Santosh Review for Block 3 Flashcards

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1
Q

Clinical Diagnosis Parameters for aseptic meningitis in a CSF sample
“A PIN”

A

Antibodies in CSF indicate Aseptic Meningitis

If the:
CSF Ab titre/Serum Ab titre > 1/100

Look for:
- High levels of protein
- Neutrophilic pleocytosis
- Intracellular pathogens

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2
Q

Prion virus:
“RABiD RAPS”

A

Turns Alpha helical PrPc into Beta-pleated PcPsc & it’s resistant to autoclaving & proteases

Causes: CJD
- High PrPsc & Ab in CSF
- Transmissible Spongiform Encephalitis
- Rapidly progressive dementia
- Sporadic

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3
Q

Hep B Serological Markers:

Acute Infection

A

HBsAg (+)
HBsAb (-)
HBcAb-IgM (acute)

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4
Q

Hep B Serological Markers:

Chronic Infection (high vs low inf)

A

HBsAg (+)
HBsAb (-)
HBcAb-IgG (chronic)
HBeAg (+= active rep & high inf)
HBeAb (+=low inf)

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5
Q

Hep B Serological Markers:

Window

A

HBsAg (-)
HBsAb (-)
HBcAb-IgM (acute)
HBeAg (+)

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6
Q

Hep B Serological Markers:

Past inf/recovery

A

HBsAg (-)
HBsAb (+)
HBcAb-IgG (chronic)

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7
Q

Hep B Serological Markers:

Immunized

A

HBsAg (-)
HBsAb (+)
HBcAb (-)

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8
Q

Meanings of Hep B serological markers

A
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9
Q

Retroviruses:
“LiaRS”
Genome

Polymerase type

2 Subfamilies

A

Linear +ssRNA

RDDP (RNA —> DNA provirus)

Oncovirinae (HTLV I/II) & Lentivirinae (HIV)

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10
Q

Epstein-Barr (herpes family)

Features (pathogenesis, infections, trans, & symptoms)

Antigens

Lab Diagnostics

EBV specific infections

A

A
Patho =
It infects B-cells via the C3 receptor site, immortalizing them

Infections = mononucleosis (kissing disease) which is Heterophile POSITIVE or monopile POSITIVE (causes agglutination in the sheep blood)

Trans= spit (active or latent inf)

Symptoms =
- Fever, headache, sore throat, & swollen lymph nodes (neck)
Sometimes causes = Splenomegaly & exudative pharyngitis

Important antigens = viral capsid antigen
Other = Early antigen + nuclear antigen

Lab Diagnostics
- IgM against VCA means an acute infection
- Ab against Early antigens + nuclear antigens is helpful to ID
- non-specific heterophile antibodies are made too

Specific infections:
- Chinese dude = nasopharyngeal carcinoma
- AIDS = lymphomas, oral-hairy leukoplakia (hairy ass tongue), & interstitial pneumonitis
- Burkitts lymphoma = mass on jaw or abdominal disease in little Afro-American kids/young adults

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11
Q

Parvovirus B19
“parvovirus is INSiDe Dusty ACs & EIther Enters From HarmFul air”

Properties (shape, genome, transmission, & effects)

Associated conditions

treat

A

An Icosahedral shaped naked virus that has ssDNA and infects humans

Trans = via airborne droplets to close contacts

Infects = It establishes infection in erythroid cells (adults’ bone marrow & Infants’ liver)

Causes =
- Febrile illness (in blood recipients)
- Aplastic crisis (patients with hemolytic anemia)
- Erythema infectiosum (aka 5th disease in healthy people)
- Hydrops fetalis (congenital infection)

Ass. with conditions =
- Encephalitis
- Neuropathies
- Myocarditis
- Nephritis
- SLE (sys. Lupus erythematosus)
- Henoch-Schonlein purpura (purpura, arthritis, & abdominal pain)
- Rheumatoid arthritis

Treatment =
- *Mainly supportive care
- fever use acetaminophen or ibuprofen
- Itching use a topical anesthetic or antihistamine
- Chronic parvovirus infection, use IV Immunoglobulins (IVIG)
- Aplastic crisis use packed RBC transfusions

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12
Q

Mechanism of action of ACYCLOVIR to treat Herpes

A

It acts against Thymidine-kinase (herpes uses it to replicate)

