Block 3 virology Q2 Flashcards
Poxvirus (poxviridae)
Properties (size, shape, & genome)
Replication
Strains
The biggest virus! It has a “brick-shape” envelope, & dsDNA (in the core) that lets it replicate in the cytoplasm of host cells.
(NOTE they’re very specific)
Replication =
The virus Attaches –>
penetrates, –>
uncoats, so its viral core dissociates to release viral DNA & enzymes
–> It uses its own RDRP to make mRNA to translate early proteins (DNA pol, Thymidine Kinase, & Recombinase)
–> The viral progeny then mature & use structural proteins to make their own membranes & exit the host cell (most lyse the cell)
Strains =
- Orthopoxvirus (variola, vaccinia, monkeypox, & camelpox)
- Parapoxvirus (Sealpox, parapox of deer, & pseudococowpox)
- Avipoxvirus (Canarypox, fowlpox, pigeonpox, turkeypox, & penguinpox
- Capripoxvirus (Goatpox & sheepox)
- Leperipoxvirus (Hare fibroma, myoma, rabbit fibroma, & squirrel fibroma)
- Suipovirus (Molluscum contagium)
- Yatapoxvirus (Tanapox & Yaba monkey tumour)
- Capropoxvirus A, B, C
“DoeS smallpox RaShed people get REC skin”
Smallpox (poxvirus)
Causal agent
Properties (shape, & genome)
Transmission
Host defences
Pathogenesis
Prevention
Causal agent = Vaccinia
It has a “brick-shape” envelope, & dsDNA (in the core) that lets it replicate in the cytoplasm of host cells.
Transmission = Respiratory
Host Defence =
- Skin
- Interferons (non-specific)
- CMI (clearing virus)
- HMI (outer membrane antigens/prevent reinfection)
Patho = IP 10-14 days
- Shedding asymptomatically starts ~7 days (Major reason for the fast-spreading & clustered outbreaks!)
Symptoms=
- Fever
- Malaise
- Centrifugally-distributed exanthems (macules, papules, & pustules)
Diagnosis=
- Symptoms
- History of animal contact
- Electron microscopy of scabs
- Cell cultures
- Egg inoculation (chorioallantoic membrane)
Prevention =
- Ring immunization containment strategy
- Live attenuated vaccinia virus
“DoeS monket WARD PLACeS?”
Monkeypox (poxvirus)
Properties (shape, genome, replication)
Strains
Source
It has a “brick-shape” envelope, & dsDNA (in the core) that lets it replicate in the cytoplasm of host cells.
Strains=
- West African (NO D14L) milder
- Central African (HAVE DL14) severe this gene disables complement-enzyme activity
Source = exotic pet trade (Gambian giant rat & prairie dogs)
Hepatitis virus types:
A, B, C, D, & E
Source
Transmission
Infection types
Prevention
Type A: ALT & AST (liver enzymes) changes + seafood
S = poop
T = Fecal-oral
I = acute
P = Pre/post-exposure vaccines
Type B:
S = Blood + body fluids
T = Percutaneous/mucosal
I = Chronic
P = Pre/post-exposure vaccine
Type C:
S = Blood + body fluids
T = Percutaneous/mucosal
I = Chronic
P = Blood donor screening & don’t be risky (IV + sexytimes)
Type D:
S = Blood + body fluids
T = Percutaneous/mucosal
I = Chronic
P= Pre/post-exposure vaccine & don’t be risky (IV + sexytimes)
Type E:
S = poop
T = Fecal-oral
I = Acute
P = Don’t drink shitty water
“RNS Get MorE HepA via unFLushed Poops”
Hep A
Features (genome & infection/symptoms)
Transmission & risk
Lab Diagnosis
Prevent & Treat
A NAKED RNA virus with one stable serotype
Infection= IP ~30 days
- Jaundice (hepatitis!!):
*less than 6yrs = 10% jaundiced
*6-14yrs = 40-50% jaundiced
*Older than 14yrs =70-80%
jaundiced
Other symptoms - nausea, abdominal pain, vomiting, malaise, & fever
Complications =
- Fulminant hepatitis
- Cholestatic hepatitis
- Relapsing hepatitis
Transmission =
- Close contact with an infected person
- Shellfish**
- Blood exposure (rare)
- Kids are a reservoir
Lab Diagnosis =
*- If there’s HAV-IgM via EIA = ACUTE infection
*- If there’s HAV-IgG via EIA = Past inf (aka immunity)
- Cell culture = tricky to grow (primary marmosets culture & in vivo chimps & marmosets)
- Direct diagnosis via RT-PCR of poop (rare)
Prevent & Treat =
- travellers, gay men, & IV drug users (higher risk)
- Pre-exposure (travellers)
- Post-exposure (within 14 days for household/close contacts)
- Selected situations (daycares/schools & food handlers (esp shellfish))
Type A: ALT & AST (liver enzymes) changes + seafood
S = poop
T = Fecal-oral
I = acute
P = Pre/post-exposure vaccines
Hep B
“DoeS HepB ACt AGainst AAL PEoPle”
Features (genome, genotypes, & infection/symptoms)
Transmission & risk
Lab Diagnosis
Prevent & Treat
A dsDNA virus (the + strand is incomplete & needs a reverse transcriptase for replication, so Lamivudine works on it)
It has a complete Dane particle core with HBcAg (single serotype) & HBeAg.
