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Block 3 virology Q2 Flashcards

1
Q

Poxvirus (poxviridae)

Properties (size, shape, & genome)

Replication

Strains

A

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

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2
Q

“DoeS smallpox RaShed people get REC skin”

Smallpox (poxvirus)

Causal agent

Properties (shape, & genome)

Transmission

Host defences

Pathogenesis

Prevention

A

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

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3
Q

“DoeS monket WARD PLACeS?”

Monkeypox (poxvirus)

Properties (shape, genome, replication)

Strains

Source

A

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)

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4
Q

Hepatitis virus types:

A, B, C, D, & E

Source
Transmission
Infection types
Prevention

A

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

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5
Q

“RNS Get MorE HepA via unFLushed Poops”

Hep A

Features (genome & infection/symptoms)

Transmission & risk

Lab Diagnosis

Prevent & Treat

A

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

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6
Q

Hep B
“DoeS HepB ACt AGainst AAL PEoPle”

Features (genome, genotypes, & infection/symptoms)

Transmission & risk

Lab Diagnosis

Prevent & Treat

A

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

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7
Q

“DoeSN’t PAPa Ad Pleasure Especially His Penis”

DNA viruses
ds vs. ss

A
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8
Q

“SpRiNT CHAP,

SpRitEd CRAFT,
DRaiN Rat”

RNA viruses
ds vs ss

A
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9
Q

Hep A genome + shape

Hep B genome +shape

Hep C genome + shape

Hep D genome

Hep E genome + shape

A

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

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10
Q

Common perinatal infections during birth

A

Hep B & C
HSV-2
HIV
HPV

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11
Q

Transmission of Hepatitis:

Hep A
Hep B
Hep C
Hep D

A

Hep A = Fecal-oral
Hep B, C, D = Blood

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12
Q

Cidofovir
“cidofovir CrusHes Naughty viral DNA pol”

mech & used against

fucked up side effects

A

Mech = inhibits viral DNA pol

Used =
- CMV retinitis (AIDS)
- HSV (that’s resistant to acyclovir)

Side effects = Nephrotoxicity

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13
Q

Ganciclovir

mech & used against

fucked up side effects

A

Mech = Inhibits DNA pol

Used = CMV (esp Aids)

Side effects = Bone marrow suppresion (leukemia, neutropenia, & thrombocytopenia), & renal toxicity

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14
Q

Acyclovir

mech & used against

fucked up side effects

A

Mech = Inhibits Thymidine-Kinase

Used = HSV & VZV (Non-latent forms only)

Side effects = acute kidney injury

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15
Q

Antiretroviral therapy (ART)

3 drugs involved

A

2 NRTI (Abacavir, Emtricitabine, Lamivudine, Tenofovir, & Zidovudine (nucleotide reverse transcription inhibitor)
&
1 integrase inhibitor (Bictegravir, Dolutegravir, Elvitegravir, & Raltegravir)

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16
Q

Hep C therapy

Multidrug therapy

NS5A inhibitor
NS5B inhibitor
NS3/4A inhibitor
Alternative drug

A

NS5A = Ledipasvir, Ombitasvir, & Velpatasvir

NS5B = Sofosbuvir & Dasabuvir

NS3/4A = Grazoprevir & Simeprevir

Alt drug = Ribavirin

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17
Q

Hep B serology markers

Acute

Window

Chronic (highly infective/active replication)

Chronic (low infective)

Recovery

Immunized

A

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

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18
Q

Infectious states of Hep B

A

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)

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19
Q

Easy Hep B Serology Markers

HBsAg =

Anti-HBs =

Anti-HBc =
- IgM-anti HBc
- IgG-anti HBc

HBeAg =

Anti-HBeAg =

A

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

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20
Q

Hep C
“HepC SPRintEd & RACEd SLoweR”

Properties (genome, infection/symptoms)

Transmission & Risk

Lab Diagnosis

A

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)

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21
Q

Hep D (Delta)
“Hep D ALMost sprinted past CJS”

Properties (genome, infection)

Transmission

A

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)

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22
Q

Hep E

Properties (genome & Infection)

Endemic info & transmission

A

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

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23
Q

Enteroviruses include…
&
Their genome
&
Infection pathway
&
Immune response

A
  • 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)