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13
Q

Hemadsorption
Infected cells with an enveloped virus containing hemagglutinin

A

The virus inserts hemagglutinins in the host’s cell membrane, so when it absorbs RBCs in modified areas of the membrane, it fuels the maturation of progeny viruses
Hemagglutinin tests will show RBCs specifically binding to the infected cells

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14
Q

CSF use in diagnostics
Main diseases it ID

A

CSF normally has little-to-no antibodies, but it’s mainly used to diagnose HSV & VZV encephalitis

If CSF titre/serum antibody titre is greater than 1/100 it means there’s meningitis

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15
Q

Polyomavirus-papovaridae
Human infections
JCV“Dumb JOCK Missed the Pass”
BKV“Bad Kidneys don’t Vent Harsh Chemicals”
MCV
Epi/Pathogenesis
Lab diagnosis & treatment

A

JCV = associated with progressive multifocal leuko-encephalopathy, a rare & fatal disease that causes demyelination. It usually impacts AIDs patients
Features= JCV reactivates & infects the CNS (via the blood), causing cytocidal infection in oligodendrocytes leading to demyelination
Sympt progression =- Early: impaired speech & mental capacity- Later (fast): Paralysis & lost motor capacity- Death: 3-6 months after symptom onset
BKV = Hemorrhagic cystitis in AIDs & nephropathic patients
Features = Urine shedding is super prevalent (more than viremia, it’s 10 times higher than shedding is serum)
Tests=- Serology (seroprevalence is nearly ubiquitous)- Infected renal tubular cells (decoy cells) deteriorate too fast (urine microscopy is limited)
Test = Steroids don’t work; use antivirals (cidofovir)
MCV = Associated with Merkle cell carcinoma, a rare & aggressive form of skin cancer
Epi/Patho =
JCV & BKV: transmitted via droplets via the resp or urine. Patients are typically infected in childhood, and normally, antibodies are made.&The infection spreads from resp + urine to the kidneys, where they can lay dormant in the tubular epi of healthy people
Lab Diag & Treat =
BKV: DNA hybridization in urineJCV: In PM, lesions in brain tissue
No antiviral treatment or vaccines (cause it’s generally asymptomatic)

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16
Q

Adenoviruses
Properties (shape, genome, effects)
Types A-G
A
B “BARs are PerFeCt for Cold Henesy”C “5 CARs CLATter”
D “DESK”
E “ Krusty Fucking EyEs”
F & G “Fucking GAG”
Testing for Adenoviruses
Using them as therapeutics

A

Shape = icosahedral, NAKED, dsDNA its capsid has:
Fibre + penton –> These are host protein receptors that determine the virus’s tissue infectivity
Hexon –> This is the most abundant capsid protein, which is a target for the immune system
Genome = It has a big dsDNA (35kbp), and it encodes its own DNA pol and regulator factors so it can replicate in the nucleus (no lysing + immunity is long-lasting)
Causes =- Hemagglutination (via the fibre capsid protein), so you can use the hemagglutination inhibition test
It infects quiescent cells (non-dividing) to make them divide & its expressed proteins block the host’s immune system/ blocks cytokines (TNFa & interferons), and increases the viruses’ replication/transcription/& translation
Types:
A = Animals only
B = Acute respiratory disease, pharyngeal-conjunctival fever, & hemorrhagic cystitis
C = 5% of acute respiratory infections in children, which can persist as latent infections in the adenoids and tonsils
D = Episodic and sporadic kerato-conjunctivitis (pink eye)
E = Epidemic keratoconjunctivitis and fever
F & G = Acute gastroenteritis
Testing for adenoviruses:
Assessing high levels of neutralizing antibody titer & ELISA (poop analysis)
Adenoviruses as therapeutic agents:- Used as antigen vectors (aka a gene delivery system via replacing deficient genes (Feline immunodeficiency virus), promoting cytotoxicity & amelioration of the disease (reducing its severity i.e. pseudorabies virus)

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17
Q

Viral receptors on host cells & their viruses
“I Pee CHAtteRing with EVery CREep in the HoTtub”
ICAM
CD4
Ach
EGF
CR2/CD21
HVEM
Sialic acid

