I&i Exam Ii

Front 1

When is the best time to collect specimen for isolation of viruses?

Back 1

As early in the clinical course as possible (HSV and VZV may not be recoverable as early as 5 days post-onset of Sx)

Front 2

Which swabs are good/bad for virology specimen collection?

Back 2

Good: sterile Rayon or Dacron
Bad: calcium alginate swabs (toxic to enveloped viruses, false(+) with DFA), wooden shafts

Front 3

What is in viral transport medium?

Back 3

Buffered saline
Stabilizers (proteins)
Abx (kill fungi/bacteria)
pH 7.2-7.4

Front 4

How many passes for each cell line?
Primary?
Diploid?
Heteroploid?

Back 4

Primary (PrRMK, RK) - 1-2 passes
Diploid (HDF) - 20-50 passes
Heteroploid (Hep-2/A549) - infinite passes

Front 5

VZV grows best in which cell line?

Back 5

HDF (diploid)

Front 6

Rabbit kidney (primary) is only permissive for which virus?

Back 6

HSV

Front 7

Adenovirus grows best in which cell line?

Back 7

Hep-2/A549 (heteroploid)

Front 8

CMW only grows in which cell line?

Back 8

HDF (diploid)

Front 9

Enterovirus grows best in which cell line?

Back 9

PrRMK (primary)

Front 10

Rhinovirus grows best in which cell line?

Back 10

HDF (diploid)

Front 11

Myxovirus grows best in which cell line?

Back 11

PrRMK (primary)

Front 12

RSV grows best in which cell line?

Back 12

Hep-2/A549 (heteroploid)

Front 13

What are mixed cell lines good for? (Mv1Lu + A549)

Back 13

Respiratory viruses (influenza A/B, RSV, Adenovirus, Parainflu)

Front 14

What are SUPER E-Mix cell lines good for? (BGMK + Decay Accelerating Factor)

Back 14

Detect all known Enteroviruses in single vial

Front 15

What are shell vial cultures good for?

Back 15

EARLY detection (24-48hr) of viruses (eg. CMV, HSV) vs. tube culture methods

Front 16

What is viral identification by Neutralization?

Back 16

(+)ID: neutralizing Abs prevent CPE

Front 17

What is viral identification by DFA staining?

Back 17

(+)ID: fluorescence with mAb conjugated FITC; rapid

Front 18

How do you detect Orthomyxoviruses/Paramyxoviruses in PrRMK?

Back 18

Hemadsorption (expression of hemagglutinin)

Front 19

What is viral identification by Enzyme immunoassay?

Back 19

(+)ID: enzyme-labeled antiviral Abs bind viruses and change color with substrate

Front 20

What is a good DIRECT way to test for Norwalk-like viruses (non-cultivable agents of gastroenteritis)?

Back 20

Immune EM

Front 21

What is viral Ab identification by Hemagglutination Inhibition Assay?

Back 21

Take pt serum with Abs, add virus.

Endpoint: Highest dilution of serum where hemagglutination of RBC's by the added virus occurs.

4-fold increase in titer is serum dilution of 1:80

Front 22

What is considered a positive Western Blot of HIV-1 Abs?

Back 22

1. gp160/120 and p24 (bobble head + core)
2. gp41 and p24 (bobble body + core)
3. gp160/120 and gp41 (bobble head + body)

Front 23

Mnemonics for HIV-1 proteins: gp160, gp120, gp41, p24, p31

Back 23

[Mn] “160 is bobble head doll w/ 120 (head), 41 (body) spanning memb)
[Mn] “kobe is at the core of his team”
[Mn] “instead of turning 31, she reversed and went to 13”

Front 24

What is a good way to detect for TORCH titers? (pernatal infections)

Back 24

IgM Capture Assay for Detection of specific IgM Abs

Front 25

What is a simplified way to define fungi?

Back 25

Non-motile eukaryotes lacking chlorophyll

Front 26

What are some characteristics of fungi?

Back 26

PM contains ergosterol instead of choletersol.
Cell wall composed of chitin and glucans, mannans, polysaccs (no PGNs so not sensitive to PCN)
Insensitive to Abx
Unicellular = "Yeast"
Mulicellular = "Mold"

Front 27

The identification of fungi in the clinical lab is often based on...?

Back 27

Colony morphology.
Yeast cells, pseudohyphae (chains of elongated yeast cells) or hyphae (long filaments).
For filamentous organism, the shape of the asexual sporulation body.
Thermal dimorphism (mold at 25oC, yeast at 37oC)

Front 28

Molds have what distinguishing morphological structure?

