spreadsheet Flashcards
flaviviruses (virus types)
hep C; St louis encephalitis virus; west nile virus; yellow fever virus; dengue virus
flaviviruses (subclasses)
hepacivirus and arboviruses
arboviruses
st. louis encephalitis virus; west nile virus; yellow fever virus; dengue virus
arboviruses - enveloped?
enveloped
arboviruses - nucleic acid/structure
+ssRNA
arboviruses - virion structure
icosahedral
St. Louis encephalitis virus - transmission route
arthropods (mosquitoes; urban/rural habitat), wild/domestic birds
west nile virus - transmission route
arthropods (mosquitoes; urban/rural habitat), wild/domestic birds
dengue virus - transmission route
Aedes aegypti mosquito, humans
yellow fever virus - transmission route
humans, Aedes aegypti mosquito (jungle yellow fever can infect tree mosquito and monkeys…tree mosquito infects human, which then is bitten by Aedes aegypti)
st. louis encephalitis virus - diseases caused
encephalitis
west nile virus - diseases caused
encephalitis
yellow fever virus - diseases caused
yellow fever
dengue fever virus - diseases caused
Classical Dengue (“bone-break fever”), dengue hemorrhagic fever (fatal)
st. Louis encephalitis - general epidemiology
how long are the two incubation periods?
Are human’s dead end hosts?
requires multiplication in arthropod host (usually 2 incubation periods; intrinsic 7 days in humans; extrinsic 14 days in arthropod), humans are dead-end hosts b/c not high enough viremia
west nile virus - general epidemiology
How long are the two incubation periods?
Are humans dead end hosts?
requires multiplication in arthropod host (usually 2 incubation periods; intrinsic 7 days in humans; extrinsic 14 days in arthropod), humans are dead-end hosts b/c not high enough viremia
yellow fever virus - general epidemiology
Where is this virus endemic?
only in rural tropical Africa and South America
dengue fever virus - general epidemiology
Where is this virus endemic?
Are humans dead end hosts?
found in tropics/subtropics, esp in S.E. Asia and Caribbean islands, humans are not dead-end hosts
st. louis encephalitis - epidemiology
How old are the usual infected patients?
What percentage of cases are fatal?
Where is this virus endemic? Where is this virus found?
Generally infects adults over 50yo, 10% cases fatal (mostly in elderly), many subclinical infections, St Louis from N America, West Nile from N Africa and Middle East
west nile virus - epidemiology
What age are the infected patients?
What percentage of cases are fatal?
Where is this virus endemic? Where is this virus located?
Generally infects adults over 50yo, 10% cases fatal (mostly in elderly), many subclinical infections, St Louis from N America, West Nile from N Africa and Middle East
yellow fever virus - epidemiology
What is the mortality rate?
Are there ever subclinical infections?
High mortality, some subclinical infections
dengue virus - epidemiology
is this virus fatal?
how many subtypes of this virus exist?
severe but not usually life-threatening disease, 4 antigenic types
st. louis encephalitis virus - pathogenesis
how long is the incubation period?
Where does the virus first multiply during viremia?
What are the prodromal symptoms?
What are the full infection symptoms?
Encephalitis after 7 day incubation period, viremia from multiplication in vascular endothelium, prodromal febrile malaise followed by encephalitis with paralysis/coma/death
west nile virus - pathogenesis
Where does the virus first multiply during viremia?
What are the prodromal symptoms?
What are the full infection symptoms?
Encephalitis after 7 day incubation period, viremia from multiplication in vascular endothelium, prodromal febrile malaise followed by encephalitis with paralysis/coma/death
yellow fever virus - pathogenesis
Where is the primary infection?
Where are the secondary infection sites?