A

ICAM = intracellular adhesion i.e polio
CD4 = lymphocyte marker (helper) i.e HIV
Ach = neurotransmitter i.e rabies
EGF = growth factor i.e vaccina
CR2/CD1 = complement factor i.e Epstein-Barr
HVEM = TNF-family i.e herpes
Sialic acid = a part of the extracellular glycoproteins i.e Influenza, corona, & reovirus

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18
Q

(-)ssRNA Replication process (Build-a-bitch) (-)–>(+)—>(-)

A

The virion uses the RDRP in its cores cytoplasm for primary transcription of (-)sense RNA to make mRNA, (+)sense RNA, & the replicative complex —> It translates its mRNAs to accumulate products (virion proteins etc) —> the virion proteins interact with the replicative complex to cause it to make more full-length (+)sense RNA intermediates (therefore more genomic/parental (-)sense RNA) —> Secondary transcription happens with the progeny (-)sense RNA (then translation and accumulation of products i.e structural proteins)—-> Finally the nucleocapsid is assembled and matured, as it buds through the host cell’s membrane it will acquire its viral envelope

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19
Q

(+)ssRNA Replication process (Host whores) (+)—>(-)—>(+)

A

The virion translates its RNA into mRNA via the host’s RNA-dependent RNA polymerase —> It then uses a (+) sense template to make (-) sense intermediates via RDRP —> from the intermediate (-) sense it makes both (+) sense & mRNA, which it translates to make proteins —> the proteins, mRNA, & (+) sense RNA are them assembled into mature viruses

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20
Q

CPE inclusion bodies

A

Adenovirus intranuclear inclusion bodies

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21
Q

CPE inclusion bodies

A

Rabies Negri bodies

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22
Q

CPE inclusion bodies

A

HSV Cowdry A bodies

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23
Q

CPE inclusion bodies

A

CMV Owl’s eye inclusions

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24
Q

CPE inclusion bodies:
HPV

A

HP bodies

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25
Q

LCMV (Lymphocytic choriomeningitis virus)

“LCMV StREtcHes MAny PIECes BeFore My REcoveRy”

-Transmission
- Genome/Family
- Lab diagnosis
- Patho
- Treatment

A

Trans:
-Common house mouse
-Vertical transmission from mom (AIDs)
- Organ transplant

Genome: -ssRNA, enveloped/helical
Family: Arenaviridae

Lab:
Clinical history
Serological ELISA
Immunofluorescence assay
PCR

Look for Leukopenia & thrombocytopenia

Patho:
It attaches to host cell receptors via its glycoproteins & causes biphasic febrile illness
(initial: fever/no appetite, head/muscle aches, malaise etc
(later: post-recovery meningitis + encephalitis

Treat:
Supportive care or
Early Ribavirin (IV)

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26
Q

Viral genetics (basics)

+ssRNA VS -ssRNA

A

+ssRNA: Code directly for protein
(+)–> (-) –> (+)

-ssRNA: Comes with its own RDRP for primary transcription
(-) –> (+) –> (-)

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27
Q

Vaccine genetics

Live attenuated vaccines
“live In MY Road Van”

Killed vaccines
“killed RHAT”

Subunit/purified (AIDS approved)
“purIfied HAB”

Virus-like particle vaccine

Protein-polysaccharide conjugate

viral vectored

bacterial/APC vectored

A

Live MMR, Yellow fever, influenza, Rotavirus, VZV etc.

Killed: Rabies, Hep A, Influenza,

Subunit/purified: Influenza, Hep B/A etc.

Virus-like: HPV

PPC: H. influenza B etc

Viral V: Ebola

B/APC: Experimental

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28
Q

Vaccine genetics pathways:

Coronavirus

A

—> Coronavirus invades cell via spike protein & ACE2 receptor (host) binding
—> Virus infuses (via M protein) & its RNA is released in host
—> Viral RNA is translated into proteins
—> Proteins assemble & are released
—> APC ingests virus & helper T-cells activate B-cells (Ab) & CD8 (Attack)

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29
Q

Viral genetics: mRNA vaccines

A

—> mRNA enters the host cell via injection
—> triggers cells to make spike proteins which are recognized by the immune system
—> Lymphocytes make Ab to trigger an immune response