Back 28

Hyphae; structurally there are:

Septate hyphae (regular crosswalls/divisions but continuous cytoplasm).

Nonseptate hyphae ("coenocytic"; no crosswalls/divisions)

Front 29

What are the 2 functional types of hyphae in a mold?

Back 29

Vegetative hyphae - the part that holds the nutrients.
Aerial hyphae - the reproductive part (spores)

Front 30

What is fungal dimorphism?

Back 30

Mold (25°C) vs. Yeast (37°C) form based on temperature

Front 31

What is the taxonomy of fungi based on?

Back 31

Structural features of the TELEOMORPH (sexual phase):

Zygomycota - fungi with nonseptate hyphae.
Ascomycota - includes most human pathogens (septate fungi, asexual spores, myotic spores)
Basidiomycota - mainly saprobes or plant pathogens.
Deuteromycota - no sexual spores

Front 32

Which antifungal drugs disrupt ergosterol?

Back 32

Amphotericin B (gold std), nystatin, azoles, allylamines

Front 33

Which antifungal drugs inhibit RNA/DNA synth?

Back 33

5-Fluorocytosine

Front 34

Which antifungal drugs inhibit mitosis?

Back 34

Griseofulvin

Front 35

Which antifungal drugs inhibit synth of glucans in cell wall?

Back 35

Echinocandins (active against Aspergillus, Candida)

Front 36

What is a dermatophyte?

Back 36

Keratinolytic fungi = use keratin as nutrient source (colonize stratum corneum).

Eg. orgs that cause Tinea

Front 37

What does dematiaceous mean?

Back 37

"Dark-colored fungi"

eg. Chromoblastomycosis
eg. Phaeohyphomycosis

Stain with Fontana-Masson Stain for Melanin.

Front 38

What are the superficial (cutaenous) mycoses?

Back 38

Piedra
Pityriasis versicolor (Tinea versicolor)
Dermatophytes (Tinea)
Onychomycosis (nails)

Tx: topical antifungals

Front 39

What is Piedra?

Back 39

Superficial/cutaneous fungal infxn: Hair shaft

Caused by:
Piedraia hortae (black) - scalp
Trichosporon beigelii(white) - beard

Front 40

What is Pityriasis (Tinea) versicolor?

Back 40

Superficial/cutaneous fungal infxn: Epidermis (chest/back)

Caused by: Malassezia spp. - dimorphic, lipophilic, linked to dandruff

Malassezia furfur - life-threatening enteric infxn in neonates

Front 41

What is Tinea (ringworm)?

Back 41

Superficial/cutaneous fungal infxn: Keratinized tissues

Caused by: Dermatophytes: Trichophyton tonsurans

mc fungal infx in peds

Front 42

What is Onychomycosis

Back 42

Superficial/cutaneous fungal infxn: Nails

Caused by: Candida and Dermatophytes

Front 43

What are the subQ mycoses?

Back 43

Mycetoma (Eumycetoma)
Chromoblastomycosis
Sporotrichosis
Lobomycosis
Rhinosporidiosis

Front 44

What is Eumycetoma?

Back 44

SubQ fungal infxn:

Chronic granulomatous infxn, swelling, deformity, sinus drainage, bone destruction

Caused by: saprophytic fungi (Pseudoallescheria boydii)

Tx: surgical debridement/amputation

Front 45

What is Chromoblastomycosis?

Back 45

SubQ fungal infxn:

Cauliflower lesions on lower extremities of agricultural men

Caused by: Dematiaceous fungi

Tx: cryosurgery, topical antifungs

Front 46

What is Sporotrichosis?

Back 46

SubQ fungal infxn: mc cutaneous myocosis in US → spreads to subQ.

"Rose gardener's Disease"
Follows lymphatics (lymphocutaneous lesions)

Caused by: Sporothrix schenckii in immunocompr (DIMORPHIC)

Tx: azoles

Front 47

What are the dimorphic fungi?

Back 47

Blastomyces dermatitidis,
Histoplasma capsulatum,
Coccidioides immitis,
Paracoccidioides brasiliensis,
Penicillium marneffei,
Sporothrix schenckii

Front 48

What is Lobomycosis?

Back 48

SubQ fungal infxn:

Keloidal lesion, granulomatous inflammatory tissue

Caused by: Loboa loboi

Tx: excision

Front 49

What is Rhinosporidiosis?