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24
Q

Coxsackieviruses (Enterovirus)

Properties (source, genome)

Transmission

Associated Diseases

A

Source = suckling mice

Genome = ss naked RNA with 2 groups that cause different lesions

–> Group A (23) virus = make diffuse myositis, acute inflammation, & voluntary muscle necrosis
–> Group (6) B = make focal areas of degeneration in the brain, necrosis of skeletal muscles, inflammation in dorsal fat pads + pancreas and sometimes myocardium

Transmission = Fecal-oral route

Associated Disease =
- Paralytic disease (usually ass. with polio & enterovirus 71)
- Meningitis (common in kids under 5)
- Encephalitis (focal or generalized can follow meningitis, patients usually recover)
- Undifferentiated febrile illness
- Hand-Foot-Mouth disease (usually from COX A)
- Herpangina (COX A)
- Epidemic Pleurodynia (aka Bornholm disease, usually COX B)
- Myocarditis (COX B usually fatal in neonates, not so much in adults)
- Respiratory infections (Common cold etc.)
- Rubelliform rashes (COX B, usually transmitted perinatally in newborns)
- Conjunctivitis (most common COX A24 & enterovirus 70)
- Pancreatitis/Diabetes (COX B)

25
Coxsackievirus A vs B groups "CAn DAVe COunt FINgers"
COX A = DAVe - diffuse myositis - acute inflammation - voluntary muscle necrosis COX B = FIN - focal degeneration in the brain - necrosis of skeletal muscles - inflammation in dorsal fat pads, pancreas, and sometimes myocardium
26
Exanthems (Rubelliform Rashes) Causal agent
Enterovirus (summer/fall)
27
Hepatitis B (HVB) Genome Pathogenesis Progression of infection Symptoms
Genome = - Circular partially dsDNA virus (incomplete shorter strand) - Reverse transcriptase (both DNA + RNA dependent functions) Transmission = - Sexy times - Parenteral (needles & blood/organ transfusions) - Vertical transmission (aka during birth from inf mom to baby) Risks = - Gay dudes + sex workers - Infected moms - Household contacts - Healthcare workers - Dialysis & blood/organ recipients Pathogenesis = - It enters the host cell and uses Reverse transcriptase to complete its shorter positive strand - Its circular DNA is converted to closed circular DNA - Its closed-circular-completed DNA is then transcribed into viral mRNA by the host DNA-dep-RNA polymerase - Viral mRNA + Reverse transcriptase leave the nucleus and are translated into HBV core proteins + a new reverse transcriptase (in the cytoplasm) - These are packaged into capsids & the viral mRNA is reverse transcribed into viral circular DNA (Progeny). They get enveloped as they leave the host cell Progression of the Infection: ACUTE infection - Patients get inf with HBV and develop an acute infection *Infected hepatocytes express HBsAg on their surface & CMI (CD8+T) attack causing liver inflammation & damage Acute (active inf) serological markers (+HBsAg, +HBcAg, +/-HBeAg, +anti-IgM, +/-anti-HBs,c,e) ACUTE SYMPTOMS Symptoms = IP 1-6 months - Serum sickness-like syndrome (rash, arthralgia, myalgias, & fever) - Asymptomatic hepatitis (70% of cases) - Symptomatic hepatitis (30% of cases) *Fever, rash, arthralgia, myalgias, fatigue, anorexia, nausea, jaundice, & Right upper quadrant pain - Acute Liver Failure (~0.5% of cases) CHRONIC INF - Some patients progress to chronic HBV via 2 ways *When our immune system can't clear the HBV- it promotes persistent hepatic inflammation (necrosis, mitosis, & regeneration) which leads to cirrhosis & hepatocellular carcinoma OR *HBV integrates its DNA into the host cells' genome to alter endogenous gene expression and cause hepatocellular carcinoma CHRONIC SYMPTOMS (6+ months) - Fatigue, malaise, nausea/poor appetite, & unspecific abdominal pain Chronic (active inf) serological markers (+HBsAg (6+ months), +HBcAg, +/-HBeAg, +anti-IgG, +/-anti-HBs,c,e)
28
Hep B infection Acute infection
ACUTE = +HBsAg anti-HBs +HBcAg (+anti-IgM-HBc) + HBeAg - anti-HBe +/- HBV DNA high (ALT > AST)
29
Hep B infection Window period (time between the onset of infection and the point where lab tests can detect HBV infection)