Primary infection in vascular endothelial cells, then viremia, then secondarily infects liver and other organs (spleen, kidney)
dengue fever virus - pathogenesis
Explain dengue hemorrhagic fever development
dengue hemorrhagic fever from massive macrophage infection –> cytokine storm (after sequential infections w/2 diff antigentically cross-reacting dengue viruses)
arboviruses - incubation period in humans?
about 7 days
st. louis encephalitis virus - signs and symptoms?
fever, malaise
west nile virus - signs and symptoms
fever, malaise
yellow fever virus - signs and symptoms
fever, nausea, jaundice
dengue virus - signs and symptoms
fevere, severe headache, muscle and joint pains, rash… dengue hemorrhagic fever causes patient to vomit blood/hemorrhage/go into shock (most often in native pop)
yellow fever virus - What kind of vaccine?
How long is protection?
live-attenuated vaccine (17-D vaccine) gives lifelong protection
togaviruses - subclasses
1) arboviruses (zoonoses)
2) nothing (Rubella is a Togavirus, but not an arbovirus)
togaviruses - virus types
western equine encephalitis virus; eastern equine encephalitis virus; rubella
togaviruses - enveloped?
enveloped
togaviruses - nucleic acid/structure
+ssRNA
togaviruses - virion structure
icosahedral
western and eastern equine encephalitis virus - transmission route
wild birds, mosquitoes (humans and horses dead-end hosts)
rubella virus - transmission route
airborne
western and eastern encephalitis virus - diseases caused
encephalitis
rubella virus - diseases caused
Rubella (German Measles), congenital rubella
western equine encephalitis virus - general epidemiology
What is the habitat of this virus?
mosquito habitat - rural
eastern equine encephalitis virus - general epidemiology
How dangerous is this virus?
How old are the usual infected patients?
In what habitat is this virus found?
most deadly arbovirus encephalitis in US, mostly infects children in swampy/wetland areas (mosquito habitats)
rubella virus - general epidemiology
how is this virus spread?
Where in the body does the virus multiply?
Does viremia occur?
Is rubella more or less contagious than measles?
airborne
after multiplies in respiratory epithelium
viremia develops
less contagious than measles
western equine encephalitis virus - epidemiology
What percentage of cases are fatal?
Are there subclinical infections?
What age groups (name two) are the infected patients?
10% clinical cases fatal
many subclinical infections
infects infants and adults over 50 yo
eastern equine encephalitis virus - epidemiology
What percentage of cases are fatal?
Are there subclinical infections?
What age group are the usual infected patients?
75% clinical cases fatal, some subclinical infections, generally infects children under 10 yo
rubella virus - epidemiology Are there subclinical infections? How severe in adults? What is a common symptom? How long is immunity after infection?
sometimes subclinical infection
can be more severe in adults
can cause transient arthritis
all infections produce lifelong immunity
western equine encephalitis virus - pathogenesis
Who are dead-end hosts?
Who are the vectors?
humans and horses are dead-end hosts, virus maintained by birds and mosquitoes
eastern equine encephalitis virus - pathogenesis
Who are the dead end hosts?
Who are the vectors?
humans and horses are dead-end hosts, virus maintained by birds and mosquitoes
rubella virus - pathogenesis
Where does this virus multiply?
Is there vertical transmission? If so, what type of vertical transmission?
multiplies in respiratory epithelium… can cross placenta during pregnancy to cause congenital rubella (earlier infectied, more likely to have defects -esp 1st trimester)
eastern and western equine encephalitis virus - incubation period in humans?
7 days
rubella virus - incubation period in humans?
18 days
rubella virus - signs and symptoms
rash lasts 3 days with fever/lymphadenopathy…
congenital rubella can cause cataracts/heart defects like patent ductus arteriosus/deafness/retardation of child (also spontaneous abortion)
rubella virus - vaccines
What type?
How many doses?
live-attenuated vaccine (MMR; 2 doses)
parvovirus - virus type
parvovirus B-19
parvovirus B-19- enveloped?
non-enveloped
parvovirus B-19 - nucleic acid/structure
linear ssDNA
parvovirus B-19 - virion structure
icosahedral
parvovirus B-19 - transmission route
airborne
parvovirus B-19 - diseases and symptoms caused
Transient aplastic crisis
erythema infectiosum (childhood rash = slapped cheek)
hydrops fetalis if infected in first or second trimester
parvovirus B-19 - general epidemiology
Are there subclinical infections?