Back 49

SubQ fungal infxn: mucous memb (nose/eye/ear/larynx)

Chronic granulomatous infxn

Caused by: Rhinosporidium seeberi (protozoa)

Tx: excision

Front 50

What is Phaeohyphomycosis?

Back 50

Dematiaceous fungi infxn that can be superficial, cutaneous, subcutaneous or systemic (immunocompr).

eg. darkly pigmented fungal structures in brain bx

Front 51

What are the systemic OPPORTUNISTIC fungi?

Back 51

Candida spp.
Aspergillus fumigatus
Cryptococcus neoformans
Pneumocystis carinii (jiroveci)
Penicillium marneffei

Front 52

What are the systemic PRIMARY fungi?

Back 52

Blastomyces dermatitidis
Histoplasma capsulatum
Coccidioides immitis
Paracoccidioides brasiliensis

Front 53

Currently, opportunitis fungi infxns are increasing in number, why?

Back 53

New susceptibilities: HIV, transplants, cancer

Front 54

Candida spp?

Back 54

OPPORTUNISTIC systemic fungal infxn: part of nl flora,

Leads to:
1. Muco-cutaneous candidiasis (from nl flora)
2. Disseminated candidiasis (from catheters, wounds→biofilms)

Front 55

Aspergillus fumigatus?

Back 55

OPPORTUNISTIC systemic fungal infxn:

Can grow at high temps (50°C).
Leads to:
1. ABPA, Allergic BronchoPulmonary Asperogillosis (IgE-mediated asthma with immune complex deposition)
2. Invasive fungal ball, lung hemorrhage
High mortality

Front 56

Cryptococcus neoformans?

Back 56

OPPORTUNISTIC systemic fungal infxn:

Pigeon droppings
AIDS-defining illness

Leads to: Meningocephalitis (mc presentation)

Hallmark: India ink (halo) stain of CSF from its capsule

Front 57

Pneumocystis carinii (jiroveci)?

Back 57

OPPORTUNISTIC systemic fungal infxn:

AIDS-defining illness
Usu colonizes lung at birth but cleared in immunocompetent

Front 58

Penicillium marneffei?

Back 58

OPPORTUNISTIC systemic fungal infxn: (DIMORPHIC)

Soluble red pigment diffuses into agar

Front 59

Blastomyces dermatitidis?

Back 59

PRIMARY systemic fungal infxn: (DIMORPHIC)

"Chicago Disease"

Diffuse pneumonitis and ARDS
Culture @ 30°C

Can convert to yeast form in body = unsusceptible to macrophages and not contagious

Front 60

Histoplasma capsulatum

Back 60

PRIMARY systemic fungal infxn: (DIMORPHIC)

Bat guano
Prevents phago-lysosomal fusion in host cells (lives in macs)
Influenza-like illness, resembles TB (cavitations)
Oral lesions

Front 61

Coccidioides immitis?

Back 61

PRIMARY systemic fungal infxn: (DIMORPHIC)

Arthroconidia easily inhaled
In tissue (37°C), forms spherule/sporangia filled with endospores.

SW US, Mexico

Front 62

Paracoccidioides brasiliensis

Back 62

PRIMARY systemic fungal infxn: (DIMORPHIC)

"Captain's wheel" morphology on stain
Ulcerative lesions (face, GI mucosa)

Front 63

What are the 3 impt HIV enzymes?

Back 63

RT
Protease (modify transcribed proteins to become fully fxnal)
Integrase (integrate viral provirus into host genome)

Front 64

What 2 major human cells does HIV infect and what do they have in common?

Back 64

CD4+ T cells
Macrophages

They both have CD4

Front 65

Explain HIV entry into host cells.

Back 65

gp120 binds CD4 → virion conf change → expose gp120 → bind chemokine receptor → allows gp41 to penetrate membrane and lead to fusion

Front 66

Name the impt host chemokine receptors for HIV entry into cells.

Back 66

CCR5 - used to ID/infect macs
CXCR4 - used to ID/infect CD4+ T cells

CCR5 mutations = resist HIV infxn!

Front 67

Why are concomitant infxns with HIV so bad?

Back 67

HIV LTRs (on both ends of HIV genome) have NK-kB binding sites.

Any activation of immune system (bact, viral, vaccine) can stim T-cells → ↑NK-kB (TF) → stim replication/pathogenicity of HIV genome

Front 68

What are the EARLY HIV genes? (regulatory)

Back 68

tat - trxn of other genes
rev - exports immature RNAs (Rev Responsive Elements) out of nucleus, req'd for late genes
nef - activates T-cells, downregulates CD4, MHCI

Front 69

What are the LATE HIV genes? (structural)

Back 69

gag - internal capsid
pol - 3 impt enzymes: RT, protease, integrase
gag/pol - due to ribosomal fram-shift
env - envelope (gp120/gp41)

Front 70

What is APOBEC3G?

