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Herpesvirus-1 Alpha herpesvirus yes IE (immediate early) proteins - bind DNA, regulate transcription immunofluorescence,
(HSV-1) (latent in sensory E (early) - transcription factors, DNA polymerase, thymidine culture, PCR
neurons) gD is main kinase (TK)
glycoprotein; L (late) - structural proteins, glycoproteins, envelope coat topical acyclovir, or
gp's B, D, H, L -DNA replicates in nucleus, but envelope received in cytosol start IV if suspect
for attachment -gp's + tegument = envelope encephalitis, even
and infectivity! Pathogenesis: CTL mediated response before results come
-evades endosomes released in infectious form! back!
-virus migrates to sensory ganglia during primary infection, lives there Ribavarin
until reactivation: during stress, vesicles appear again, may be due
to a deficiency in IFN- no vaccine
-blisters contain multinucleated giant cells and intranuclear inclusions
Receptors: heparan sulfate, Hve A,B,C,M, Nectin 1,2,
Diseases: virus + immune response (although many are asymptomatic)
1. Gingivostomatitis - swollen vesicles on mucous membranes
2. Whitlow - watery finger pustule spread from primary infection
3. Keratitis - corneal infection, very common cause
4. Encephalitis - fever, personality change, focal seizures
5. Eczema herpeticum - in presence of underlying eczema
Latency = transcription but no translation
Herpesvirus-2 Alpha herpesvirus yes pathogenesis same as HSV1, just antigenically distinct (diff. gp's) immunofluorescence,
(HSV-2) (latent in sensory genital infection, usually with self-limited meningitis culture (24-48 hrs),
neurons) gD is main Diseases: PCR
glycoprotein 1. neonatal infection - transplacental viral transfer, attack rate higher
if mother is newly infected near time of birth (otherwise do C-section) acyclovir, oral or IV
a) skin and mucous membrane infection - skin rash, DIC if untreated (fam or valacyclovir
b) CNS infection - fever, lethargy, seizures, CSF abnormal is oral)
c) disseminated - hepatosplenomegaly, jaundice, high mortality!
no vaccine yet
Varicella-zoster Alpha herpesvirus yes no asymptomatic shedding, only infectious when clinically apparent culture (5-7 days)
virus (VZV) (latent in sensory can be transmitted during pregnancy and delivery - give newborn IgG immunofluorescence
neurons) gE is main cell-mediated immune response most important PCR
glycoprotein Pathogenesis: inhaled virions infect respiratory mucosa
-cell-cell spread only, unless talking about skin vesicles - enveloped acyclovir, oral or IV
infectious virions produced in vesicles (famciclovir or
-T lymphocytes infected, viremia ensues, get skin vesicles valacyclovir for elderly
-virions in vesicles migrate up sensory root and are latent in ganglia with zoster)
only to reappear in zoster
-lytic infection, regulatory protein expression nuclear; latent infection, vaccine is live
regulatory protein expression is cytoplasmic attenuated, 85%
-ORF 62 (open reading frame) protein is critical in formation of new viruses effective - contraindicated
and maintenance of latent infection in immunocompromised
Receptors: heparan sulfate, mannose-6-phosphate receptor
1. Varicella (chickenpox) in children - skin vesicles (adults are 25x
more likely to have severe disease)
2. Zoster (shingles) in adults only as reactivation of latent VZV
rash distributed along sensory nerve root one on side of body
3. Post-herpetic neuralgia, a rare development after zoster reactivation
Cytomegalovirus Beta herpesvirus yes Pathogenesis: infection is through saliva, tears, urine, sexual contact tissue culture looks
(latent in lymphoid -not airborne! no skin lesions inclusion bodies,
and other cell types gB and gH -infectious virus can persist on table-tops day care problem immunofluorescence
like salivary glands -latent in bone marrow precursors of monocytes
and the kidney) -down-regulates MHC class I, evades immune system no acyclovir! Use
Diseases: ganciclovir, foscarnet,
1. self-limited mono in immunocompetent patients cidofovir
2. CMV infection in immunocompromised - pneumonia, fever, retinitis,
colitis, lymphadenopathy, rash, encephalitis, neutropenia no vaccine
-reactivation common in transplant pts, AIDS pts
3. Congenital CMV - transfered during pregnancy, risk highest during
1st trimester. If acquired at birth, disease not as bad.