&
A coat with free HBsAg’s (adr, ayw, & ayr)
Genotypes = A-H
Infection = IP 60-90 days
- Jaundice:
* Less than 5yrs old = 10%
* 5yrs old = 30-50%
- acute case: less fatal (>1%)
- chronic case:
Less than 5yrs old (high risk 30-90%
& 5yrs (>10%)
- Premee-mortality = 15-25% (no jaundice yet)
Infection = Chronic diseases
- Chronic persistent (asymptomatic, aka carrier)
- Chronic active (symptomatic, i.e. Cirrhosis & Liver cancer)
Symptoms of the Acute disease
- Right upper quadrant pain
- Nausea
- Anorexia
- Malaise
- Jaundice
- Dark urine
- Black tarry stool
- Elevated liver enzymes
Symptoms of convalescent period
- Jaundice
- Malaise
- Anorexia
- Dark urine
Transmission & Risk:
+HBsAg +HBcAb-IgM = Acute infection
+ HBsAg + HBcAb-IgG = Chronic/late acute infection
+HBcAb-IgM = Acute infection (window period before HBaAb seroconversion)
+HBsAb +HBcAb-IgG =Past infection
+HBsAb = Immunized
Trans continued …
Supercarriers = Their blood has high titres of HBsAg + HBeAg (very infectious and may have HBV & DNA pol)
Simple carriers = Their blood has low levels of HBsAg (No HBeAg, HBV, & DNA pol)
Risks =
- Sex (Sex workers + Gay dudes)
- Parenteral (IVDA + healthcare pers)
- Perinatal (HBeAg-positive mom can infect their baby)
Lab Diagnosis=
- Serological tests:
* HBsAg (infection marker)
* HBsAb (recovery/immunity
marker)
* anti-HBc IgM (Acute infection
marker)
* anti-HBc IgG (Past/chronic
infection)
* HBeAg (Active replication/
high infectiousness)
* anti-HBe (No replication but
can still be +HBsAg
via HBV)
* HBV-DNA (indicates active
replication
most accurate)
Treatment =
- Interferon (use for + HBeAg carriers with chronic active infection (low resp rate)
- Alpha-interferon 2b (original)
- Alpha-interferon 2a (newer)
-**Lamivudine (nucleoside analogue that acts against Hep B’s reverse transcriptase)
- Adefovir (less drug resistance risk than Lamivudine)
Prevent =
- Vaccination (recombinant vaccines)
- Hep B immunoglobulin (HBIG protects post-exposure (esp within 48hrs can be used for neonates with +HBs&eAg moms)
- Screen blood donors
Type B:
S = Blood + body fluids
T = Percutaneous/mucosal
I = Chronic
P = Pre/post-exposure vaccine
“DoeSN’t PAPa Ad Pleasure Especially His Penis”
DNA viruses
ds vs. ss
“SpRiNT CHAP,
SpRitEd CRAFT,
DRaiN Rat”
RNA viruses
ds vs ss
Hep A genome + shape
Hep B genome +shape
Hep C genome + shape
Hep D genome
Hep E genome + shape
Hep A = +ssRNA, non-segmented, & icosahedral
Hep B = dsDNA (incomplete + strand) + reverse transcriptase,
Hep C = +ssRNA, non-segmented & icosahedral
Hep D = -ssRNA (circular)
Hep E = +ssRNA non-segmented (linear) & icosahedral
Common perinatal infections during birth
Hep B & C
HSV-2
HIV
HPV
Transmission of Hepatitis:
Hep A
Hep B
Hep C
Hep D
Hep A = Fecal-oral
Hep B, C, D = Blood
Cidofovir
“cidofovir CrusHes Naughty viral DNA pol”
mech & used against
fucked up side effects
Mech = inhibits viral DNA pol
Used =
- CMV retinitis (AIDS)
- HSV (that’s resistant to acyclovir)
Side effects = Nephrotoxicity
Ganciclovir
mech & used against
fucked up side effects
Mech = Inhibits DNA pol
Used = CMV (esp Aids)
Side effects = Bone marrow suppresion (leukemia, neutropenia, & thrombocytopenia), & renal toxicity
Acyclovir
mech & used against
fucked up side effects
Mech = Inhibits Thymidine-Kinase
Used = HSV & VZV (Non-latent forms only)
Side effects = acute kidney injury
Antiretroviral therapy (ART)
3 drugs involved
2 NRTI (Abacavir, Emtricitabine, Lamivudine, Tenofovir, & Zidovudine (nucleotide reverse transcription inhibitor)
&
1 integrase inhibitor (Bictegravir, Dolutegravir, Elvitegravir, & Raltegravir)
Hep C therapy
Multidrug therapy
NS5A inhibitor
NS5B inhibitor
NS3/4A inhibitor
Alternative drug
NS5A = Ledipasvir, Ombitasvir, & Velpatasvir
NS5B = Sofosbuvir & Dasabuvir