Back 70

Host antiviral protein; induces mutation in viral DNA (C→U) so that the virus can't replicate

Only works in Vif(-) HIV.
HIV that are Vif(+) degrade APOBEC3G.

Front 71

What are the important helper T cell cytokines in normal viral infxns and what happens in HIV?

Back 71

Th1 - produce IL-2, IFN-γ → help CTLs (CD8+) to kill infected cells

Th2 – produce IL-4 → help B-cell produce neutralizing Abs

HIV kills these helper T cells

Front 72

What is the timecourse of HIV-1 infxn?

Back 72

-2-6 wks: Flu-like Sx
-~10yrs: aSx phase (depletion of CD4 -T cells)
-Symptomatic phase
-AIDS: CD4<200 (opportunistic infxns)

Front 73

What is the origin of HIV-1?

Back 73

Cross-species transmission of Simian Immunodeficiency Virus

Front 74

2 impt viral wapons for HIV:

Back 74

Integrase: can establish latent infxns
RT: error-prone enzyme (muts)

Front 75

Name a complication/syndrome of HAART.

Back 75

Immune reconstitution inflammatory syndromes - reestablishing your immune system causes you to detect/attack latent infxns

Front 76

Orthomyxoviruses: Genome, Transmission, Clinical.

Back 76

(-)ssRNA

Transmxn:resp secretions

Clinical: first URT then LRT; high fever, tiredness, m ache, HA

Front 77

What are the 3 types of Influenza virus?

Back 77

Type A: Ag shift/drift
Type B: Ag drift only
Type C: Ag drift only

Front 78

Structure of influenza virus

Back 78

Spikes:
HA (80%) - binds SA, endocytosis
NA (20%) - cleaves SA

M1 - packaging of RNA, budding
M2 - ion ch involved in penetration

Front 79

What are influenza virus' pathogenic talents?

Back 79

Cap stealing - viral endonuclease steals host cap and transfers it to viral mRNA
High mutatation/recombo rate of ssRNA
Molecular evolution due to selective pressures

Front 80

What is Antigenic Drift? (influenza)

Back 80

Minor changes → seasonal epidemics

Front 81

What are the important helper T cell cytokines in normal viral infxns and what happens in HIV?

Back 81

Th1 - produce IL-2, IFN-γ → help CTLs (CD8+) to kill infected cells

Th2 – produce IL-4 → help B-cell produce neutralizing Abs

HI kills these helper T cells

Front 82

What is the timecourse of HIV-1 infxn?

Back 82

-2-6 wks: Flu-like Sx
-~10yrs: aSx phase (depletion of CD4 -T cells)
-Symptomatic phase
-AIDS: CD4<200 (opportunistic infxns)

Front 83

What is the origin of HIV-1?

Back 83

Cross-species transmission of Simian Immunodeficiency Virus

Front 84

2 impt viral wapons for HIV:

Back 84

Integrase: can establish latent infxns
RT: error-prone enzyme (muts)

Front 85

Name a complication/syndrome of HAART.

Back 85

Immune reconstitution inflammatory syndromes - reestablishing your immune system causes you to detect/attack latent infxns

Front 86

Orthomyxoviruses: Genome, Transmission, Clinical.

Back 86

Genome:(-)ssRNA
Transmxn:resp secretions
Clinical:first URT then LRT; high fever, tiredness, m ache, HA

Front 87

What are the 3 types of Influenza virus?

Back 87

Type A: Ag shift/drift
Type B: Ag drift only
Type C: Ag drift only

Front 88

Structure of influenza virus

Back 88

Spikes:
HA (80%) - binds SA, endocytosis
NA (20%) - cleaves SA

M1 - packaging of RNA, budding
M2 - ion ch involved in penetration

Front 89

What are influenza virus' pathogenic talents?

Back 89

Cap stealing - viral endonuclease steals host cap and transfers it to viral mRNA
High mutatation/recombo rate of ssRNA
Molecular evolution due to selective pressures

Front 90

What is Antigenic Drift? (influenza)

Back 90

Minor changes → seasonal epidemics.

eg. errors in RNA replication

Front 91

What is Antigenic Shift? (influenza)

Back 91

Major changes → pandemics

eg. recombination with other strains

Front 92

What is the H & A variant of Avian Flu?