Epstein-Barr virus Gamma herpesvirus yes Pathogenesis: asymptomatic people shed virus in saliva (+) heterophile test
-lytic infection, tumor virus monospot test =
gp350 binds to -evades immune system with 1L-10 mimics, IFN, inhibits apoptosis Viral capsid antigen -
CD21 on B -latent EBV lives in memory B cells (VCA) early test
cells Diseases: EBV nuclear antigen-
1. Infectious mononucleosis - fever, malaise, pharyngitis, myalgias, (EBNA) late test
lymphadenopathy, hepatosplenomegaly
2. Nasopharyngeal carcinoma no good treatment
3. B-cell lymphoma steroids for
4. Leiomyosarcoma complications
5. Oral hairy leukoplakia in AIDS pts
6. X-linked lymphoproliferative disease (in males only) no vaccine
Kaposi Sarcoma Gamma herpesvirus yes only appears in immunocompromised patients treat with chemo or
herpes virus (HHV8) (latent in lymphoid strongly linked to male-male sex radiotherapy
cells) Pathogenesis:
-pirated human genes for it's own repertoire, such as IL-6, Bcl-2, no vaccine
chemokine genes
Disease: oncogenesis is via transformation
1. Kaposi's Sarcoma in AIDS pts
2. primary effusion lymphoma = body cavity B-cell lymphoma
3 Castleman's disease - malignant lymphoproliferative disease
Influenza A Orthomyxoviridae yes 8 segments of RNA, so can shift and drift! Shift causes major epidemics - if one cell clinical symptoms,
infected with two strains, they can mix - not recognized by any human antibodies nasopharyngeal
RNA replicates in the nucleus, which allows for easier antigenic shifting / drifting swab or rapid antigen
A has greatest mutation rate test
-HA is hemagglutinin glycoprotein, binds sialic acid residues on host cells like RBCs Amantadine,
sticks out of viral outer membrane; anchored by M-proteins Rimantadine (interfere
-NA is neuraminidase protein, cleaves mucin neuraminic acid, exposing sialic acid with viral uncoating)
residues beneath so HA can bind; also anchored by M-proteins only for flu A;
-M1 protein anchors HA and NA, provides stability Zanamivir (inhaled-bad for
-M2 becomes ion channel in endosomes once endosome is acidified - acid activated asthmatics)
-also has viral polymerase, nucleocapsid, and nonstructural proteins and Oseltamivir (oral)
Pathogenesis: good for A and B, work by
Tryptase Clara (protease) secreted by non-ciliated Clara cells in bronchial epithelia cleaves inhibiting NA protein;
HA into 2 subunits, which allows fusion of virion and host cell membrane Ribavarin interferes with
viral HA attaches to host cell and is endocytosed mRNA, stops RNA
once endosome is acidified (via M2 in influenza A), virus uncoats polymerase
viral RNA is released and transported to nucleus, mRNA is transported out of nucleus
and translated; copies of RNA with ribonucleoprotein also transported out of nucleus 2 vaccine:
HA and NA brought to surface of host cell and stick out, M proteins accumulate, injected is whole
packaged RNA is incorporated and virion buds off killed;
Disease: inhaled is live
1. Influenza - fever above 101F; myalgia, chills or malaise; cough or respiratory discharge attenuated
abrupt onset, lasts for 2-4 days but some symptoms can persist for 2 weeks
a) complications: pneumonia, either viral or bacterial
-if viral, can be from actual influenza - lower tract involvement, can be fatal in young adults!
-if bacterial, two most common infections are S. pneumo and Staph aureus - can be fatal,
especially in older adults and pts with chronic medical conditions
-also neurological - post-infectious encephalitis - self-limited
Influenza B Orthomyxoviridae yes segmented RNA , so can shift and drift diagnosis same as
no M2 protein! above, can also use
Pathogenesis basically same as above DFA
Disease same as above
-can have myositis as complication of Influenza B neuraminidase inhibitors
effective for
flu A and B

Influenza C Orthomyxoviridae yes segmented RNA, but not associated with significant morbidity/mortality yes
no NA protein! No real shift associated with flu C
see above for general info about influenza

Parainfluenza virus Paramyxoviridae yes Disease: Ribavarin

1. respiratory infections that are a little milder than flu - rhinitis, pharyngitis, sinus
congestion, bronchitis and flu-like symptoms no vaccine
2. Croup - infection of larynx and upper resp. tract, coughs sound like barks