30
Q

Common causes of encephalitis & meningitis are

A

Enteroviruses (Naked icosahedral ssRNA virus)

  • 70 ( hemorrhagic conjunctivitis)
  • **71 ( aseptic meningitis, encephalitis, paralytic poliomyelitis, HFM disease) HIGH PATHOGENICITY
  • 72 (Related to Hep A)

Note:
Polio/cox- encephalitis
Polio/cox/echo- meningitis

31
Q

Coxsackie

A
&
B

A

A: Diffuse myositis, acute inflammation, & necrosis of voluntary muscle
- Herpangina

B: Focal areas of brain degeneration, skeletal muscle necrosis, & changes in inflammation of the pancreas, fat pads, & myocardium
- HFM disease
- Endemic pleurodynia (Bornholm disease)
- Myocarditis
- pancreatitis/diabetes

32
Q

Mumps sequelae (complications)
“DreaMy PyJAMas”

A

Meningitis (15%)
Deafness (rare)
Pancreatitis
Myocarditis
Joint pain/ arthritis (adults)

33
Q

HPV
“PINcH & PoKE”
Serotypes
Oncogenes
Lab findings
Vaccines

A

Serotypes: HPV 16 & 18
Cause cancer in the oropharynx/genitals
&
Condylomata/ venereal warts

Oncogenes:
E6 = Blocks P53
E7 = Blocks PRb

Lab findings:
- Koliocytes (Papanicolaou staining), aka cells with structural changes:
Nuclear enlargement
Irregular membranes
Hyperchromasia
Perinuclear halos

34
Q

Surface receptors of adenoviruses

Fibre
Hexon
Penton

A

Fibre: Mediates hemagglutination

Hexon: target for the immune system (most abundant)

Penton: tissue specificity

35
Q

Hep E

Family/Genome
Transmission source
High-risk patient
Serology markers (acute +chronic)

A

Family: like calciviridae

Genome: +ssRNA, unenveloped virus

Trans-source:
- unclean water & raw shellfish/fruits/vegs

High risk: Preggos
1-3% case fatality rate

Serology:
Acute (+IgM-HEV, High ALT, & virus in poop)

Chronic (+IgG-HEV, Low ALT, & NO virus in poop)

36
Q

Parvovirus

Genome
Main diseases (2)

A

Genome: Naked, Icosahedral +ssDNA virus

Diseases:

1: Erthymatous infectiousum (Slapped cheek syndrome/5th disease)

2: Aplastic anemia/reticulocytosis (Sickle-cell) B19 infects the progenitor erythroid cells

37
Q

Targets for HIV meds

“FIRP”

A

Fusion inhibitors
—>(Block virion binding/entry)

Reverse transcriptase inhibitors
—> (in cyto, they block the translation of viral RNA to DNA)

Integrase inhibitor
—> (in nucleus, they block viral integrase from inserting the viral genome into the host’s DNA)

Protease inhibitor
—> (in cyto, they block proteolytic cleavage of protein precursors so mature virions can’t be assembled)

38
Q

Disease & Drug of choice

Influenza
A, B, C

RSV

Hep B
“LEAThEr”

Hep C

JC

A

Influenza
A= Amantidine, Rimantidine, Oseltamivir, & Zanamivir
B & C= Oseltamivir & Zanamivir

RSV = Ribavirin

Hep B =
- Lamivudine (3TC)
- Emtricitabine (FTC)
- Adefovir
- Tenofovir
- Entecavir

Hep C = Alpha-INF (Pegylated) + Ribavirin

JC = Cidofovir

39
Q

Drugs & diseases

Acyclovir

Ganciclovir

Cidofovir

A

A: HSV, VZV, & some CMV

G: HSV, VSV, & CMV

C: CMV, HSV, HPV, & POX

40
Q

Hep B & C treatments (more detail)

A

B:
Alpha INF (pegylated)
** Lamivudine (nucleoside analogue @ 100mg/day)

  • Adefovir dipivoxil (is nephrotoxic at high doses use 10mg/day)
  • Entecavir (0.5-1 mg/day)

C:
Alpha-INF (pegylated)
+
Ribavirin (Triphosphorylated by the host’s cell, it inhibits MP-ionosine 5’ monophosphate DH to deplete GTP)

41
Q

AZT (Azidothymidine/Zidovudine)
“MY LATe BMS”
Side effects

A

Bone marrow suppression
Lactic acidosis
Myopathy

42
Q

Rabies

Category
Treatment
Labs

A

Catagory III: Transdermal bite (Treat!)