- HBsAg - anti-HBs +HBcAg + seroconversion of anti-IgM --> anti-IgG - HBeAg +/- anti-HBe +/- HBV DNA high (ALT > AST)
30
Hep B infection Chronic inf with high transmissibility Chronic infection with low transmisibility
(High trans) + HBsAg - anti-HBs + HBcAg (+anti-IgG-HBc) + HBeAg - anti-HBe High HBV DNA Normal or high (ALT > AST) (Low trans) + HBsAg - anti-HBs + HBcAg (+anti-IgG-HBc) - HBeAg + anti-HBe low HBV DNA Normal
31
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
32
Differential Diagnosis of HAV "HAVeN't FOund Good PIRAted Movies" HBV HDC
HAV * Trans = fecal-oral * IP = 2-6 weeks * Clinical course = 3 phases 1: prodromal (1-2 weeks) early 2: icteric (2 weeks) 3: resolution (2-4 weeks) ** NO CHRONICITY (recover in 3 months * Serum markers = +anti-HAV IgM (Active inf) +anti-HAV IgG (Past inf or vaccine) * Associated condition = RARE Thrombocytopenia & Pancreatitis * Treat = Supportive care * Prevent = HAV vaccine (active) Anti-HAV immunoglobins (passive) HBV
33
*Coxsackievirus (groups A & B) General characteristics Associated conditions
GC = - A (cause diffuse myositis, acute inflammation, & necrosis of voluntary muscle fibres) - B (cause focal degeneration in the brain, necrosis in skeletal muscles, & inflammation in dorsal fat pads/pancreas/myocardium Ass. Cond. = - Meningitis (A+B) - Undiff febrile illness (A+B) - Hand-Foot-Mouth Disease (A) - Herpangina (A) - Epidemic Pleurodynia (Bornholm disease) (B) - Myocarditis (B) - Rubelliform rashes (A+B) - Neonatal Inf (B) - Conjunctivitis (A24) - Pancreatitis/Diabetes (B)
34
The reason why Coxsackie B & Enterovirus 71 don't have a vaccine
Because their multiplicity of serotypes
35
Echoviruses (Enteric-cytopathic human orphan viruses)
Source human poop no Ag but they can have heterotypic cross-reactions
36
Enteroviruses 70, 71, 72
70 (epidemic acute hemorrhagic conjunctivitis) 71 (highly pathogenic & ass with acute aseptic meningitis, encephalitis, paralytic poliomyelitis, & hand-foot-mouth disease epidemics) 72 (was supposed to be Hep A, now it's in the heptovirus family)
37
Rhinoviruses (picornaviruses) General Characteristics Replication site Causes Types of infection "Treatment"
GC= - Acid-stable & somewhat thermostable enteroviruses Rep site= - Epithelium of nasal mucosa Causes = IP 1-2days - common cold (healthy) - can exacerbate asthma Types of Inf: - Repeated attacks (Headache, myalgia, mild cough, & chills) - Secondary bacterial inf (otitis media, sinusitis, bronchitis, or pneumonitis) Treatment = 100 serotypes! (means no vaccine) - 5-day intranasal interferon can prevent spreading
38
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
39
Paramyxovirus & Rubella virus
- Measles (Morbillivirus) - Parainfluenza (1-4) (paramyxovirus) - Mumps (paramyxovirus) - Respiratory syncytial virus (pneumovirus) -Metapneumovirus (pneumovirus) - Hendra, Nipah, & Cedar viruses (Henipavirus)
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Orthomyxoviridae
They are all influenza viruses & an affinity for mucins Strucuture= - Spherical - (-)ssRNA genome - Helical nucleocapsid - Enveloped (from budding) Replication Process = *The Matrix proteins include - Hemagglutinin which binds sialic acid on the glycoprotein/glycolipid receptors of the host cell *Then Receptor-mediated endocytosis happens (M2 has a role in early & late stages of replication) - M2 acidifies the endosome, causing pH-dependent membrane fusion & viral uncoating - Releases the vRNPs with the M1 - Replicates to form the cRNAs - M2 takes part in glycosylation in rER, polymerization & acetylation of viral proteins - Transported to the surface + M1 & packaged into nascent viral particles - During exit- M2 weakens the binding M1 in the matrix & neuraminidase destroys the sialic acid to release the progeny viruses Hosts= - Influenza A ( Humans + animals (pigs, horses, birds)) - Influenza B (Humans) - Influenza C (Human)
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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)
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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
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Influenza virus types A B C
