Virology 2

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What makes up a virion?: NA
proteins
sometimes a lipid envelope w/glycoproteins
What are nucleocappsids??: regularly organized nucleoprotein structures that can be crytallized, are robust, yet permiable to small molecules
/what are viroids?: Plant pathogens:

small, covalently closed circular ssRNAs that have no ORFs

Appear to be regulatory RNAs whach are never packaged into protein jackets as per viruses;

essentially transmissible RNA plasmids
What is a virion made of?: NA
proteins
sometimes a lipid env w/glycoproteins
What is a capsid made of?: small number of repeating protein units called capsomers or cpsomeres
What is the nucleoocapsid?: viral genome + capsid
3 generalforms of nucleocapsid morphology/symmetry: 1) helical/rod
2) icosahedral/spherical
3) complex
How many faces in an icosaedron?: 20
How many vertices in an icosohedron?: 12
Process of envelope acquiring: 1) viral env proteins synthesized and trafficked to specific cell membrane
2) initially insert at random, but attractive forces cause them to cluster
3) cyto-side domains in nucleocapsid interact with cytoplasmic side domains of the membrane proteins; "docking" occurs
4) nucleocapsid buds through this patch
What characteristics do envoloped viruses have?: 1) need envelope to survive
2) sensitive to lipid solvents (chloroform, ether, detergents, bile_
3) few are stable in GI tract (bile) and transmitted fecal-oral
4) istable in dry/nonaqueous environment
Where are the proteins in certain viruses that cause syncitium formation?: in the lipid envelope
Pox family members: variola
vaccinia
monkey pox
molluscum contagiousum
Herpes family members: HSV
VZV
LMV
EBV
HHV 6/7
HHV 8
Monkey B
Papova family members: Polyoma
Papilloma (HPV)
Vacuolating agent
Hepadna family members: HBV
Retro family members: HIV
HTLV
Picorna family tree: Subsets:
1) rhino
2) entero
3) Hepato (hep A)

Entero members:
1) coxsackie
2) echo
3) polio
4) entero
Calici virus members: Norwalk agent
Togavirus members: rubella
alpha virus
Flavivirus members: Hep C
SLE
JE
TBE
WNV
Dengue
Yellow fever
Rhabdo family members: rabies
Bunya faamily members: hemorrhagiv fever + renal
Hantaan pulmonary syndrome
Arenavirus family members: Lasaa fever
Argentine + Bolivian hemorrhagic fever
Filo family members: Ebola
MArburg
Reovirus members: Rotavirus
How many segments in rotavirus?: 11
What do you treat with ribavirin?: Bunya and arenaviruses (hemorrhagic fevers, etc)
which DNA dep RNA pol is used to make mRNA?: DNA dep RNA pol II
summarize reverse transcription: 1) (+) ss RNA --> ds RNA/DNA hybrid [RTase]
2) RNA/DNA hybrid --> ss (-) DNA [RNase H]
3) ss (-) DNA --> ds DNA [RTase]
which 2 virus families use RT path?: Retro
Hepadna (HBV)
Once you have ds DNA, where do the stages of RTase pathway occur?: 1) ds DNA --> mRNA : nucleus (via host RNA pol II)

2) mRNA --> ds DNA : cytoplasm (RTase and RNase H)
is there net amplification in reverse transcription?: No. 1 ss RNA --> 1 DS DNA. no neta mplification.
WHat do you use ganciclovir on?: CMV
What is the deal with a infidelity of on in 10^-4?: Roughly 1 error per genome synthesized.