What is the most common symptom?
What is effect of infection during pregnancy?
often subclinical infection, can cause acute arthritis (most common symptom), infection during pregnancy can cause fetal death via edema (hydrops fetalis)
parvovirus B-19 - epidemiology
Who is affected most severely?
Patients with pre-existing RBC deficit (anemia, sickle cell anemia) have more severe infection = Transient Aplasic Crisis
parvovirus B-19 - pathogenesis
What cells does paro B-19 infect?
Why are certain patients more susceptible to consequences?
infects RBC precursors (inhibits RBC production during incubation)
patients with either anemia or sickle cell anemia are susceptible due to their already low RBC counts.
parvovirus B-19 - incubation period
7 days
parvovirus B-19 - signs and symptoms
normal people have asymptomatic infection OR ///fever, malaise, rash (erythema infectiosum caused by immune complexes)… keratitis presents with red eye/irritation/photophobia (can cause blindness)
parvovirus B-19 - chemotherapy ie what is treatment?
Passive immunization with pooled IgG for people with immunological defects that result in prolonged anemia
papovaviruses - subclasses
Polyomavirus (now its own family apart from Papovaviruses but this is not in our notes)
papovaviruses
What viruses are part of papovirus class?
papilloma virus (HPV); JC virus
papovaviruses - enveloped?
non-enveloped
JC virus - nucleic acid/structure
circular dsDNA
papovaviruses - virion structure
icosahedral
JC virus - transmission route
aerosols
JC virus - diseases caused
progressive multifocal leukoencephalopathy (PML)
JC virus - general epidemiology
Who does this illness occur in?
(ie, this is a slow virus and is present for a long time before becoming an illness)
Occurs in immunocompromised, slow virus
JC virus - pathogenesis
What is the progression of the illness?
How long before death once the illness begins?
Demyelinating disease of brain that infects oligodendeoglia
no inflammation!
reactivation of JC virus causes PML that progresses to blindness/dementia/coma/death within 6 months
Note: progressive multifocal leukoencephalopathy (PML)
kuru - transmission route
consuming brains
creutzfeld-jakob disease (CJD) - transmission route
inherited mutations, spontaneous mutations, corneal transplants + GH preparations (iatrogenic)
variant CJD (mad cow) - transmission route
Consuming beef from infected cows (who were fed brains/bone marrow of cows/sheep)
prions - diseases caused
kuru
creutzfeld-jakob disease (CJD)
variant CJD (mad cow)
kuru - epidemiology What group of people does this effect? What was its peak mortality rate? What is the transmission route? What is the rate now?
limited to stone-age tribe in New Guinea (Fore tribe), caused 1/2 total mortality at peak, transmissible via brain products, low incidence now with reduced cannibalism
CJD - epidemiology
How common is this illness among prions?
Who are the hosts?
What are the causes?
Most common human spongiform encephalopathy
transmitted to primates
Causes:
can be result of inherited mutation (most spontaneous)
some iatrogenic via corneal transplants and GH preparations
vCJD - epidemiology
What started this illness?
Outbreak in England linked to eating beef from infected cows
Kuru - pathogenesis
What is the progression of this illness?
Progressive degenerative disorder of CNS (especially cerebellum), causes spongiform encephalopathy
CJD - pathogenesis
Spongiform encephalopathy
vCJD - pathogenesis
What illness?
What is the cause of this illness?
Spongiform encephalopathy of cows (mad cow disease) from using brains/marrow of cow/sheep for bovine food
herpesviruses - virus types
HSV-1, HSV-2, VZV, CMV, EBV, HHV-6, HHV-7, HHV-8/KSHV
herpesviruses - enveloped?
If so, which ones?