Respiratory Paramyxoviridae yes occurs in winter months characteristic

Syncytial virus Th2 response - cell-mediated immune response most important formation of syncytia
Virulence: glycosylated surface proteins F (fusion), G, and SH mediate attachment & fusion (fusion of multi-nuc
-proteins N, L, P assc. with nucleocapsid, M (matrix) proteins, NS (nonstructural) proteins giant cells)
which may play a role in RNA replication
Pathogenesis: inoculation is via eyes or nose, infection limited to respiratory tract -aerosolized Ribavarin
-G and SH mediate attachment to host cell (interferes with viral
-F protein helps virion fuse RNA polymerase)
-replication of RNA and formation of mRNA can be given to high
-virion assembly and budding risk pts, but is
-if lower tract involvement, atalectasis and trapped air, especially in young children teratogenic
-easily transmissible, reinfection is common b/c immunity is not complete -treat high risk infants
Disease: with RSV-Ig or
1. Bronchiolitis in infants - nasal congestion, sore throat, fever, increased RR, can see Palivizumab
retraction of intercostal muscles (means lower tract involvement); lungs are hyperinflated (monoclonal
-duration = 7-21 days RSV antibody)
2. Pneumonia in adults - nasal congestion, cough - significant mortality! 20% in older pts
no vaccine

Adenovirus Adenovirus no transmission by respiratory droplets, fecal-oral route, and direct contact Ribavarin
outbreaks occur in crowded conditions
Pathogenesis: capsid contains a fiber that helps the virus attach to host cells only military uses vaccine
-pharyngitis, conjunctivitis, cystitis, pnuemonia, gastroenteritis
Rhinovirus Picornavirus no occurs in early fall and spring clinical symptoms
optimal growth at 33C, which is temperature of nose and large airways
uses ICAM-1 can survive on environmental surfaces for hours - efficient transmission treatment is
as receptor Virulence: noncytolytic - host immune response is responsible for most of symptoms symptomatic - treat
-many differect serotypes, so vaccine not really possible with over-the-counter
Pathogenesis: cold remedies
-virus enters via nasal or ophthalmic mucosa not antibiotics!!
-replication occurs in lymphoepithelial cells in nasopharynx - no viremia
-usually upper respiratory infections, but can involve lower tract no vaccine
-IL-8 released from infected cells causes more rhinorrhea and nasal congestion
1. Common cold! sneezing, coughing, rhinorrhea, nasal congestion, pharyngitis - 1 week
-high fevers, myalgias, chills are not commonly seen
-green nasal discharge not indicative of bacterial infection! color is from myeloperoxidase
a) also acute sinusitis, otitis media, exacerbations of chronic bronchitis, asthma attacks

Rabies virus Rhabdovirus yes transmission via bite from infected animal diagnosis uses RT-PCR
100% fatal if untreated! high neuroinvasiveness, high neurovirulence of brain, Negri bodies
Virulence: RNA encodes: in brain tissue, CSF
L protein (polymerase) - capping, methylation P protein - transcriptional activator culture, urine, saliva
M protein - bridges RNA and envelope N protein - wraps the template
G protein - antigenic glycoprotein spike treatment is post-
Pathogenesis: virus enters through a break in the skin, across a mucosal surface or inhaled exposure prophylaxis
-virus replicates and infects muscle spindle infects nerve to muscle, travels centrally (vaccine + Rabies Ig)
-once it reaches the spinal cord, virus spreads to CNS with almost every neuron infected
-after CNS spread, there is peripheral spread to the rest of the body (saliva, stool, etc) 2 vaccines:
Disease: whole killed administered
1. Rabies - incubation may be 1-week to a year! biphasic at 0, 3, 7, 14, 28 days;
a) febrile prodrome followed by excitation phase or passive Ig shot
b) paralysis - paresthesias at site of bite, spasm of laryngeal muscles, coma, paralysis injected at site
inevitable death
Vaccine does not work if clinical symptoms have already started.
Poliovirus Picornavirus no Pathogenesis: enteroviruses enter through GI tract from fecally contaminted material diagnosis from throat
(enterovirus) -virus replicates in submucosal lymphatic tissues in gut secretions in 1st week
-virus penetrates host cells, uncoats, and releases RNA into cytoplasm of illness;
-4 viral capsid proteins and 8 non-structural proteins are transcribed can't use CSF;
-inhibition of host cell protein synthesis serology
-release not necessarily cytolytic
-minor viremia in lymphatic tissue, major viremia in bloodstream no treatment
-polio specifics: hematogenous spread to CNS motor and autonomic neurons (not sensory)
attacks gray matter of anterior horn and motor nuclei of pons ans medulla 2 vaccines:
Disease: OPV (oral) can revert to
1. Asymptomatic - 95% wild-type, also assc. w/
2. Abortive poliomyelitis - fever, headache, abdominal pain, anorexia - self-limited paralytic dz;
3. Nonparalytic poliolyelitis - looks like aseptic meningitis IPV (inactivated) given
4. Spinal paralytic poliomyelitis - 0.1% - biphasic illness IM as series of 4 shots
a) minor: looks like abortive polio, lasts a few days, then well for 2-5 days
b) major: headache, fever, vomiting, neck stiffness, muscle pain relieved by motion
results in weakness and eventually flaccid paralysis (can be 1 muscle or many)
5. Bulbar paralytic poliomyelitis - paralysis of cranial nerves, usually IX and X
6. Polioencephalitis - rare, can occur in infants; changes in mental status