If it were 10 -3, you'd get 10 errors per genome and probably no viable progeny virus
Name the 2 "periods" of infection: 1) exclipse period: time from initial infection until intracellular assembly of the virions

2) latent period: time from the initial infection until the first infectious virions are released
What is the MOI?: multiplicity of infection

Number of infectious virions per cell, at the outset of infection process in a ell culture.
Describe subdivisions of eclipse period for Most DNA viruses: 1) early synthesis phase: before viral DNA synthesis. Sythhesis of viral enzymes and regulatory proteins that will play roles in viral DNA synthesis and late viral transcription

2) late synthesis phase: begins rougly with onse of DNA synthesis. Late proteins are predominantyly virion/structural proteins
do most viruses replicate in human RBC's?: no, but RBC's often nevertheless have virus receptors. utilized in hemagglutination and hemadsorption tests.
what are the 2 general types of fusion-type penetration of enveloped viruses: 1) virion has active fusogenic protein in its envelope, which initiates the fusion. This usually causes infected cells to fuse with adjacent uninfected cells forming GIANT cells

2) virion has an inactive or CRYPTIC fusogenic protein in envelope. Vurus gets in via RME. Fusion protein activated withi n the vesicle and fusion occurs. This DOES NOT induce giant cell formation
what are viral inclusion bodies?: assemblages of virus particles or viral antigens that aggregate and accuulate in an infected cell. Can be used to identify viral infections
Where are rabies inculsion bodies?: cytoplasm
Where are smallpox inclusion bodies?: cytoplasm
Where are measles inclusion bodies: nucleus and cytoplasm
Where are JC virus inclusion bodies?: nucleus
What are WIN compounds?: Anti Rhinovurs agents (common common cold virus)

80% of rhinoviruses use same receptor (ICAM-1) for docking and enntry.
WIN compounds were designed to fit in the putative receptor binding domain.
They prevent Rhinovirus entry
What is Amantadine and Rimantadine?: Act on Flu A virus M2 protein (bokcing its role as an ion channel_. This prevents release of viral nucleocapsid into the cell cytoplasm from thhe endocytic vesicle. Infection is thus aborted.
What do amantadine and Rimantadine NOT work on?: Flu B virus
Acyclovir: what is it, what is it used for: dG analog

use on HSV and VZV
Ganciclovir: what and what for: dG analog

use on CMV (NOT HSV, etc)
what is AZT?: dT analog
What is 3TC? what ussed for?: dC analog.

used for HIV and HBV
what is adefor? what used for?: nucleoside MMONOPHOSPHATE analog (of dAMP)

used for HIV and HBV
what is foscarnet? what used for?: Pyrophosphate analog

used for HSV, CMV, HIV
What is neviparine? where used?: Non nucleoside analog. BInds directly to HIV RT and inhibits the pol activity.

HIV
What is ribavirin? where used?: rG analog
inhibits reactions involving rGTP (RNA synthesis). Inhibits 5' capping of mRNA, GTP synthesis

Also may act as an immunomodulator in HCV infection

Used on: RSV, Lassa, HCV
How do interferons work?: Cytokines induced in infected cells
can induce antiviral and immmunomudulatory responses
can be induced by administering ds RNA

Some downstream IF effects can block RNA and protein synthesis, thus stopping those infection steps
What kind of viruses are Interferons most useful for? examples?: Best for RNA viruses

Uses: HCV, papilloma

Can theoretically be used prophylactically for: Rhinovirus, RSV, coronavirus, influenza
What are Indinavir, Saquinavir, Ritonavir? What for?: protease inhibitors

HIV
What is Zanamivir: (relenza)

Analog of sialic acid, the essential compoinent of the viral receptor for Flu A and B. Thus inhibits viral neuraminidase.

Given nasally
inhibits viral maturation and egress
which "age" of virus tends to be more pathogenic?: viruses that are "newer" on the scene are less well adapted to the new host and thus are more pathogenic
Polio: acute or chronic: acute
Polio: local or systemic?: systemic
Are most polio infections symptomatic?: NO
WHat is the me chanism of most polio pathogenesis?: Only overt pathogenesis due to death of infected CNS neurons
Does polio evade host response?: No. "hit and run" infection strategy
Flu A: acute or chronic? Systemic or local?: Acute, localized (respiratory)
name a hallmark of all herpes viruses: latency and reactvation
Are progeny viruses produced by latently infected cells: never
how do latent herpes infections avoid immune system?: infected neurons do not express and display HLA-I
Give examples of host determinants of pathogenesis: HBV:

gender of patient is a host determinant of virulence: higher PERSISTANT carriage rate in males.
what is the natural portal for smallpox virus: oropharynx and respiratory tree
smallpox: systemic or loca?: systemic
What is the deal with adenovirus and portal of entry?: Normally a minor cause of respiratory infection
More serious where large number of persons are housed together (boarding schools, military camps)