Back 92

H5N1, very high mortality rate, strong environmental survival

Front 93

What is the flu vaccine production timeline?

Back 93

Jan-May: Virus selection and production
Summer: FDA approval and packaging
Fall: Vaccination

Vaccines are usu an inactivated vaccine

Front 94

Paramyxoviridae: Genome, Major genera, Unique features

Back 94

(-)RNA

Morbillivirus (measles)
Paramyxovirus (parainfluenza)
Rubulavirus (mumps)
Pneumovirus (RSV)
Henipaviruses (Nipah and Hendra virus)

Abs are not effective bc can spread directly from cell-to-cell via host cell fusions (cell-mediate immunity is critical!!)

Front 95

Paramyxoviridae: Morbillivirus (measles): Genome, Hallmarks, Complications

Back 95

(-)RNA

Koplik spots (white spots on buccal mucosa) maculopapular rash that starts on head and spreads

Live attenuated vaccine is good

Complications: Subacute sclerosing panencephalitis (Δmental, spasticity, blindness)

Front 96

Rubulavirus (mumps): Genome, Hallmarks

Back 96

(-)RNA

Parotitis (salivary glands), orchitis, meningoencephalitis

MMR vaccine: 95% lifelong imm

Front 97

Pneumovirus (RSV): Hallmarks

Back 97

Rales (auscultation), CXR hyperexpansion, patchy infiltrates;
NO viremia/systemic spread; syncytia formation (multinucleated "giant cell"), immunity doesn't protect against reinfxn

Infants: Pneumonia/bronchiolitis
Adults: URT Infxn

Front 98

Paramyxoviridae: Paramyxovirus (parainfluenza): Genome, Hallmarks

Back 98

(-)RNA

Limited to resp tract (URT), NO viremia/systemic spread

Front 99

Henipaviruses (Nipah and Hendra virus): Genome, Hallmarks

Back 99

(-)RNA

Hendra/Nipah more closely related to eachother (70-80%) than other paramyxo's (50%)

Extended Zoonotic virus:
Hendra - bats, horses
Nipha - bats, pigs

Front 100

Rhabdovirus: Lyssavirus (rabies): Genome, Hallmarks, Tx

Back 100

(-)ssRNA

Hydrophobia, anxiety, cardiac arrest, Negri inclusion bodies in brain, long incubation phase bc virus takes longer to replicate in muscle

Tx:pre/post-exposure before Sx (if symptomatic, only supportive care)

Front 101

Togavirus, Flavivirus: ArBoviruses: Genome, Hallmarks

Back 101

(+)ssRNA = "capped" mRNA

Togavirus - Equine Encephalitis
Flavivirus - Dengue & Yellow Fever, West Nile

Cytolytic, arthropod-borne, systemic/viremia, can induce host IFN

Some vaccines, otherwise supportive care

Front 102

Togavirus: Rubella virus: Genome, Hallmarks

Back 102

(+)ssRNA = "capped" mRNA

Resp virus that ONLY infects humans

Fetus: severe congenital defects
Children: rash, lymphadenopathy
Adults: bone/joint pain, thrombocytopenia, encephalitis

Front 103

HBV: Genome, Hallmarks, Complications, Vaccine, Tx

Back 103

Circular, partially dsDNA, enveloped

Jaundice

Outcome based on age of infxn
Birth: aSx, chornic, no anti-HBs
Adult: Sx, not chronic, anti-HBs (resolution)

Complications: cirrhosis, hepatocellular carcinoma (5yr survival 3%)

Vaccine: 3 shots, long-lasting
Tx: (NOT curative, but helps liver regen) - IFN, nucleoside analogues

Front 104

HDV: Genome, Hallmarks

Back 104

Circular ssDNA, enveloped

Obligatory coinfxn with HBV, "superinfxn" when HDV happens on top of a CHRONIC HBV infxn

Again anti-HBs is the key to resolution in acute coinfxn

Front 105

Adenovirus: Genome, Hallmarks, Impt genes

Back 105

linear dsDNA, non-enveloped = lytic

Disease (serotype):
Resp (4/7), conjunctivitis (8), gastroenteritis (11), cystitis (40/41)

Can persist and reactivate

E1A – inhibits host pRB (TSG)
E1B – inhibits host p53 (TSG)
E2 – pol/replication
E3 – immune evasion
L1-L5 – Late proteins (structural)