1-5 are enveloped
herpesviruses - nucleic acid/structure
1-5 are linear dsDNA
herpesviruses - virion structure
1-5 icosahedral
herpesviruses - how virus multiplies
1-5: virion adsorbs to cell, fuses with PM, nucleocapsid goes to nucleus, synthesis of proteins/DNA/mRNA, progeny nucleocapsids assembled in nucleus (nuclear inclusion bodies), glycoproteins inserted into nuclear membrane that nucleocapsids bud through, glycoproteins in PM can result in cell fusion (multinucleate giant cells like measles), also has tegument proteins btw envelope and nucleocapsid
HSV-1 - transmission route
saliva
HSV-2 - transmission route
sex, perinatal infection
VZV - transmission route
airborne, contact with lesions
CMV - transmission route
close contact, nasopharyngeal fluid, semen, urine, vaginal secretions
EBV - transmission route
first-basing (kissing, duh!), close oral contact, shared items
HSV-1 - diseases caused
symptoms
herpes, cold sores, herpes simplex encephalitis/keratitis
HSV-2 - diseases caused
symptoms
genital herpesm neonatal herpes simplex (perinatal infection, 6 days after birth)
VZV - diseases caused
chickenpox (primary infection), zoster/shingles (recurrent disease), congenital varicella syndrome
CMV - diseases caused
mononucleosis-like, most frequent viral congenital infection
doesn’t this also cause some degradation of the brain if there is an nervous system infection?
EBV - diseases caused
mononucleosis, oral hairy leukoplakia or tumor (in immunocompromised), Burkitt’s lymphoma (esp African boys), nasopharyngeal carcinoma,hepatitis, fatal lymphoproliferative disease in pts w/mutation that blocks cell-mediated immunity
HHV-6 - diseases caused
roseola infantum (system infection w/rash in infants), MS, CFS, epilepsy
HHV-7 - diseases caused
none known
HHV-8/KSHV - diseases caused
Kaposi’s sarcoma
HSV-1 - general epidemiology
Are there subclinical infections?
Are primary or secondary infections worse?
primary infection often subclinical… often recurrent infections
Primary is worst
HSV-2 - general epidemiology
When is this virus most fatal and to whom?
What is the major disruption caused?
most fatal perinatal infection is acute primary infection around time of delivery
hepato-adrenal necrosis in neonates
VZV - general epidemiology
When do epidemics occur?
Who is most affected?
winter-spring epidemics every few years
patients with impaired immune response get severe/fatal chickenpox
CMV - general epidemiology
What are the cellular feature of a CMV infection?
During what age in life are infections subclinical?
how common is this infection in newborns?
infected cells large with nuclear inclusion
primary infections before puberty often subclinical and
infection of nursing infants is asymptomatic
most frequent viral congenital infection
EBV - general epidemiology
What illness does EBV usually cause?
What age group of people usually see a clinical infection?
How does EBV affect the immune system?
Where in the body does the virus reproduce/shed?
most common cause of infectious mononucleosis
disease of teenagers and young adults
immortalizes B-cells
virus found in saliva and produced by lymphoid cells in oro-pharynx
HHV-6 - general epidemiology
What is the prevalence? in human populations?
90% prevalence worldwide, 1% have HHV-6 integration
HHV-8 - general epidemiology
What co-infection is HHV-8 usually found with?
most frequent neoplasm in persons with AIDS
15-20% AIDS patients develop KS
HSV-1 - epidemiology
What brings an latent infection into clinical infection?
Where in the body is the virus latent? Where does it travel to become clinical?
What is the prevalence of infection in adults?
- latent infections activated by…
fever, UV light, emotion - virions transported down axon to site of initial infection, produce cold sores
- 80% seroprevalence in adults
HSV-2 - epidemiology
Are infections once and done or recurrent?
What percentage of the U.S. population is sero-positive?
What precautions during birth should be taken if the mother has an active infection?
can cause recurrent infection
20% of US population seropositive
vaginal lesions before delivery indication for C-section
VZV - epidemiology
What age group is most affected by Zoster clinical infection? Why?
What other type of patients is at risk for Zoster infection?