PET (Post Exposure Treatment:
- 5 doses of HDCV at 0,3,7,14, & 28 days post-exposure
- HRIG (Rabies immunoglobulins + equine form) injections most at the wound site, the rest in the glutes

Note: Vaccines are purified

Labs:
Negri bodies

43
Q

Coronavirus “PoRSH”

Genome
Surface proteins
Causes
Treatment

A

Genome: Helical enveloped +ssRNA virus

Surface proteins:
- Spike (mediates attachment)
- E (envelope protein that binds ACE2)
- M (membrane protein)
- N (nucleocapsid protein)

Causes: reps in cyto
- SARS (Asia): binds to ACE2 receptor on the mucosa (atypical pneumonia, fever, non-productive cough, dyspnea, hypoxia, rigors, malaise etc.)
- MERS (Middle-East): binds to CD26 receptor on mucosa
- ARDS
- Cold

Treatment:
- Pfizer
- Astrazeneca
- Mederma
- Johnson/Johnson

44
Q

Hanta virus
“Hanta ERRS”
Family/Genome
Vector
Labs
Diseases

A

Family: Bunyavirus

Genome: Helical enveloped -ssRNA (3 segments) virus

Vector: RAT poop/pee (inhaled)

Labs:
PCR- shows viral RNA in lungs
Serum- IgMAb

Diseases:
- Hantavirus Pulmonary Syndrome/Sin Nombre virus (cough, dyspnea, tachycardia, pulmonary edema, effusion, & hypotension)
- Korean Hemorrhagic fever (shock, headache, petechial hemorrhages, & renal failure)

45
Q

Retroviruses

Genome
2 subfamilies

A

Genome: Linear Icosahedral +ssRNA virus with an RDDP
(RNA–> DNA)

Subfams:
- Oncovirinae (HTLV I/II)
- Lentrivivinae (HIV)

46
Q

HIV

Genome
Patho

A

Genome: Complex/conical +ssRNA virus

Patho: Genes
gag –> p55 –> P17(Matrix), P24(Caspid), P7,9 (other)

pol –> p100 –> Protease, Reverse transcriptase, Integrase

env –> gb160 –> cleaved gb120 (ext. envelope) & gb 41 (transmembrane)

  1. gb120 adheres to CD4 on helper T-cells
  2. gb41 allows membrane fusion/entry

Note the virus binds CD4, CXCR4, & CCR5
People with CCR5
Homozygous = resistant
Heterozygous = longer disease progression time

47
Q

CD4 Counts for HIV

  1. CD4 More than 500
    “5+ Nice stARS”
  2. CD4 between 500-200
    “Pay CHeCK”
A

1.
- Acute retroviral syndrome
- HIV-associated nephropathy (Focal segmented glomerulosclerosis)

    • Oral candidiasis
    • TB & Community acq pneumonia
    • Kaposi’s sarcoma
    • Herpes Zooster
    • Cervical intraepithelial neoplasia
48
Q

CD4 Counts for HIV

  1. CD4 less than 200 (AIDS)
    “2 PoT SHoW”
  2. CD4 less than 100 (AIDS)
    “1 CAFe Latte TSP”
A

3.
- PCP/PJP (Pneumocystis jiroveci pneumoni)
- Sulfamethoxazole & Trimethoprim
- Diss histoplasmosis
- Extrapulmonary TB
- Wasting
- HIV Dementia

4.
- CNS Toxoplasmosis (Rx Sulfadiazine & Pyrimethamine
- Toxo IgG +ve (Prophylaxis Sulfamethoxazole & Trimethoprim)
- CNS Lymphoma
- Cryptococcus (Rx Amphotericin B & Flucystosine/Fluconazole)

49
Q

CD4 Counts for HIV:

  1. CD4 less than 50 (AIDS)
    “50’s PM CRAM”
A

5.
- Non-specific spots, aka disseminated mycobacterium avium intracellulare (Rx Clarithromycin + Ethambutol + Rifabutin) & (Prophylaxis is Azithromycin or Clarithromycin)