Front 106

Parvovirus: Erythrovirus B19: Genome, Hallmarks, Complications

Back 106

(+)DNA and (-)DNA

Child: Erythema infectiosum - "Fifth / Slapped Cheek Disease"
Adult: arthritis
Infects nasopharynx, URT, BM (RBC precursors, anemia)

Complications:
Aplastic anemia in sickle cell pts
Chronic anemia in immunocompr
Hydrops fetalis in pregnancy

Front 107

Papovovirus: Papillomavirus: Genome, Hallmarks, Impt genes, Vaccine

Back 107

Circular dsDNA

Tropism to stratified squamous epith
HPV16, 18, 31 → cervical cancer

E6/E7 inhibits p53/pRB (TSGs)

Gardasil against HPV6/11/16/18

Front 108

Papovovirus: Human Polyomavirus: 2 types

Back 108

JC - Progressive Multifocal Leukoencephalopathy (PML) in HIV
BK - hemorrhagic cystitis in BM transplant, ureter stenosis in renal transplant

Front 109

Picornaviruses: Genome, Impt ones

Back 109

(+)ssRNA = "capped mRNA," non-enveloped = lytic

Enterovirus (Poliovirus) - bind CD55
Rhinovirus - bind ICAM-1

Front 110

Picornavirus: Poliovirus: Genome, Hallmarks, Vaccine

Back 110

(+)ssRNA

Fecal-oral transmxn, lots of serotypes, Sx depend on secondary target tissue

90% aSx > resp/gut > meningitis > poliomyelitis > paralytic disease

UMN: Bulbar poliomyelitis
LMN infx: Paralytic poliomyelitis
mm deterioation: Postpolio syndrome

Polio enterovirus vaccine (no non-polio enterovirus vaccines):
Salk - inactivated, 4xIV
Sabin - attenuated, oral=easy

Front 111

Picornavirus: Rhinovirus: Genome, Hallmarks, Tx

(Respiratory viruses)

Back 111

(+)ssRNA

Lots of serotypes!, mcc common cold, limited to resp tract due to acid sensitivity (inactivated pH<6) and grows better in colder temp in lung (33°C) vs. GI;

I-CAM-binding receptor is hidden in groove, not recog'd by Abs

Tx: cough suppressant, decongestant, fluid/rest (No Abx or antihistamines)

Front 112

Coronavirus (SARS): Genome, Hallmarks

(Respiratory viruses)

Back 112

(+)RNA, largest RNA virus, has 5'cap/polyA tail, synthesizes nested set of subgenomic RNAs, enveloped, glycoprotein "corona" is protective in intestine

Coronaviruses (a/w enteric infxn) are URTI (2nd mcc common cold after Rhinovirus), but SARS can also cause serious LRTI

SARS begins with ssytemic Sx (high fever >38°C!!), followed by resp Sx (infiltrates)

Supportive care

Front 113

Reovirus: Rotavirus: Genome, Hallmarks

(Respiratory viruses)

Back 113

Segmented dsRNA, non-enveloped, two-layer capsid

Single most important cause of severe diarrheal illness in young (lots of virus in stool)
R(resp), E(nteric), O(rphan) virus

Two-layer capsid (non-infxs), cleaved in GI and can infect enterocytes

Vaccine, Supportive care

Front 114

Flavivirus: HCV: Genome, Hallmarks, Tx

Back 114

(+)RNA, enveloped, quasispecies (Abs don't protect against recurrent)

Acute: 70% aSx > jaundice, LFT
Dx: Bx (gold std)
Global challenge: No preventative vaccine, Tx ineffective, leads to CHRONIC infxn → hepatitis, steatosis, insulin-resistance, cirrhosis

Transmxn (blood): IV drug use > sex

Tx:
Genotype 1a/1b don't respond to IFN
Genotype 2/3 respond to IFN
Genotype 3a → steatosis
Transplant

Front 115

Picornavirus: HAV: Genome, Hallmarks, Vaccine

Back 115

(+)ssRNA, non-enveloped, 1 serotype

mcc acute viral hepatitis > HBV > HCV; replicates slowly without direct CPE
Fecal-oral, jaundice more severe >14yo; no chronic sequelae (only acute)

Acute/current infxn: anti-HAV-IgM
Past infxn: anti-HAV-IgG

Pre-exposure: Vaccine, Ig (travelers)
Post-exposure: Ig

Front 116

What are the 8 HHV?

Back 116

HSV1
HSV2
VZV
CMV
HHV6
HHV7
EBV
Kaposi's Sarcoma assoc HV (HHV8)

Front 117

What are the differences between the 3 groups of HHV?