- zoster risk increases after 50 yo (decline in cell-mediated immunity)
- immunosuppressed pts at risk for disseminated zoster (spread by viremia)
CMV - epidemiology
What similarities and differences exist between CMV and mononucleosis?
* Where is infection common (age group and external location?
* Do recurrent infections occur?
appears like mononucleosis with negative heterophile test
- transmission common in nursery schools
- can be post blood transfusion complication
- recurrent disease only in immunocompromised
EBV - epidemiology
What cancer does this cause?
What is the prognosis for young males, if untreated?
What are the different illnesses that this virus causes (aside from mono)?
Burkitt’s lymphoma most frequent childhood tumor in Africa, boys at greater risk, if untreated will die in 6 months… can also cause nasopharyngeal carcinoma, Hodgkin’s disease, gastric carcinoma, AIDS patients tumors
HSV-1 - pathogenesis
Where (body part) does this virus first infect?
Where does this virus remain as a latent infection?
primarily infect nose/eyes/fingers/mouth… travels into sensory ganglia for latent infection
HSV-2 - pathogenesis
Where does this virus remain as a latent infection?
primarily infect sensory ganglia in genital region (sacral ganglia)
VZV - pathogenesis
Where (in the body) does the virus initially infect?
Where is the virus latent?
What immune feature is present in the latent virus location?
infection in respiratory tract followed by viremia, latency established in sensory ganglia, monocyte infiltration of involved ganglion
CMV - pathogenesis
How does vertical infection occur?
virus can cross placenta to cause congenital disease, latent infected cell type unknown
EBV - pathogenesis
What cells are infected?
What is the process by which the cancer causes infection?
infects B-cells (attacked by CTLs)… for Burkitt’s lymphoma, often involves translocation placing c-myc protoncogene under Ig promoter
HHV-8 - pathogenesis
What growth factor does this virus cause to be expressed?
tumor cells express high cellular VEGF (for vascularization)
HSV-1 - incubation period
7-14 days
HSV-2 - incubation period
7-14 days
VZV - incubation period
14-21 days
CMV - incubation period
3-12 weeks
EBV - incubation period
4-6 weeks
HSV-1 - signs and symptoms
cold sores, stomatitis (with vesicles in mouth), encephalitis (temporal lobe), keratitis (red eyes)
HSV - 2 - signs and symptoms
lesions on genitalia, primary infection - bilateral lesions or asymptomatic, recurrent disease - fewer lesions that are unilateral
VZV - signs and symptoms
fever, rash, lesions… congenital varicella can result in limb atrophy/scarring of skin… post-herpetic neuralgia (pain after zoster lesions heal), zoster lesions have unilateral, dermatomal distribution
CMV - signs and symptoms
Also, if the patient has a co-infection with AIDS, what symptoms are common?
congenital CMV can result in microcephalic mental retardation with intracerebral calcifications, neuro-sensory deafness, jaundice, enlarged liver/spleen, anemia// immunosuppressed get generalized infections, AIDS pts have high incidence of retinitis and gastroenteritis caused by CMV
EBV - signs and symptoms
fever, sore throat, lymphadenpathy… oral hairy leukoplakia (white patches on tongue/buccal mucosa)
HHV-6 - signs and symptoms
systemic infection with rash in infants, high fever
HHV-8 - signs and symptoms
multiple, pigmented, highly-vascularized nodules on skin
HSV-1 - lab diagnostics
PCR detection in CSF for herpes simplex encephalitis
CMV - lab diagnostics
mononucleosis with negative heterophile test, owl’s eye inclusion bodies
EBV - lab diagnostics
Also, do antibodies neutralize EBV?
heterophile test (antigenic cross-reactivity of Abs to EBV and sheep RBCs), Ab does not neutralize EBV
VZV - vaccines
live-attenuated (reduces clinical infecions by 85%, reduces severe infections by 97%, elderly should receive booster
CMV - vaccines
experimental live virus vaccine
HSV-1 - chemotherapy
trifluridine for recurrent keratitis
adenine arabinoside for encephalitis
acyclovir for systemic infection and for encephalitis
HSV-2 - chemotherapy
acyclovir
VZV - chemotherapy
- Passive immunization with IgG (VZIG)
- acyclovir (can reduce risk of post-herpetic neuralgia too)
- foscarnet
CMV - chemotherapy
ganciclovir, Foscarnet (PPi analogue)
papovaviruses - virus types
papilloma virus (HPV)
HPV - enveloped?