WT portal of entry: URT and oropharynx
Vacccine: released in GI, where it develops into nonpathogenic infection and gives excellent immunity to respiratory adenovirus
what is the influenza receptor? what does it bind to: sialic acid poymers (ubiquitus)

Binds to HA
how does flu enter host cell: HA binds to sialic acid
RME envelops whole virion
what is required for viral release into cytoplasm: Acidification of endosome
Acidification of viral particle via M2 ion pore
when it gets acid enough, HA is cleaved into H1 and H2, revealin the fusogenic peptide activity in H
this causes fusion of viral envelope with endocytic vesicle
The protease that does the cleaving is released by specialized respiratory epithelial cells and bacteria
name barriers to viral entry via respiratory tract: mucus
ciliated epithelium
secretory IgA
lymphocytes, neutrophils, alveolar macrophages
name barriers to infection via GI route: 1) stomach acid dissociates virus proteins
2) digestive enzymes
3) bile salts (destroy envelopes)
4) maternal IgA in milk

Note: enteric viruses are usually stable at low pH and require proteolytic digestion
Which enteric viruses are limited to localized infections?: rota
calici
What enteric viruses can establish systemic infection? how?: polio
HAV

transported across specialized M-cells in Peyers patches
How do viruses invade GU tract? what goes in there?: Usually through tears in the mucosa

HIV, HSV, and some HPV goes in there
What can infect the conjunctiva? is it localized or systemic?: adenoviruses
herpesviruses

usually remains localized, but can be a secondary result of systemic infection started elsewhere
how can virus be cleared from the blood?: direct uptake of virus by cells of the RES
or by opsonization fo virus/AB complexes
how does the site of maturation of virus in the cell affect systemic v local infection?: Basolateral membrane surface maturation allowa for deeper penetration

Apical maturation allows for release back into lumen
how can viru traverse the BBB?: replication within the barrier cells
passive transport via endocytic vesicles
via an infected lympbhocye/monocyte (trojan horse)

can enter CSF via choroid plexus capps where caps are fenestrated
what does CPE stand for: cytopathic effects
describe examination of paired sera for diagnosis: acute v. convalescent sera

??
what kind of ABs are associated with acute hep B infection?: IgM
which type of CTL cells recognize MHC loaded with viral proteins and kill infected cell?: CD8
what aeffects other than death can cell mediated immunity trigger?: local release of cytokines, chemokines, other factors that may cure cell without lysis
why are nonspecitific immune responses important early in viral infection?: bc immune responses are slow:

IgM: 3-4 days post inf
IgG, IgA: 7-14 days post inf
How fast do non specific immune responses come up?: 12-24 hours
What interferons sre induced in virus infected cells?: IFN alpha and beta
What do IFN alpha and beta do?: after secretion by viral infected cell, they bind to a common receptor on healthy cells to induce synthesis of proteins designed to prevent virus growth, creating surrounding antiviral protection
what can IFN be used to treat?: Hep B
Hep C
Rhinovirus
what causes most hep B pathology?: not direct induced damage:

rather, the CTL attack and lysis of infected hepatocytes
what is immune complex disease?: caused by virus:AB complex deposition in the kidney
What is immune enhancement?: When AB binding to virions does not result in neutralization of infectivity...giving the V:AB complex access to Fc receptor-bearing cells, such as MPhages, to which the virus might not ordinarily bind. this can cause more serious disease in individuals with partial immunity...
2 classifications of hepatitis: Acute: symptoms less htan 6 mo; a few are fulminant w/poor prognosis