NS3/4A = Grazoprevir & Simeprevir
Alt drug = Ribavirin
Hep B serology markers
Acute
Window
Chronic (highly infective/active replication)
Chronic (low infective)
Recovery
Immunized
Acute = HBsAg, HBeAg, & anti-HBc (IgM)
Window = anti-HBe (IgM)
Chronic = HBsAg, HBeAg, anti-HBc (IgG)
(highly infective/active replication)
Chronic = HBsAg, anti-HBe, & anti-HBc
(low infective)
Recovery = anti-HBs, anti-HBe,
& anti-HBc (IgG)
Immunized = anti-HBs
Infectious states of Hep B
Susceptible pers with no immunity or inf =
HBsAg (-)
Anti-HBs (-)
Anti-HBc (-)
Immune person with a previous inf but no active inf =
HBsAg (-)
Anti-HBs (+)
Anti-HBc (+)
Immune person with no active inf but they’re immunized =
HBsAg (-)
Anti-HBs (+)
Anti-HBc (-)
Pers with an active, acute & previous inf without immunity =
HBsAg (+)
Anti-HBs (-)
Anti-HBc (+)
IgM-Anti-HBc (+)
Pers with an active, chronic & previous inf without immunity =
HBsAg (+)
Anti-HBs (-)
Anti-HBc (+)
IgG-anti-HBc (+) (or - IgM)
Easy Hep B Serology Markers
HBsAg =
Anti-HBs =
Anti-HBc =
- IgM-anti HBc
- IgG-anti HBc
HBeAg =
Anti-HBeAg =
HBsAg = Active inf
Anti-HBs = immunity
Anti-HBc =previous or ongoing inf
- IgM-anti HBc (acute) +
- IgG-anti HBc (chronic) +
HBeAg = high transmissibility (high rep rate)
Anti-HBeAg = low transmissibility
Hep C
“HepC SPRintEd & RACEd SLoweR”
Properties (genome, infection/symptoms)
Transmission & Risk
Lab Diagnosis
Genome =
+ssRNA (similar to a flavivirus). It has 6 genotypes, with types 1-4 having worse outcomes
Infection = IP 6-7 weeks
- Jaundice (30-40% of cases)
- Chronic hepatitis (70% of cases)
- Persistent infection (85-100% of cases)
- no protective antibodies
Symptoms of chronic infection =
- Chronic/persistent hepatitis
- Chronic active hepatitis
- Cirrhosis
- Liver cancer
Transmission/risks =
- Transfusion/transplant from an inf donor
- Injectable drug use
- Hemodialysis
- Needle stick injuries
- Sexual/household exposure to an anti-HCV (+) contact
- Sexy times (multiple partners)
- Birth via infected mom
Lab Diagnosis =
- Test for IgM & G via ELISA if + use PCR to confirm & monitor antiviral therapy
Treatment =
- Acute (alpha interferon)
- Chronic (interferon + ribavirin relapse if stopped)
- Chronic genome 1 (ledipasvir + sofosbuvirvir)
Prevention =
- Screening blood/organ donors
- Don’t be risky
- Blood/fluid safety handling
Type C:
S = Blood + body fluids
T = Percutaneous/mucosal
I = Chronic
P = Blood donor screening & don’t be risky (IV + sexy times)
Hep D (Delta)
“Hep D ALMost sprinted past CJS”
Properties (genome, infection)
Transmission
Genome =
- small ssRNA that’s contained in a delta antigen & outer HBsAg coat (needs Hep B to cause infection)
Infections=
- Simultaneous primary co-infection
* HVD + HBV incubate at the
same time = Severe acute
infection
- Chronic co-infection
* HDV + HBV incubate at the
same time to cause the acute
inf & then they progress to a
chronic inf
* Causes a superinfection & is a
high risk for severe chronic
liver disease - Primary HDV inf of a person with a chronic HBV infection
* Person has a chronic HBV inf
then gets inf with HVD =
SEVERE acute hepatitis which
progresses to chronic inf
Transmission =
- Percutaneous exposure (injectable drugs)
- Permucosal exposure (sexy times)
Prevention =
- HBV-HDV coinfection (use for pre/post-exposure prophylaxis to prevent HBV inf)
- HBV-HDV Superinfection (Don’t be risky)
Type D:
S = Blood + body fluids
T = Percutaneous/mucosal
I = Chronic
P= Pre/post-exposure vaccine & don’t be risky (IV + sexytimes)
Hep E
Properties (genome & Infection)
Endemic info & transmission
The genome is an unenveloped + RNA virus that is very labile and sensitive (like calicivirus)
Infection = IP 40 days
- Causes fatality in < 3% overall & 15-25% in preggos