Back 117

α – short replication cycle
β – long replication cycle
γ – generally infects immune cells (eg. B cells)

Front 118

HHV: HSV1/2: Genome, Hallmarks, Impt genes, Complications, Tx

Back 118

dsDNA, α (short replication cycle)

Prevalence: HSV1 > HSV2
HSV1 - oral/eye
HSV2 - genital

Lytic and Latent cycles
Acute/lytic: VP16 gene - master ctrl gene that turns on gene expression

Latent: viral DNA remains as episome in ganglionic cells (antiviral drugs ineffective here)

Immunocompr - disseminated infxn, CNS, HSV can enhance HIV acquisition

Tx: acyclovir - targets HSV-1 thymidine kinase to stop DNA elgonation

Front 119

HHV: VZV: Genome, Hallmarks, Tx

Back 119

dsDNA, α (short replication cycle)

Primary: Varicella - mostly children, rash
Reactivation of latent from DRG: Zoster - pain along affected nerves

Tx: acyclovir

Front 120

HHV: EBV: Genome, Leads to 4 diseases, Hallmarks, Tx

Back 120

dsDNA, γ (infects immune cells)

Acute: in epith cells
Latent: in B-lymphocytes (can cause immortalization here → malignancy)

Leads to:
1. Infectious mononucleosis (Heterophile Abs; Triad: lymphadenopahty, splenomegaly, pharyngitis)
2. Burkitt's Lymphoma (t(14;18), c-myc)
3. Nasopharyngeal Carcinoma
4. Hair oral leukoplakia in AIDS

Supportive care (no Abx/vaccine), life-long immunity

Front 121

HHV: HHV8/Kaposi's Sarcome-associated HV: Genome, Hallmarks

Back 121

dsDNA, γ (infects immune cells)

Found in AIDS-related B-cell lymphomas

Front 122

HHV: CMV: Genome, Hallmarks, Tx

Back 122

dsDNA, β (long replication cycle)

OI, latency in leukocytes, 80% of all adults have CMV Abs, Owl eye inclusions

1. Cytomegalic inclusion disease - mc viral cause of congenital defects
2. CMV mononucleosis
3. CMV retinitis, pneumonia (immunocompr)

Tx: Gancyclovir and Foscarnet – inhibit CMV DNA pol

Front 123

Name a strategy of immune evasion (1)

Back 123

Ag variation

S. pneumonia: lots of subtypes that differ in capsular polysaccs
Influenza virus:
Ag drift - mutations in H epitopes → seasonal
Ag shift - reassortment b/w strains → pandemics

Front 124

Name a strategy of immune evasion (2)

Back 124

Latency - for escaping eradication and for reactivation

HSV: hides in sensory neurons (also VZV, EBV)
M. tuberculosis - hides in macs

Front 125

Name a strategy of immune evasion (3)

Back 125

Manipulation of immune system - resistance to immunity

M. tuberculosis: prevents phagosome-lysosome fusion (hids in macs)

Front 126

How does HIV avoid immune response?

Back 126

Avoid Abs;
1. HIV envelope is heavily glycosylated
2. gp41 is masked until CD4 is engaged by gp120
3. high mutation rates (RT)

Avoid CTLs
1. Downregulate MHCI
2. Tat/Rev system turbocharges HIV gene expression
3. Virions can be released b4 immune recog

Chen's research:
Mutation in CTL epitope of AIDS helps it escape MHCII

Front 127

Filovirus: Genome, Genera, Hallmarks

Back 127

Linear (-)ssRNA

Marbug virus
Ebola virus

Leads to: severe hemorrhagic fever

Host fruit bats don't die bc they carry PKR (dsRNA-dep protein kinase R)

Front 128

Poxvirus (Smallpox): Genome, Hallmarks

Back 128

dsDNA, replicates in cytoplasm

Guarnieri inclusion bodies

Smallpox (vs. Chicken Pox):
1. Rash on lower extrem (face/trunk)
2. Vesicles appear all at same time (diff stages)

Front 129

Bunyavirus: Genome, Hallmarks

Back 129

(-)ssRNA

Transmission via Aedes mosquito in California encephalitis
Hanta virus (no insect vector, a/w rodent feces)

Front 130

Areavirus: Genome, Hallmarks, Tx

Back 130

(-)ssRNA, ambisense RNA that fxn as both (+) and (-)

Rodent feces/urine
Infects Macs → activate T cells → tissue damage due to T-cell-mediated inflamm

Non-fatal: Lymphocytic choriomeningitis
Fatal: Lassa fever, Machupo, Junia

Tx – Ribovirin

Front 131

- What is a key charac of picornaviruses that contrib. to ability to be transmitted effic via oral fecal rotue?