Chroinic: Symptoms >6 mo
Staes of chronic liver disease (from biopsy): 1) chronic persistant hep (CPH)
2) Chronic active hep (CAH)
3) cirrhosis
4) primary hepatocellular carcinoma (PHC)
HAV family: picorna (entero)
HBV family: hepadna
HCV family: flavivirus
HDV family: delta
HEV family: calici
describe and name members of the 2 subgroups of hepatitis: 1) Bile secretion: HAV, HEV
2) blood/fluid secretion: HBV, HCV, HDV
HAV family?: picorna
how does hep A replicate?: like poli (another enterovirus)
is 5 end of viral RNA of HAV capped?: no
Where does translation of HAV RNA start?: IRES: internal ribosome entry site in 5 NTR
What is VpG: Viral protein covalently linked at 5 terminus of HAV RNA
how is HAV different from proliovirus?: viral protease does NOT inactivate host cell protein that associates with capped mRNAs (so translation of normal host mRNAs can continue)
is HAV cytolytic?: no
does HAV replication overstress the hepatocyte?: on
how do you diagnose HAV?: seology for anti-HAV-specific IgM
What is likely site for primary HAV replication?: GI site
Describe pathogenesis of HAV: 1) primary entry at GI
2) resulting viremia
3) goes via portal system to liver
4) hepatocytes damaged PROBABLY due to Cytotoxic t cell action
5) virus shed into blood
is there a chronic carrier state for HAV?: no
Is there a lifelong immunity for HAV?: no
is htere progressionto hepatocellular carcinoma in HAV?: no
symptoms of HAV in the young?: usually asymptomatic (maybe due to less mature CMI)
How is HAV spread: 1) fecal-oral (anal sex, day care center)
2) fecal contamination of source (concentrated in shellfish)
How do you prevent HAV?: 1) vaccine (killed): recommended for foreign travelers
How do you treat HAV?: No drugs
Can give pooled immunoglobulin, although it is notbecoming low in titers of anti-HAV
Family of HEV: calici
how is HEV spread?: fecal oral
Describe diffence in infectious course of HAV and HEV: HEV like HAV, but there is a much higher incidence of fulmiknant hepatitis, with high mortality in pregnant wommen
is there an HEV chronic carrier state?: no
does HEV progress to hepatocellular carcinoma?: no
How do you diagnose HAV: usuallty thru history + clinical signs

serology requires SPECIAL TESTS
How do you prevent and treat HEV: no vaccine
no antiviral therapy

supportive treatment only
what is the "new wrinkle" wrt HEV: HEV-related virus found in pigs--worry about transmission of this to humans via hog farm contamination
Hep B family: hepadna
What is the shape of hepadna genome: circular, partial ds (+ strand incomplete)
Describe the core antigen story in HBV: HBe and HBc in same ORF (pre c + C)

Prec is a target for secretion, so prec+c product gets secreted, pre c gets cleaved off, leaving the c core protein (essentially) that is secreted.

but another ORF just produces the C protein alone--C is the core CAPSID protein
What envelope proteins are there in HBV?: Large, medium and small

All contain the S protein epitope: but the others have either pre s2 or pre s1 and pre s2
what is X gene?: encodes a regulatory protein (transcriptional transactivator) in HBC; not believed to be in the virion particle
Why is there more HBs antigen in the blood then HBV virion?: Extra HBs antigen buds off as spherical paricles with no nucleocapsid. "Australia antigen."