Coxsackievirus Picornavirus no infections occur in late summer, early fall CSF is clear with PMNs
(enterovirus) replication, pathogenesis and epidemiology same as polioviruses at first, then lymphos
Disease: (glucose + protein nl) -
1. Aseptic meningitis - common in children - fever, followed by headache, stiff neck, URI culture or PCR
self-limited, all pts recover
2. Summer cold - rhinorrhea, sore throat, etc. treat symptomatically
3. Encephalitis (rare) - lethargy, seizures, but excellent prognosis
4. Hand-Foot-and-Mouth disease - fever and vesicles in mouth, hand, feet; mouth pustules no vaccine
help differentiate between this and chickenpox; very contagious!
5. Herpangina - vesicular rash in oropharynx; fever, vomiting, sore throat, painful to swallow
6. Transient paralysis - flaccid paralysis
7. Epidemic pleurodynia - sharp muscular pain with spiking fevers after each paroxysm
8. Myopericarditis - inflammation of heart muscle; virus replication in myofibers necrosis
seems to attack young adults, esp. males; can lead to dilated chronic CHF
9. Neonatal myocarditis or hepatitis
Echovirus Picornavirus no infections occur in late summer, early fall PCR, viral culture
(enterovirus) replication, pathogenesis and epidemiology same as polioviruses
Disease: symptomatic treatment
1. Aseptic meningitis - fever, followed by headache, stiff neck, URI
2. Summer cold - rhinorrhea, sore throat, etc. no vaccine
3. Chronic meningoencephalitis only in patients with defects in B-cell function - can be fatal
4. Transient paralysis
5. Acute hemorrhagic conjunctivitis - pain, swelling of eyelids - contagious, bilateral!
6. Myopericarditis - inflammation of heart muscle; virus replication in myofibers necrosis
seems to attack young adults, esp. males; can lead to dilated chronic CHF
7. Neonatal myocarditis or hepatitis
Rotavirus Reovirus no segmented RNA, but major antigenic shifts don't occur clinical diagnosis
infections occur during 3-4 months in winter ELISA or PCR to
responsible for 10-20% of all diarrheal-related deaths in children detect rotavirus in
spread by fecal-oral route, resistant to stomach acid since no envelope stool
-since ds RNA, must package own RNA polymerase to make mRNA supportive treatment
-binds to sialic acid residues with fluids, don't use
-once swallowed, infects mature villus epithelial cells of small intestine death of cells anti-diarrheals
leading to decrease in absorptive area, may result in lactase deficiency
Disease: Rotashield vaccine
1. Gastroenteritis - vomiting and watery diarrhea, nausea, high fever pulled from US market

