Block 3 virology Q1 Flashcards
(91 cards)
(+)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
(-)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
viroids
“VaNS”
unencapsulated (Naked) ssRNA viruses (these replicate and usually only cause plant diseases (except Hep D)
Icosahedral vs. Helical shaped viruses
Icos= Can either be naked or enveloped (easy to kill)
Heli = Always enveloped
Prion viruses
Only made of infectious proteins, these cause slow diseases, transmissible spongiform (CJD) encephalopathies
Susceptible = UV light, NaOH, Autoclaving, Hypochlorite
Resistant = Formaldehyde & nucleases
DNA vs RNA viruses
It’s either one or the other, not both!
DNA = has an Owls eye appearance (intranuclear inclusions) & they’re usually dsDNA
RNA= has cytoplasmic inclusions & are usually ssRNA (except retroviruses)
Steps of the typical infectious cycle
“Apply Pressure Under The Right ARmpit”
Attachment
Penetration
Uncoating
Transcription (-ssRNA) &/or Translation ((+/-)ssRNA)
Replication
Assembly
Release
Eclipse (prep-load) vs Exponential growth period (fire)
Eclipse= ~1-20hrs; it’s from when the virus attaches a host cell and can’t infect other cells (viral load appears to be 0 on a chart)
- Initial entry + disassembly of the parental virus —> assembly of the first progeny active synthesis ( aka from Attachment —> Assembly)
EXP= ~8-72 hrs. This is when the number of assembled progeny viruses increases exponentially over a period of time & then reaches a plateau (with no other increase in viral load)(can give 100-10,000 virions per cell!!!
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
Reveptor-mediated fusion of an enveloped virus: envelope fusion vs endocytotic entry
Envelope fusion:
The virion attaches to the host cell via its receptors, then the viral and host cell’s envelopes fuse to bring in the nucleocapsid, and the viral envelope forms a patch on the host’s membrane
Endocytotic entry:
The virion attaches to the host cell and forms a clathrin-coated endocytotic vesicle via virion-receptor interactions, it’s amplified, and the nucleocapsid is released inside the host cell
Forming a viral envelope (Budding)
Glycoproteins are made in the ER and glycosylation begins—>
The glycoproteins are moved in a vesicle to the golgi to continue glycosylation until the viral glycoproteins are moved in a vesicle to the host’s cell membrane —->
From there, the viral glycoproteins bind to the host’s membrane and form a patch to wait until a nucleocapsid migrates to it to bud outside the host cell to be released as a free virion
Methods of transmission:
Respiratory “AIR”
Fecal-oral “FOE”
Blood-borne “HIgH”
Sexy times “Hump”
Animal or bugs “Rabid”
Resp = Influenza A & rhinovirus via aerosols, sensitive to drying, & closer contact means more infectiousness
F&O = Enteroviruses (i.e polio) they replicate in the gut
Blood-Borne = Hep B & HIV, via sharing needles (IV drug abuse)
Sex = HIV
Animals/bugs = rabies
Egg inoculation:
Chorioallantoic membrane innoculation “CHoPpeR”
Amniotic inoculation “AIM”
Yolk sac inoculation “YeaH”
Allantoic inoculation “All Her gAINs”
CMI = Herpes, Poxvirus, & Rous Sarcoma
AI = Mumps & Influenza
YSI = Herpes
AI = HIV, Avian Adenovirus, Influenza & Newcastle disease
Poliovirus
“polio ENTeRs FrOm the gut”
Properties (type, genome, transmission)
Disease
An Enterovirus with RNA genome that’s transmitted via the fecal-oral route
It infects the gut and can be excreted in poop & also enter the blood (viraemia). From there, it infects both non & neuronal tissues (paralysis)
It causes poliomyelitis (iron lung patients) & gastro illness
Influenza A virus
Properties (type, genome, transmission)
Disease
An Myxovirus that’s enveloped with a segmented RNA genome
Its got a wide infectious range from people to animals because of its extensive antigenic variation
It causes respiratory infections
Tumour causing viruses
Epstein-Barr “Eat BLeuberries”
HPV (Human papillomavirus) “HP the Basilisk’s Chamber”
HTLV-1 (Human T-cell leukemia virus)
Hep C “Hard Cider & Liquor”
EB = Burkitts Lymphoma
HPV = Benign warts & Cervical carcinoma
HTLV-1 = Leukemia
Hep C = Liver carcinoma
Tumour-causing virus infectious pathways
General
Exceptions
The virus infects a cell and integrates its own nucleic acid & DNA into the host’s genome. This way it can alter gene expression by either activating certain host genes or activating its own genes to promote uncontrolled replication and delay cell growth (aka tumour making 101)
Exceptions include:
Herpes = causes latent infection, but its own nucleic acid stays separate from the hosts’ genome
Retroviruses = have an RNA genome so they need to make a DNA copy of their genome to replicate
Treating & preventing viral infections
Antivirals, vaccines, & immunization
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)
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
Erythema Infectiosum aka 5th virus (inf agent is the Parvovirus B19)
Features (IP, Phases)
IP ~ 7-10 days
Phase 1 (peak virus levels and RBC destruction)
- Fever, malaise, myalgia, chills, & bright red rashes (raised slapped cheek app)
Phase 2 (Rash & arthralgia)
- Virus disappears (not infectious anymore)
- Erythematous maculopapular rash on the arms and trunk (lace-like app) due to the immune complexes in the capillaries of the skin
Phase 3
- Frequent reoccurrence & clearance, triggered via exercise, irritation, heat, & Sun)
Aplastic crisis (inf agent is the Parvovirus B19)
Effects on anemic, healthy, & thrombocytopenic patients
anemic patients = causes symptoms by destroying RBCs (pallor, fatigue, reduced hemoglobin)
Thrombocytopenic patients = Bruising & hydrops fetalis
Hydropis fetalis
Associated virus
Treatment/prophylaxis
Test
Ass. virus = associated with a maternal or fetal infection of the B19 parvovirus
Treat/pro = Preggos exposed to B19 should get IgG & M serology done (then repeated in 3 weeks)
Test = If IgMs develop, then there’s an acute infection
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 urine
JCV: In PM, lesions in brain tissue
No antiviral treatment or vaccines (cause it’s generally asymptomatic)