A- Human & animal B- Human C- Human & swine
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Typing & variation
Typing = - NP, M1, & M2 (A, B, &C) - HA & NA (only A) influenza A H1-15, N1-9 avian H1-15, N1-9 human H1,2,3,5 & N1,2
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Antigenic Shift
Involves = - Genetic reassortment (between strains) - Sequence analysis (shows all influenza derived from avian influenza)
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What host serves as a reassortment vessel in influenza viruses between avian & human
Pigs
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Pandemic influenza stages 1-3 4 5-6 post-peak post-pandemic
1-3 = animal inf 4 = jumps to humans 5-6 = widespread in humans PPeak= possible recurrence PPandemic = normal activity
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Symptoms of influenza Who's most at risk
Symptoms = - Fever - Headache - Myalgia - Cough - Rhinitis - Occular issues (Type C = milder) Risk= - Very young & old - AIDs - Heart & lung disease
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Pulmonary symptoms of influenza
- Croup (young) - Primary influenza pneumonia - Secondary bacteria inf (strep. pneumonia, staph aureus, or H. influenzae)
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Non-pulmonary complications of influenza "MC GREggor"
- Myotis (rare type B that gets kids) - Cardiac comp - Encephalopathy -Reye's syndrome (brain edema, fatty liver. vomiting, lethargy, & coma use aspirin) - Guillian-Barre syndrome
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Recovery of influenza Interferon pathway 2 other mechs that happen during recovery
interferon = - triggers immune defence against RNA viruses - then, dsRNA is formed as an intermediate during viral replication - This activates PRRs to engage interferon receptors & stim the JAK-STAT pathway causing positive feedback of interferon production to kill the virus Side effects= - Fever, myalgia, fatigue, & malaise 2 recovery mechs= - CMI - Tissue repair
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Viral response to the host immune system "host's Body KIlls CrAzy Monsters"
- Block interferon binding - Inhibit interferon-induced proteins - Inhibit NKs - Fuck with MHCI/II expression - Block the complement activation - Inhibit apoptosis
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Protection against re-infection of influenza
- IgG & IgA (long lasting) - Ab against HA & NA
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Treating H1N1 2009 & influenza B
Oseltamivir or zanamivir
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Lab Diagnosis Process of Influenza "influenza lab SPEC"
- Culture (1-10days) - RT-PCR (2-4hrs) - Ag detection (2-4hrs via ELISA) - Serology > 2 weeks - Ag detection (15-30 min, Rapid EIA-like)
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Treating Influenza A H1N1 2009
A= Rimantadine (M2) & Amantadine (M2) given early H1N1 2009 = Zanamivir & Oseltamir (also good for A,B,C)
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fuck
it
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Types of influenza easy Severity Reservoir Human pandemics & epidemics Antigenic changes Segmented genome Amantadine, Rimantidite Zanamivir Surface glycoproteins
TYPE A Severity = SEVERE Reservoir = animals Human pandemics & epidemics = causal agent Antigenic changes = Shift & Drift Segmented genome = Yes Amantadine, Rimantidite = Sensitive Zanamivir = Sensitive Surface glycoproteins = 2 TYPE B Severity = MODERATE Human epidemics = causal agent Antigenic changes = Drift Segmented genome = yes Zanamivir = Sensitive Surface glycoproteins = 2 TYPE C Severity = MILD Human epidemics = sporadic Antigenic changes= Drift Segmented genome = 7-segments Zanamivir = Sensitivee Surface glycoproteins = 1
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molluscum contagiosum "DoeS molluscum contagios SUPrise you?"
dsDNA RDRP + Thiamine kinase Suipovirus

Microbiology SJSM (12 decks)

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