non-enveloped
HPV - nucleic acid/structure
circular dsDNA (10 genes so relies greatly on host proteins)
HPV - virion structure
icosahedral
HPV - how virus multiplies
has early and late (capsid) genes… early gene can bind promoter to recruit DNApol for genome replication, all genes essential for virus growth,
HPV - transmission route
direct contact, sexual contact, perinatal
HPV - diseases caused
Papillomas (plantar genital, and anogenital warts), cervical carcinoma, condylomas, association w/H&N cancers
HPV - general epidemiology
what is the prevalence in college-aged women?
What is a common disease caused by HPV?
- 1/3 college women have HPV in cervix
- 80-90% of cervical carcinomas have HPV integrated into host genome
- other cofactors like smoking can cause cervical carcinoma
HPV - epidemiology
What illnesses are caused by HPV 6b and HPV 11?
What illnesses are caused by HPV 16 and HPV 18?
condylomas (from nononcogenic HPV 6b and 11), >75% cervical carcinomas from HPV16 and HPV18
HPV - pathogenesis
Is there virus integration in warts?
Is there virus integration in cervical cancers?
What is the mechanism of uncontrolled cell proliferation?
- in warts the viral genome is not integrated
- in cervical tumors, early genes are integrated
- early genes E6 binds p53 to inactivate it and E7 binds Rb to inactivate it (both tumor suppressors)
HPV - lab diagnostics
Pap smears
HPV - vaccines
recombinant vaccine based on viral capsid protein
retroviruses - virus types
human T-cell Leukemia virus-1 and 2 (HTLV 1/2) and HIV
retroviruses - virus types
disregard, repeated question
disregard, repeat
retroviruses - subclasses
oncoviruses and lentiviruses
retroviruses - subclasses
oncoviruses and lentiviruses
oncoviruses - virus types
HTLV 1 and 2
oncoviruses - virus types
HTLV 1 and 2
HTLV-1 and 2 - enveloped?
enveloped
HIV - enveloped?
enveloped
HTLV-1 and 2 - nucleic acid structure
+ssRNA, two identical copies
HIV - nucleic acid structure?
+ssRNA, two identical copies
HTLV-1/2 - how virus multiplies
RT makes DNA from RNA, DNA integrates into host genome
HTLV-1/2 - how virus multiplies
RT makes DNA from RNA, DNA integrates into host genome
HTLV-1/2 - transmission route
sexual contact, blood, breast milk (horizontal transmission)
HTLV-1/2 - transmission route
sexual contact, blood, breast milk (horizontal transmission)
HTLV-1/2 - disease caused
adult T-cell leukemia (ATL; from HTLV-1), cutaneous T-cell lymphoma
HTLV-1/2 - disease caused
adult T-cell leukemia (ATL; from HTLV-1), cutaneous T-cell lymphoma
HTLV-1/2 - general epidemiology
endemic in southern Japan, central Africa, Caribbean… 0.025% incidnece in US
HTLV-1/2 - general epidemiology
endemic in southern Japan, central Africa, Caribbean… 0.025% incidnece in US
HTLV-1/2 - epidemiology
ususally asymptomatic, 0.1% infected individuals develop ATL after 10-30 year latency
HTLV-1/2 - epidemiology
ususally asymptomatic, 0.1% infected individuals develop ATL after 10-30 year latency
HTLV-1/2 - pathogenesis
viral tax protein is transcription factor that induces IL-2 and receptor for autocrine loop for transformation
HTLV-1/2 - pathogenesis
viral tax protein is transcription factor that induces IL-2 and receptor for autocrine loop for transformation