this spurred the notion of a protein subunit vaccine
how does HBV replication occur?: 1) gapped ds DNA is completed
2) moves to nucleus and converted to covalently closed circular DNA (ccc DNA)
3) ccc DNA transcribed by HOST DNA dep RNA Pol II
4) subgenomic mRNAs made then for protein synthesis in the cytoplasm
5) genome sized RNA (pregenome) also synthesized
6) pregenome packaged into HBc antigen along with viral polymerase protein (primer+RTase+RNaseH)
7) RT reactons occur, creating dsDNA. Viral DNA is NEVER packaged, but is created after packaging)
8) THEN the nucleocapsid leaves thee hepatocyte
What is HBV viral polymerase: multifunctional protein containing a priming domain, a RTase and a RNase H. Protein is involved in RT in the nucleocapsid
what is clinical course of most HBV primary infections?: mostly subcinial and asymptomatic
What is clinical course of HBV in immunosupprssed?: Always asymptomatic and persistant
What might develop from chronic carriage of HBV?: 1) chronic persistant hep
2) chronic active hep
3) primary hepatocellular carcinoma
How long does staging of liver patholoogy take in chronic cariers: usually 30+ years, sometimes as few as 2
What is the range of clinical manifestations of HBV?: subclinical to fatal acute/fulminant
What is a good clinical sign for HBV?: Development of anti HBe antibodies. This correlates with reduced viermia and lesser rate of damage to liver, and portends coming of anti HBs antibodiies.
What happens wrt ag/ab complexes in HBV?: can deposit, causeing polyarteritis or glomerulonephritis
Does HBV overstress the cell?: no
Is direct cytopathology evident in HBV?: no
What causes most damage in HBV?: CTL response, directed probably at HBc or HBe antigens
Can HBV cause PHC?: yes. HBV likely does not integrate, but 80% of tumors have integrated HBV DNA
What accomanies (serologically) resolution of persistant HBV infection?: anti HBs antibodies
What is pre-core mutant?: A mutant HBV strain that is often associated with a more fulminant course. Doesn't make secreted HBe, which may normally work as a tolaragen and mediate the destructive immune reaction
Can HBV patients have infection in extrahepatic sites?: Yes:

bile duct epithelium
pancreas
spleen
kidney
lymphocytes
how is most U.S. HBV transmitted? How else transmitted? How is it generally transmitted?: sex
also IV drugs, tattooos, piercing, mother to neonate

Titer highest inblood; it seems that most transmission is via inapparent parenteral inocculations of blood, saliva, etc
how is HBV diagnosed?: serology
Describe serology of acute HBV: 1) HBs antigen rises
2) Host response takes care of HBV
3) window period where HBs is gone, andti HBs is not yet detectible. Only marker now is anti-HBc. Anti HBc coincides with clinical symptoms
4) Anti HBs rises.
5) If recovering, ant HBe arieses before antiHBs is apparent.
Chronic HBV serology: 1) HBsAg rises during acute infection; maintained during chronic infection
[note: there may be just direct progression to chronic with no acute phase]
Prevention of HBV: 1) vaccination (HBs antigen subunit)
2) passive immunization: neonates of carrier given immune globulin along with vaccination course
Who gets HBV vaccination: 1) universal vaccination of newborns
2) vaccination for infection risk jobs (cops, docs, trainers, etc)
Treatment of HBV: 1) Interferon alpha can help
2) 3TC (dC nucleoside analog)
3) 3TC (lamivvudine) + Penciclovir: used in liver transpant patients with HBV
3) Adefovir (dAMP analog). Adefovir diphosphate (dAMP-PP) is the active form and acts as a chain terminator of HBV DNA synthesis)
5) NOT AZT: is conjgugated with gglucuronic acid in the liver, preventing host kinase from converting it to active form)
6) cant use protease inibitors, since HBV does not encode an analogous viral protease
Hep C family: flavivirus
Does hep C have a virion associated polymerase?: no
Describe genome of hep C: one ORF
translated as one polyprotein
cleaved by cellular and viral proteases

C: nucleocapsid
E1 and E2: envelope glyocoproteins
NS: nonstructural - proteases, RNA dep RNA polymerase
Compare clinical features of Hep C with Hep B: Hep C is liek HBV infection but with lower serum ALT; often presents as sequential episodes.

Many asymptomatic infections.