Back 131

o Nonenveloped viruses with relatively stable capsid

Front 132

- When delivered to cyto of a permissive host cell, the genome of picornaviruses:

Back 132

o These are positive strand so….. serve as template for host ribosomes to translate the viral proteins

Front 133

- Enteroviruses are one of several groups of viruses which gain access to human body thru GI. However, rarely cause GI disease and in fact cause wide range of diff clinical manifestations. Why do these viruses cause a wide variety of disease syndromes?

Back 133

o The secondary target tissues to which specific enteroviruses spread and replicate are different.

Front 134

- Frustrated teacher comes in with 3rd rhinovirus infxn of year. Why does she keep getting it?

Back 134

o Reinfxn is common cuz there are >100 serotypes.

Front 135

- Which of the following viruses is hep A most closely related to?

Back 135

o Poliovirus (picornavirus)
HAV is a Picornavirus

Front 136

- 14 yo with acute illness with jaundice, fatigue, nausea and tests indic elev ALT. what form of viral hepatitis do you suspect he has contracted?

Back 136

o Hep A: distinguishing feature is acute

Front 137

- Of the following chronically infected Hep C pts, which statistically has highest probability of achieving SVR (sustained viral response) in response to combo therapy with IFN and ribavarin?

Back 137

o 30yo Caucasian female infected with genotype 2a

Front 138

- HBsAg negative person comes into clinical complaining that she has chronically felt tired with ab discomfort, loss of appetite and digestive disturbances for years and now appears jaundice. Blood transfusion in 1991. What hep virus?

Back 138

o Hep C

Front 139

- To avoid flu virus spread the use of a regular face mask ...

Back 139

o May offer reasonable protection

Front 140

- 3 mo infant presents with 3 day Hx of fever, cough and poor feeding. On exam, baby appears ill and temp of 102 and RR 32. CXR shows bilateral patchy infiltrates in lungs. Which is most likely etiologic agent?

Back 140

o Respiratory syncytial virus (infants under 1yo RSV is most common cause of pneumonia like symptoms)

(Corona and Rhinoviruses stay in upper resp tract so not that)

Front 141

- 1yo had common cold but now has voice that is hoarse and cough= that sounds harsh and brassy and worse at night. On exam, child has trouble drawing air into lungs btwn coughs and trouble drawing air into lungs. Visible stridor on inhalation. Most likely to be...

Back 141

o Parainfluenza

Front 142

- Which of the following disease can be prevented by vaccine except:

Dengue, Measles, Polio, Rubella, Flu

Back 142

o Dengue fever

Front 143

- Vaccination strategy for child born to chronic carrier mother (Hep B)

Back 143

o 3 Hep B vaccine (0, 1, 3 mo) + HB Ig

Front 144

- What determines if a newborn will become a chronic carrier or not

Back 144

o Viral load of mother

Front 145

- Antiviral Tx for Hep B:

Back 145

o IFN
o Nucleoside analogs: target reverse transcriptase

Front 146

- Who gets hep D infxn?

Back 146

o Those with hep B
o Coinfected: worse than Hep B alone.
o Superinfected: get worse and stay worse

Front 147

- Chronic HBV criteria:

Back 147

o longer than 6 mo with HBsAg circulating

Front 148

- Why does geographic distrib of hep B matter?

Back 148

o People are travelling to those areas.
o Carriers.

Front 149

- Chronic Hep B rates going down because:

Back 149

o vaccines.

Front 150

- How do you get hep B?

Back 150

o Bloooooooooooooooooooooooood

Front 151

- What are the important reqts for HIV-1 entry into target cells?

Back 151

o Receptor is CD4rec
o CCR5,CCL4 are coreceptors

Front 152

- What is the consequence of HIV 1 infxn?

Back 152

o Cd4 drops cuz this is the target.
o Also macrophages are infected but for some reason the functional aspect is not as striking as CD4 T cell.

Front 153

- Why does T cell activation lead to inc in HIV replic—molecular mech?

Back 153

o Infection causes T cell activation and this is what HIV targets CD4 T cells so it increases.
o 2 binding sites for NF-kB

Front 154

- How does HIV establish latency?

Back 154

o Integrate its DNA into host.

Front 155

- What is the possible mech whereby swine flu virus H1N1 evolves?

Back 155

o Antigenic shift. Segments changed through recombination