Rubella virus Togavirus yes transmission via respiratory droplets serology

envelope contains HA (hemagglutinin) protein and F (fusion) protein
Pathogenesis: virus enters via nasopharynx, replicates in regional lymph nodes symptomatic
-viremia follows, hematogenous spread
Disease: live attenuated vaccine
1. German measles - mild fevers, rash on head and neck, spreads to body part of MMR
resolves in 2-3 days, but contagious for 7 days
2. Congenital rubella syndrome - rubella acts as a teratogen severe birth defects
don't give vaccine to women during pregnancy or within 3 months of conceiving
Calicivirus Calicivirus no spread by fecal-oral route clinical, epidemiological
encodes 4 proteins - helicase, protease, RNA polymerase, capsid protein diagnosis; ELISA
can withstand heat and chlorination (swimming pools, disinfectants)
Pathogenesis: causes blunting of small intestinal villi, esp. jejunum supportive treatment
-virus shedding in stool highest in first 1-2 days with fluids
-extremely contagious!
Disease: no vaccine
1. Gastroenteritis - vomiting and diarrhea, fever, myalgias, malaise; 2-3 days then done

Coronavirus (SARS) Coronavirus yes infections occur in winter and spring clinical diagnosis
virulence probably due to recombination event of 2 different coronaviruses viral cultures and PCR
infects multiple species, cats, dogs, etc - spread by respiratory droplets and other secretions being tested now;
Disease: ELISA (+) after 1 month
1. SARS - 2-7 day incubation, but up to 10 days - important for sequestering possible pts
a) fever - then chills, headache, malaise, maybe diarrhea supportive treatment
b) dry cough, shortness of breath, which may rapidly progress to respiratory distress that
requires mechanical assistance no vaccine
-CXR shows increasing infiltrates and consolidations
-lymphopenia, thrombocytopenia, elevated creatinine and LFT's
Human Retrovirus yes carries 2 identical copies of RNA and reverse transcriptase enzyme acute - use ELISA,
Immunodeficiency ten billion virions are produced and destroyed each day; HIV is not latent! Western blot, and RNA
viruse (HIV) -gp120 amd viral set point reached at ~6 months, lose about 50 CD4 cells per year viral PCR
gp41 most Virulence: AIDS - use CD4 count
important -gag codes for internal structural proteins and RNA viral load
-pol codes for reverse transcriptase, protease, integrase
-memory CD4 -env codes for gp120 (binds to and gp41 Treatment: almost
cells do not -tat (transcription factor) binds RNA LTR sequence to enhance transcription always triple combo!
have viral -rev regulates export of full genomic (unspliced) RNA Resistance if less
surface -nef down-regulates host cell MHC class I and CD4 expression, enhances release of virus (see syllbus for combos)
proteins (nef deletion results in much slower progression of disease)
-virion maturation is completed as it is budding off the host cell no vaccine
Pathogenesis: acute infection - dendritic cell binds HIV with DC-SIGN receptor,
brings to lymph node, where extensive replication occurs
-gp120 binds to CD4 and CCR5/CXCR4, then gp41 inserts into membrane and allows
fusion with host cell
-clinical latency for up to 10 years or more - depends on immune response, HLA type, etc
1. Acute HIV infection - fever, lymphadenopathy, macular rash, fatigue, sore throat
can treat at this stage to delay onset of AIDS
2. AIDS/Opportunistic infections - usually with CD4 counts under 200, reactivations of latent dz
a) TB: CD4 = 300
b) PCP: CD4 = 200
c) Toxoplasmosis: CD4 = 100
d) Cryptococcal dz: CD4 = 100 - diarrhea may be dominant symptom
e) M. avium complex: CD4 = 50 - diarrhea may be dominant symptom
f) CMV: CD4 = 50
g) cryptosporidium - diarrhea