But 40% of chronic carriers later develop cirrhosis-->hepatocellular carcinoma
What is pathology of HCV due to?: Both cytotoxic T cells AND virus induced cell death (unlike HBV, which causes no direcy cytopathology)
What percentage of HCV infections become chronic?: 70-100%

(and 40% of those will get cirrhosis and PHC)
What is the leading cause of chronic hepatitis/cirrhosis and liver x-plant requests?: HCV
what does positive serology for anti-HCV mean?: It means that infection is ongoing! not recovery.
How is HCV mainly transmitted?: via blood; also sex and mother to child.
which is better transmitted thru sex: HBV or HCV?: HBV.
How do you diagnose HCV?: ELSIA to find anti HCV antibodies
Also can do RT-PCR for viral dna
correction: viral RNA, not viral DNA
prevention of HCV: 1) no vaccine available (high antigenic drift rate)
2) screen blood for HCV Antibodies
3) no hyperimmune serum available
Treatmetn of HCV: 1) Interferon alpha can be used with mixed results
2) interferon + RIBAVIRIN (response depends on HCV genotype)
what is the general deal with HDV?: Apparently an intrinsically defective RNA virus: no genes for its env nor for replication
What is host range for HDV?: Can ONLY replicate in cells that are infected with HBV, since it has none of its own machinery
where does HDV get its viral env lipoprotein?: it parasitizes it from HBV
What is the structure of HDV?: HDV RNA surrounded by the HD antigen (core protein)

HD is all the genome coads for
What is unique about what HDV codes for?: Unique in that it is a negaitve sense RNA genome that does NOT encode for an RNA dependent RNA pol. It uses host cell DNA dep RNA pol II
Clinical features of HDV?: When coinfected with HBV, it follows a more aggressive clinical course
what are the 2 types of HDV infection settings"?: 1) patient acquries HBV and HDV simultaneously. Clinical hep often appears biphasic. High but transient viremia.

2) HBV carrier acquires HDV. If immune system clan clear HBV from liver (acute) then it also clears HDV. If not, it keeps both.
How is HDV transmitted?: Likely like HBV. Sex, drug users.
How do you diagnose HDV?: detect HD antigen or anti-HD antigen
How do you prevent HDV: HBV vaccination effective against HDV
no specific HDV vaccination
How do you treat HDV?: Lamivudine (3tc) or penciclovir inhibit HBV RT, but thhey do Not inhibit the synthesis of HBs antigen. thus they cannot affect course of HDV antigen (???)
what family: Measles: paramyxo
clinical features of measles: Respiratory exposure
10-14 days
high fever
cough, conjunctivitis
rashon head and neck
diagnosis of measles: usually based on symptoms especially the pathognomonic red lesions wiht white centers that appear on the buccal mucosa
potential complications of measles: 1) encephalomyelitis
2) giant cell (primary) pneumonia in immunocompromised
3) secondary bacterial pneumonia
4) keratoconjunctivitis
5) SSPE: subacute sclerosing panencephalitis. rare, 7-10 years later
What is atypical measles: Seen in people who got killed vaccine from 63-67
they later get infected
they get an atypical rash, and frequently a serious pneumonitis
Killed vacccine now longer used
describe measles spkes: Two:

1) Hemagglutinating (H)
2) fusing (F)

NO Nueraminidase on its spikes
describe how the F protein works: F protein is synthesized in the cell as an inactive precursor
Cleaved by host protease
F protein displayed on surface of infected cells can themselves cause cell-cell fusion, forming giant cells
WHAT causes measles rash: host CMI response
how many measles serotypes?: 1
Disease course of measles: 1) breathe in droplets
2) 10-14 days asymp incubation
3) then high fever
4) cough, head cold, conjunctivitis
5) characteristic rash on head and neck
6) Koplik's spots on buccal mucosa
what has happened to number of measles cases from 84-92: gone up
due to failure to immunize preschoolers and failure of vaccine when given before 15 months of age
measles vaccine?: 2 doses

