Q

Chronic persistent hepatitis presentation?

A

Acute hepatitis episodes

64
Q

Chronic active hepatitis presentations?

A

Frequent hepatitis episodes cause liver damage, increased liver enzymes, and bilirubin levels

65
Q

Hep strain that has a higher risk of developing cancer?

A

Hep B

66
Q

How do we screen for HBV?

A
  1. Markers of acute and chronic infection
  2. HBV antigens (triple panel test: HBsAg, anti-HBs, anti-HBc)
  3. Elevation in aminotransferases, billirubin, prothrombin time
67
Q

Structure of HCV?

A
  1. Flavivirus
  2. Enveloped, icosahedral
  3. Two envelope glycoproteins (E1 and 2 that help with viral attachment)
    • sense ssRNA genome
  5. RNA dependent RNA polymerase (error-prone)
68
Q

What are outcomes of having so much variability with HCV?

A
  1. Antigentic variability
  2. Different envelope glycoproteins
  3. High mutation rate
  4. Genotyping for tx protocols
69
Q

How does HCV replicate?

A
  1. Envelope proteins mediate receptor-mediacted endocytosis by binding to CD81 (tetraspanin) on hepatocytes
  2. Virus is uncoated
  3. +ssRNA is released, translated and processed into different viral proteins
  4. Virions are packaged with viral RNA and are released by budding
  5. Replicates in the liver and is then released into the blood (viremia)
70
Q

Transmission of HCV?

A
  1. Contaminated blood
  2. Less Vertical and sexual
71
Q

Lab tests for HCV?

A
  1. Immunoassay to detect anti-HCV antibodies
  2. NAAT to detect presence HCV RNA (qualitative)
  3. NAAT to detect levels of HCV RNA (quantitative)
72
Q

Pathogenesis of HCV?

A
  1. Inhibits interferon response blocking apoptosis of hepatocyte -> mutates quickly
  2. Cytotoxic T cell respond to kill the virus but also damage the liver (indirect damage)
73
Q

Clinical presentation of HCV?

A
  1. Aymptomatic
  2. Acute hepatitis
  3. Chronic hepatitis
  4. Damage is caused by cytotoxic T cell response
  5. Predisposes host to hepatocellular carcinoma
74
Q

What is the difference between flu virus?

A

A: seasonal flu epidemics and pandemics
B: infects humans only and causes epidemics

75
Q

Describe the structure of flu?

A
  • Segmented - sense ssRNA genome allowing genetic reassortment
  • Contains viral RNA polymerase: Transcribes the –ssRNA to mRNA
76
Q

What is reassortment?

A

Occurs when 2 strains of segmented virus infect the same host cell -> stable change in genome

77
Q

What are the membrane proteins of flu?

A
  1. Hemaglutinin (HA)
  2. Neuraminidase (NA)
  3. Matrix proteins 1 and 2 (M1 and M2)
78
Q

Function of hemagglutin?

A
  1. Viral attachment
  2. Binds to host sialic acid on mucous secreting, ciliated epithelial cells
  3. Agglutininates RBCs in clinical blood tests
  4. Target of neutralizing antibodies
  5. Antigenically variable
79
Q

Function of neuraminidase?

A
  1. Facilitates viral release
  2. Cleaves sialic acid on host cell to release progeny virions
  3. Degrades mucous in the respiratory tract
  4. Antigenically variable
80
Q

Function of matrix proteins?

A

M1: virion assembly
M2: serves as an ion channel and involved in uncoating

81
Q

How are influenza subtypes identified?

A

Hemagglutinin and neuraminidase proteins (type-specific antigens)

82
Q

How many subtypes do HA and NA have?

A

HA: 16
NA: 9

83
Q

Portal of entry for flu A?

A

Respiratory

84
Q

How does flu A replicate?

A
  1. Influenza infects mucous secreting ciliated epithelial cells of the respiratory tract
  2. HA binds to sialic acid on surface of host cell and enters cell by receptor-mediated endocytosis
  3. Viral proteins synthesized in the cytoplasm
  4. vRNPS enter the nucleus to combine with new RNA
  5. +strand acts as a template for the viral RNA polymerase to synthesis (-) RNA strand
  6. Host machinery will produce +strand of RNA
  7. As the virion is budding from the membrane HA/sialic interactions hold the virion to the host cell
  8. NA cleaves sialic acid to release viral progeny at the apical cell surface
  9. Promotes cell to cell spread
85
Q

What cause influenza diversity?

A
  1. Antigenic drift
  2. ANtigenic shift
86
Q

Seasonal flu vaccines are based on flu’s antigenic ____?

A

Drift

87
Q

What is antigenic drift?

A

Minor changes based on mutations in RNA genome year to year

88
Q

What is antigenic shift?

A

Major changes in flu A RNA genome that alters H and N proteins -> genetic reassortment of entire segments of RNA genome

89
Q

Lab test for flu?

A
  1. RAT
  2. NAAT to measure viral RNA
90
Q

Type of flu infection?

A
  1. Uncomplicated URTI
  2. Viral pneumonia
  3. Respiratory viral infection followed by a secondary bacterial infection
91
Q

What is the immune response to flu?

A
  1. Cytotoxic T cells work to clear the virus by killing virus infected cells
  2. B cells produce neutralizing antibodies against type-specific antigen hemagglutinin to prevent disease
  3. Antibodies against neuraminidase do not neutralize infectivity, but reduce budding (reducing viral spread)
  4. Influenza vaccine is a killed vaccine containing multiple strains of virus (grown in embryonated eggs)
92
Q

Components of trivalent flu vaccine?

A

2 strains of A and 1 of B

93
Q

Components of quadrivalent flu vaccine?

A

2 strains of A and 2 of B

94
Q

Structure of coronavirus?

A
  1. Enveloped virus with large + sense ssRNA genome
  2. Structure formed by envelope protein (E), membrane protein (M), nucleocapsid protein (N) and spike protin (S)
  3. S protein is involved in attachment to host cells
95
Q

What is SARS CoV 2 binding?

A
  1. Spike glycoprotein homotrimers binds to Angiotensin-Converting Enzyme 2 Receptor (ACE2) on ciliated cells of the nasopharynx or trachea and alveoli
96
Q

Structure of RSV?

A
  1. Enveloped, - sense ssRNA virus
  2. Subtypes RSV-A and RSV-B
  3. Envelope contains 3 surface proteins G, F, and SH
97
Q

Function of RSV surface proteins?

A

G helps attach to host cells
F is responsible for fusion to host cell and syncytium formation
SH improves viral infection through an unknown mechanism

98
Q

Describe the binding of RSV?

A

Binds to ciliated epithelial cells of the airway and type I alveolar cells

99
Q

Transmission of RSV?

A
  1. Respiratory droplets
  2. Direct contact (e.g. kissing infected infant)
  3. Contact with contaminated surfaces and fomites
100
Q
A

Drug Action IV (28 decks)

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