West Nile virus Flaviviridae yes vector-borne disease - transmitted by mosquito bite, usually in late summer clinical diagnosis
previously described virus, but in new location and serology
human-human transmission possible because of blood transfusions, organ transplantation,
and breast-feeding supportive treatment
single polyprotein made from RNA - encodes M (membrane), E (envelope) and many NS (IFN + Ribavarin in
(nonstructural) proteins clinical trials)
neurons don't express MHC class I, so CTL's can't kill infected neurons
Pathogenesis: mosquito bite leads to viral replication in peripheral sites no vaccine yet
-viremia in blood follows, with eventual CNS invasion and disease
1. Asymptomatic - most common
2. Flu-like illness, abrupt onset with fever, headache, sore throat, rash, lymphadenopathy
3. Encephalitis - flu-like syndrome progresses to encephalitis, with changes in mental status
and focal neurological abnormalities profound muscle weakness prominent feature
-neuronal apoptosis induced by virus, CSF pleocytosis
-elderly at greatest risk; overall mortality ~5%
Dengue virus Flaviviridae yes vector-borne disease - transmitted by mosquito bite, usually in late summer clinical diagnosis
most common arthropod-borne viral infection; worldwide distribution in warmer climates
same structure for all flaviviridae (see above) supportive treatment
same pathogenesis as above (mosquito bite, viremia, CNS invasion) essential for survival;
major exception - cross-protective immunity does not occur, reinfections are often worse! Ribavarin?
1. Dengue fever (DF) encephalitis - 2-7 day incubation period vaccine becoming
a) joint/bone pain, fever, headache, retro-orbital pain, then vomiting, respiratory symptoms available
b) fever, rash, lymphadenopathy, cytopenia
-NO fatalities!
2. Dengue Hemorrhagic fever (DHF) - dengue-like illness with thrombocytopenia and
increased hematocrit - usually 2nd infection, but can be first
-increased vascular permeability = TNF, IL-8, apoptotic endothelial cell death
-bleeding diathesis = cytokines, vascular injury, viral antibodies to platelets
-circulatory failure with GI bleeding, pulmonary edema, neurological manifestations
-can lead to shock
-10% fatal if untreated, less than 1% fatal if treated
Reasons why re-infection is worse: pts have non-neutralizing antibodies to DF that will bind
the virus, and simply target it more efficiently to the Fc receptors on macrophages, where
it can replicate faster; this is called antibody-dependant immune enhancement
-also, memory CD4+ and CTL's results in increased cytolysis of Dengue-infected
macrophages, which results in much higher amounts of cytokines and vasoactive mediators

Yellow fever virus Flaviviridae yes vector-borne disease - transmitted by mosquito, usually in late summer serology, viral culture
same structure as above (flaviviridae) no liver biopsy!
occurs exclusively in Africa and Americas, not Asia - no human-human transmission
different mosquitos transmit different diseases - jungle yellow vs. urban yellow supportive treatment;
Pathogenesis: mosquito bits leads to replication in regional lymph nodes, followed by Ribavarin?
hematogenous dissemination and liver infection - degeneration and "Councilman bodies"
caused by direct viral injury live attenuated vaccine
-vasoactive and inflammatory cytokines are released hemorrhagic diatheses, shock boosters given q. 10yrs
1. Yellow fever - 3-6 day incubation period, 3 stages of disease
a) viremia - fever, chills, headache, back pain
b) remission, lasts 1 day
c) intoxication - jaundice, "black vomit" hematemesis, shock - no viremia
-in pts with jaundice, mortality is 20-50%
Measles virus Paramyxoviridae yes transmission via respiratory droplets Koplik spots are
envelope contains HA and F proteins, virion also comes with RNA polymerase diagnostic
Th2 response
Pathogenesis: virus infects epithelium of respiratory tract, spreads to local lymph nodes symptomatic treatment
-viremia follows, hematogenous spread Ribavarin?
1. Measles - 7-14 day incubation - fever, rhinitis, cough, conjunctivitis, photophobia live attenuated vaccine
Koplik spots appear in the mouth, followed by rash on head and then trunk - not part of MMR - 2 doses are
contagious at this point recommended

Prions Prions (different) proteinaceous infectious particles clinical syndromes,

no genome, not inactivated by UV light, heat, or formaldehyde history
Biology: PRPc is a normal human protein on chromosome 20. Infection results in PRPsc.
PRPc = It is -helical, protease sensitive, located on cell surface no treatment
PRPsc = -sheets, protease insensitive, located in cytoplasm
-insolubility b/c of protease insensitivity thought to cause storage problems and aggregation
Diseases: TSE = transmissible spongiform encephalopathies
1. Kuru - spread by exposure to brains/mucous membranes of infected individuals
headaches, arthralgias, neurologic disease and death within 3months - 1year
2. CJD (Creutzfeldt-Jakob disease) - can be sporadic or from infected surgical instruments
vCJD = mad cow disease (variant); death within 3-6 months
-looks like Alzheimer's disease, lack of coordination, dementia, motor weakness
3. Fatal familial insomnia - autonomic dysfunction and sleep disturbances
thalamic, cerebellar changes
4. Gerstmann-Straussler-Scheinker (GSS) disease - autosomal dominant,
progressive spinocerebellar degeneration and accumulations of plaques in cerebellum