  • Disseminated CMV
  • Progressive Multifocal Leukoencephalopathy (JC reaction)
50
Q

HIV

Labs
Best treatment choice & combo

A

Labs:
- 1. ELISA (HIV Abs)
- Western blot (confirms)
- CD4 Count (severity)
- HIV RNA PCR (fast)

Treatment:
2 NRTI (Nucleotide reverse transcriptase inhibitor)
+
1 PI (Protease inhibitor)
OR
1 NNRTI (non-nucleoside reverse transcriptase inhibitor)

51
Q

HIV Protease inhibitor’s side effects

A

All = lipid dystrophy
Atazanavir = Hyperbilirubimia
Fosamprenavir= Hyperlipidemia
Indinavir= Nephrolithiasis
Nelfinavir= Diarrhea
Ritonavir = circumoral paraesthesia & numb extremities
Saquinavir= Central obesity & peripheral wasting

52
Q

HIV NRTI’s side effects
‘‘AFTeR SPiLLeD PiLs”

A

Abacavir = fatal hypersensitivity reaction
Didanosine= Peripheral neuropathy, pancreatitis, & lactic acidosis
Stavudine = peripheral neuropathy, lactic acidosis, & lipodystrophy
Tenofovir = Renal insuff & Fanconi synd

53
Q

Poxviridae:

Molluscum Contagiosum
“EaRNS Kash via RAIDS”

Characteristics

A

-ssRNA with RDRP that replicates in the dermis

Eosinophilic cytoplasmic inclusions (Guarneri/B-type inclusions) in keratinocytes

Dome-shaped rash on trunk/hands/feet in AIDS

54
Q

Smallpox characteristics
“ReCC BalLs”

A

Brick-shaped (inhaled) virus that replicates in the cytoplasm & causes lesions that all look the same

Contraindicated Vaccine (vaccine virus immunoglobulin)

55
Q

Polyomavirus (papovaridae)
- Polyoma causes

  1. JCV
  2. BKV
A
  1. JCV
    - Progressive Multifocal Leukoencephalopathy (demyelinating CNS disease) in AIDS

MRI/CT shows:
- Asymmetrical focal zones of low attenuation (Periventricular + subcortical)
- White matter cytocidal infection of oligodendrocytes

Labs:
DNA Hybridization
PM lesions in the brain

  1. BKV
    - Hemorrhagic cystitis & nephropathy in AIDS

Labs:
Urine microscopy shows Decoy cells & high urine shedding

Treat Cidofovir (IV)

56
Q

Orthomxyovirus (influenzas)

M1/M2 Proteins

A

M1= Matrix protein that’s activated by M2

M2 = Acidifies the endosome to uncoat influenza (pH-dependent membrane fusion) to release activated M1 & Viral RNP’s (replicate to form cRNA and do glycosylation+acetylation in RER)

57
Q

Influenza

Antigenic Shift vs Drift

A

Shift: new strain + Pandemics
Influenza A only (major changes = new strain)

Drift: Epidemics
Influenza A+B (minor changes = varied strains)

58
Q

Influenza genetic reassortment

A

Happens in pigs when avian +human combine in swine to make a reassorted human strain

59
Q

Influenza A

Labs

A

Labs:
- Rapid immunofluorescence (detect Ag in pharyngeal swab)
- Serological ELISA (Ab titre)
- Haemagglutination inhibition test
- RT-PCR
Viral culture

60
Q

Influenza

Treatment

A

A:
Rimantidine + Amantadine
(work against M2)
Oseltamivir + Zanamivir
(Prevent sialic acid destruction & progeny release)

B+C:
Oseltamivir + Zanamivir
(nausea) (exacerbate reactive
airway disease)

61
Q

RSV (Respiratory Syncytial virus)

Family/Genome
Diseases
Patho
Treatment

A

Family: Pneumovirus

Genome: ssRNA

Patho: invades resp epi & causes necrosis of bronchi/ioles to form mucus plugs (fibrin/mucus/debris) which obstruct the narrower airways in kiddos (its big virion is activated by dryness/acid)

Diseases :
- Infant 6-7 months = respiratory distress/atypical pneumonia
- pneumonia
- bronchiolitis
- cold (adults)