- Severity increases with age
- no chronicity
Epidemical info =
- poop in drinking water (India, USSR, China, Africa, & Mexico)
Transmission =
- Oral fecal route (usually via drinking water)
Prevention
- Travelers (avoid unbottled water + ice, raw shellfish & fruit/veggies)
- Immunoglobulins from Western country donors don’t prevent inf
- NO VACCINE
Type E:
S = poop
T = Fecal-oral
I = Acute
P = Don’t drink shitty water
Enteroviruses include…
&
Their genome
&
Infection pathway
&
Immune response
- Poliovirus
- Coxsackievirus (A & B)
- Echovirus
Genome =
- ss naked RNA (acid-stable fuckers)
Infection pathway=
- inhaled/ingested (rep in the oropharynx & peyers patches)
–>
Then primary viremia (multiplies in the blood) –>
Then secondary viremia (multiplies in target tissue)
Immune response =
- Innate immune (first response & regulates the adaptive Imm resp)
- HMI (protection & life-long immunity)
- CMI (Pathogenic & NOT protective)
Exanthems (Rubelliform Rashes)
Causal agent
Enterovirus (summer/fall)
Hepatitis B infection
Immunity
Resolved inf
vs
HBV vaccination
(Resolved)
- HBsAg
+ anti-HBs
+ HBcAg (+ anti-IgGHBc)
- HBeAg
+ anti-HBe
No HBV DNA
Normal
(Vaccinated
(Resolved)
- HBsAg
+ anti-HBs
- HBcAg
- HBeAg
- anti-HBe
No HBV DNA
Normal
Poliovirus
General characteristics
Host
Susceptible to
Lab Diagnosis
Pathogenesis
Symptoms
Prevention
GC=
- An enterovirus with 3 serotypes, no common Ag, & little shared nucleotide homology (despite identical physical properties)
Host = Only infects humans
Susceptible to =
- Inactivated via heat ~55c (30 mins) + chlorine concentration of 0.1ppm
Lab diagnosis =
- Cultures (Human or monkey kidney/testes/muscle)
- Usually swabbed from poop, rectum, & throat
- Molecular tech to diff serotypes
- Serology is more used for immune screening
Pathogenesis = IP 7-14dats
- Spread fecal-orally
- Ingestion & replication in oropharynx & intestine mucosa
- Invades lymph system (via Peyer’s patches & tonsils)
- Enters blood causing transient viremia
- Some can infect CNS (dissemination, i.e. via blood, axons of peripheral nerves & lower motor nerves)
Symptoms = 3 outcomes
- Subclinical infection (majority) inapparent
- Abortive infection (4-8%), minor flu-like illness & possible aseptic meningitis
- Major illness (1-2%) can appear sporadically or 2-3 days after the minor illness causing aseptic meningitis, flaccid paralysis, respiratory paralysis & death
Prevention=
- Intramuscular Poliovirus vaccine ( formalin-inactivated virus for all 3 serotypes (Salk) only causes the body to make Ab (prevents paralytic poliomyelitis)
- Oral Poliovirus vaccine (The live-attenuated virus of all 3 serotypes (Sabin) causes the body to make local immunity via an IgA response. Don’t use in AIDS) - 3rd world countries use this one more
Changes in Antigenicity
When two strains of influenza mix to cause
Genetic re-assortment (makes a new strain with different hemagglutinin & neuraminidase combos)
Antigenic shift (only happens with influenza A usually causes pandemics)
Mutated genomic RNA (cause minor changes in antigenicity aka antigenic drift, can happen in influenza A & B epidemics)
Swine Flu H1N1 causes Antigenic Shift & drift
“sudden shift is more deadly than a minor drift”
Antigenic shift
- Major, abrupt, drastic changes due to reassortment of the RNA genome segments & entire segments are exchanged)
- Seen in type A influenza
- Major pandemics
- Animal viruses are sources of RNA segments for epidemics
&
Antigenic drift
- Minor, gradual, sequential changes that happen in regular intervals due to mutations in RNA)
- Usually in Influenza B (only human virus) & A (periodical epidemics)
- No animal source of new RNA segments
What host serves as a reassortment vessel in influenza viruses between avian & human
Pigs
