Santosh Review for Block 3 Flashcards
Clinical Diagnosis Parameters for aseptic meningitis in a CSF sample
“A PIN”
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
Prion virus:
“RABiD RAPS”
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
Hep B Serological Markers:
Acute Infection
HBsAg (+)
HBsAb (-)
HBcAb-IgM (acute)
Hep B Serological Markers:
Chronic Infection (high vs low inf)
HBsAg (+)
HBsAb (-)
HBcAb-IgG (chronic)
HBeAg (+= active rep & high inf)
HBeAb (+=low inf)
Hep B Serological Markers:
Window
HBsAg (-)
HBsAb (-)
HBcAb-IgM (acute)
HBeAg (+)
Hep B Serological Markers:
Past inf/recovery
HBsAg (-)
HBsAb (+)
HBcAb-IgG (chronic)
Hep B Serological Markers:
Immunized
HBsAg (-)
HBsAb (+)
HBcAb (-)
Meanings of Hep B serological markers
Retroviruses:
“LiaRS”
Genome
Polymerase type
2 Subfamilies
Linear +ssRNA
RDDP (RNA —> DNA provirus)
Oncovirinae (HTLV I/II) & Lentivirinae (HIV)
Epstein-Barr (herpes family)
Features (pathogenesis, infections, trans, & symptoms)
Antigens
Lab Diagnostics
EBV specific infections
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
Parvovirus B19
“parvovirus is INSiDe Dusty ACs & EIther Enters From HarmFul air”
Properties (shape, genome, transmission, & effects)
Associated conditions
treat
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
Mechanism of action of ACYCLOVIR to treat Herpes
It acts against Thymidine-kinase (herpes uses it to replicate)
Hemadsorption
Infected cells with an enveloped virus containing hemagglutinin
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
CSF use in diagnostics
Main diseases it ID
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
Polyomavirus-papovaridae
Human infections
JCV“Dumb JOCK Missed the Pass”
BKV“Bad Kidneys don’t Vent Harsh Chemicals”
MCV
Epi/Pathogenesis
Lab diagnosis & treatment
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)
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
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)
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
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
(-)ssRNA Replication process (Build-a-bitch) (-)–>(+)—>(-)
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
(+)ssRNA Replication process (Host whores) (+)—>(-)—>(+)
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
CPE inclusion bodies
Adenovirus intranuclear inclusion bodies
CPE inclusion bodies
Rabies Negri bodies
CPE inclusion bodies
HSV Cowdry A bodies
CPE inclusion bodies
CMV Owl’s eye inclusions
CPE inclusion bodies:
HPV
HP bodies
LCMV (Lymphocytic choriomeningitis virus)
“LCMV StREtcHes MAny PIECes BeFore My REcoveRy”
-Transmission
- Genome/Family
- Lab diagnosis
- Patho
- Treatment
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)
Viral genetics (basics)
+ssRNA VS -ssRNA
+ssRNA: Code directly for protein
(+)–> (-) –> (+)
-ssRNA: Comes with its own RDRP for primary transcription
(-) –> (+) –> (-)
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
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
Vaccine genetics pathways:
Coronavirus
—> 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)