1 given from 12-15 months
2d given at least a year later (usually 4-6 yo)

but all kids have a window of susceptibility
mumps family: paramyxovirus
clinical features of mumps: incubation for 18 days
spread to parotiid glands
Causes swllen, tender glands
can cause orchitis in 1/4 of males
Describe mumps spikes: One has: H AND NA activity
Other: F (fusing) activity
diagnosis of mumbps: clinical symptoms alone (swollen parited glands)

may culture it
rubella family: toga
clinical course of rubella: like measles
starts with face rash
goes to extremities
rubella copmplications:: can cause abortion or "congenital rubella syndrome" (hearing loss, cataracts) if it infects a nonimmunized bpregnant woman
what is congenital rubella syndrome?: when mom gets rubella and is not immunized, baby can immediately or distantly develop hearing loss, cataracts
rubella: fusion protein?: no
rubella diagnosis?: usually clinically
symptoms of hhv6/7: high fever and red rash (roseola)
usually resolves in 3-5 days without complications
usually get it very early in life (under age 2)
what is VAHS: rare reactivation of HHV-6 reactivation causeing phagocytosis of blood cells
when is parvo b19 serious?: if you have underlying hemolytic disorder, it can cause life threatining aplastic crisis

May also infect fetus in utero (severe annemia)
what is parvo b19 misdiagnosed as: measles, sometimes
what does b19 do in the body: kills erythropoeitic cells in bone marrow
causes rash due to immune-cmplex formation
coxcackivirus family: picorna
clinical features of cosxackie?: multiple serotypes
cause tons of diseases

herpangia-fever, st, acute onset (A)
and, foot, mout (A)
aseptic meningitis (A)
epidemic conjunctivitis (A)
pleurodynia (chest pain and fecer) (B)
myocarditis/pericarditis (B)
neonatal infection (B)
what causes common cold: rhinovirus
coronavirus
what causes pharyngitis: rhinovirus
what causes laryngitis: influenza
rhino
adeno
prainfluenza
What causes laryngotracheobronchitis: paraflu
what causes ronchitis: variety
what causes bronchiolitis: RSV
what causes pneumonia?: RSV
paraflu
iinflu
what is SARS: coronavirus
what diseases do adenoviruses cause: ARD: acute respiratory disesase--in young military recruits
adenovirus transmission: fecal oral
prevention and therapy of adenovirus:: vaccines for certain types
not licensed for civilian use
adenovirus serotypes?: dozens
rhinovirus family?: picorna
rhinovirus serotypes?: over 100
rhinovirus treatment?: WIN compounds
Anti receptor compounds
what are WIN compounds:: capsid binding antiviray agents
bind to a canyon on rhino surface and prevent binding and entry
not effective agains non-rhino colds
difficult to administer
what are anti-receptor compounds: directed against ICAM-1
prevent whino binding and entry into cells
tratment after sickness ineffective
may help to add soluble ICAM receptor to the anti-receptor.
problems in developing cold treatments: 1) hard to tell early on what disease it is
2) no easy way to tell if it is whino, corona, adeno prior to treatment
3) drugs have short half life
4) hard to target drugs to nasal mucosa
5) drug resistant mutants
why no cold vaccine?: large number of seotypes
RSV family: paramyxo
RSV surfface proteins: G protein binds cellular receptor
Fuses vie F protein
Where do RSV life cycle events occur?: cytoplasm
general features of RSV infection (clinically): can cause Severe LRT infection in kids, mild URT in adults
describe bronchiolitis: acute inflammation and necrosis of respiratory epithelium in the bronchioles

acute onset of wheezing and hyperaeration, tahcypnea

mainly due to RSV
does RSV infection go systemic?: no, never penetrates deeper than superficial layers of respiratory epithelium
spread of parainfluenca: person to person contact or spread of contaminated secretions
sypmtoms of flu: acute illness
aching muscles (esp leg and back)
dry, hacking cough
HA
ST
fever
blocked, but not runny, nose
How is flu spread?: person to person via inhaling droplets from exhalations of others
what causes a pandemic?: introduction of a novel influenza A
describe structure of flu: 8 viral RNA (-) segments wrapped in nucleoprotein. Enveloped.

contains viral RNA polymerase in the virion (as it must, as a - rna virus)
viral glycoproteins?: HA
NA

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