Treatment:
- healthy infants = supportive therapy
- AIDS = Ribavirin (guanosine nucleotide analog)
- Pre-mee infants = Palivizumab (Humanized RSV monoclonal AB) to prevent complications of RSV in lungs

62
Q

HSV

Lab
HSV1 vs 2
Space occupying lesions

A

Labs:
- Tzank stain shows Cowdry A bodies & multinucleated giant cells

HSV1: Trigeminal
- Gingivostomatitis
- Diss infection in esophagus (AIDs)
- Herpetic Whitlow

HSV2: Sacral
- Primary/recurrent genital herpes
- Neonatal herpes
- Aseptic meningitis

Space-occupying lesions:
- Fulminant + sporadic hemorrhagic necrosis of the temporal lobes
- Oral vascular lesions

63
Q

Paramyxoviruses (childhood)

Mumps “LiaRS”
- Genome
- Symptoms
- Sequelae (complications)
- Labs
- Treatment

A

Genome: Linear -ssRNA

Symptoms:
- Fever, malaise, parotitis (big ass neck)
- Anorexia, swollen parotid gland
- swollen testicles + orchitis

Sequelae:
- Meningitis (~15%)
- Deafness (rare)
- Pancreatitis
- Myocarditis
- Joint paint + arthritis

Labs:
- PCR
- ELISA

Treatment:
- MMR vaccine ( 3 live attenuated viruses (long-term immunity)

64
Q

Mumps

Sequelae (complications)
patho

A

Sequelae:
- meningitis (~15%)
- Deafness (rare)
- Pancreatitis
- Myocarditis
- Joint pain & arthritis

Patho:
7-10 days = spreads to spleen + lymph
15 days = viremia
18 days = disease

65
Q

Paramyxoviruses (childhood)

Measles
Symptoms
Complications
Labs
Treatment

A

Symptoms (inhales trans)
- Fever, cough, runny nose, conjunctivitis, maculopapular rash (starts at the head and moves down ~14 days) & Kopliks spots (irregular bright-red spots with blue/white center)

Complications:
- Ear infection
- Pneumonia
- Diarrhea
- Post-infection measles encephalitis

Lab:
PCR-Ab (swabs/blood)
Viral isolation on monkey human kidney culture shows giant-multinucleated cells + inclusion bodies)

Treat:
Live attenuated virus MMR (2 dose program (12-15 months) & (8-12yrs)
side effect= pneumonia & atypical measles

66
Q

Parainfluenza

Serotypes & ass condition

Genome

characteristics

A

Serotypes: 1-3

Ass. condition:
Laryngotracheobrochitis (Croup) with SEAL BARKING COUGH

Genome: Large enveloped (-) sense RNA activated via dryness/acid

Characteristics:
- Giant cells & lyse

67
Q

Acyclovir

Composition
Treats
Mech of action

A

Comp: A cyclic nucleoside guanosine analog + active triphosphate moiety

Treats: HSV,VZV, CMV

Mech of action:
—> Thymidine kinase turns it into acyclovir monophosphate
—> cellular kinases then turn it into acyclovir triphosphate
—> Acyclovir triphosphate competitively inhibits Viral DNA Pol & terminates the Viral DNA Chain

Note mutations to thymidine kinase = drug resistance

68
Q

EBV (Epstein-Barr virus)

Genome/Family
Diseases
Patho
Labs

A

Genome: linear dsDNA

Family: HHV4 (Herpesviridae)

Diseases:
- Burkitts lymphoma (mass in jaw)
- Nasal pharyngeal carcinoma (Chinese)
-** Infectious mononucleosis (heterophile & monopile + (agglutination in sheep blood)
- Exudative pharyngitis
- Lymphomas
- Oral-hairy leukopenia (tongue)
-Interstitial pneumonitis

Patho:
- EBV blocks interferon synthesis & binds via viral receptors CR2/CD1 to the complement pathways (CD3)

Labs:
- IgM vs VCA = Acute infection
- Ab vs early Ag ID
- Mononuclear spot

69
Q

Describe each corner of the flow cytometry chart

A
70
Q

Why do we have drugs that target HIV & HEP B?
“RIPE”

A
  • RDDP
  • Incomplete
  • Partial + strand
  • Need enzyme