Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
342 Cards in this Set
- Front
- Back
|
What are the three genera of reoviridae that infect humans?
|
orthoreoviruses
rotaviruses coltiviruses |
|
|
How many RNA segments are in reoviruses?
|
10
|
|
|
How many RNA segments are in rotaviruses?
|
11
|
|
|
How many RNA segments are in coltiviruses?
|
12
|
|
|
What types of infections are caused by coltiviruses?
|
Generalized & CNS infections
|
|
|
What types of infections are caused by reoviruses?
|
Asymptomatic GI and respiratory tract infections
|
|
|
What types of infections are caused by rotaviruses?
|
GI infection
|
|
|
What is the structure of a rotaviruses?
|
At least 3 concentric protein layers-->wheel appearance
Non-enveloped 3 protein layers include a core single-shell and a double shell |
|
|
What type of genetic information is carried by rotaviruses?
|
dsRNA
Segmented |
|
|
What types of proteins are in a rotavirus?
|
6 structural proteins
5 nonstructural proteins |
|
|
What are some important physical properties of rotaviruses?
|
Stable over a wide range of pHs and temperatures
Resistant to drying, detergens & proteases |
|
|
How does trypsin enhance the growth of rotaviruses?
|
Cleaves VP4 into VP5 and VP8-->enhances viral infectivity
|
|
|
Where does replication of rotaviruses occur?
|
Cytoplasm
|
|
|
How does rotavirus cause infection?
|
Mature enterocytes are destroyed, sloughed-->diarrhea
NSP4 has been implicated as a viral toxin molecule-->enhance Cl secretion WATERY DIARRHEA |
|
|
What virus can increase the risk for celiac disease?
|
Rotavirus
|
|
|
What rotavirus gene codes for VP4?
|
Gene 4
|
|
|
What rotavirus gene codes for VP7?
|
Gene 9
|
|
|
What type of protein is formed by VP4?
|
Hemaglutinin
|
|
|
What leads to G-serotypes in rotaviruses?
|
Glycoproteins (G proteins) from VP7
Neutralizing epitopes |
|
|
What leads to P-types and subtypes?
|
VP4
|
|
|
Where are group antigens found in rotaviruses?
|
VP6 on inner capsid
|
|
|
What is the major source of rotaviruses?
|
Young children
|
|
|
What happened to the first vaccine for rotaviruses?
|
Discontinued due to intussecption (intestinal obstruction)
Live, tetravalent vaccine=RotaShield |
|
|
What is used for rapid dx of rotavirus infection?
|
VP6
|
|
|
What is the prototype virus for other SRSVs in the Calicividiae family?
|
Norwalk virus (NV)
|
|
|
What is the structure of caliciviruses?
|
Non-enveloped
|
|
|
What is the genetic material of caliciviruses?
|
Postive RNA with 3 ORFs
|
|
|
What proteins are involved in caliciviruses?
|
1 structural protein
|
|
|
Can caliciviruses be cultured in vitro?
|
Nope.
|
|
|
How do caliciviruses cause disease?
|
Infected cells have altered water adsorption-->blunted villi.
Symptoms include vomiting, diarrhea, nausea, abdominal cramps, low-grade fever |
|
|
Once infected with a calicivirus, how long does immunity last?
|
Short.
Re-infectio ncan occur with same genotype. |
|
|
How are noroviruses genetically classified?
|
Genogroupss GGI-GGV.
Only GGI and GGIV infect exclusiveily humans. GGII infects both humans & swine. |
|
|
What is the morphological difference between NLVs and SLVs?
|
NLVs=small round w/ragged surface
SLVs=cup-shaped indentations w/6-pointed star shape |
|
|
What types of infections are typical of SLVs?
|
Infections in infants & young children.
GI infections |
|
|
What types of infections are typical of NLVs?
|
Family & community outbreaks of gastroenteritis
|
|
|
What is the incubation time for NLVs?
|
24-48 hours
|
|
|
What is the sickness duration for NLVs?
|
24-48 hours
|
|
|
How are caliciviruses transmitted?
|
Fecal/oral route
|
|
|
Where are NLV outbreaks most common?
|
Nursing homes and hospitals
|
|
|
What can be used to dx NLV-gastroenteritis?
|
Serology, EM, or RT-PCR
|
|
|
What is the structure of astroviruses?
|
non-enveloped
|
|
|
What is the genome of astroviruses?
|
ssRNA & (+) polarity
|
|
|
What are the proteins of astroviruses?
|
1 structural
2 nonstructural |
|
|
What characterizes illness caused by astroviruses?
|
Diarrhea, headache, malaise, nausea, low-grade fever
|
|
|
What is the incubation period of astroviruses?
|
3-4 days
|
|
|
What is the duration of astrovirus-related illness?
|
2-3 days
|
|
|
Is viral shedding in stool common in astroviruses infection?
|
NO.
|
|
|
How are astroviruses transmitted?
|
Fecal-oral
Person to person by fomites & contaminated food & water |
|
|
Are there vaccines or antivirals for astroviruses?
|
none
|
|
|
What type of virus is Hep A virus?
|
picornavirus
enterovirus 72 |
|
|
What type of virus is the Hep B virus?
|
Hepadnavirus
|
|
|
What type of virus is the Hep C virus?
|
flavivirus
|
|
|
How does Hep A replicate?
|
Similar to other enteroviruses w/little or no shut down of host cell macromolecular synthesis
|
|
|
How does Hep A cause infection?
|
Reachs liver via blood after local replication in GI tract.
NO CHRONIC INFECTION severity is age related (severity increases w/age) |
|
|
What immunity is associated with Hep A?
|
Antigens for immunity are on surface of virions.
Immunity is lifelong |
|
|
How is HepA spread?
|
Fecal-oral
Day care centers are common source of virus Viral shedding can occur before appearance of illness |
|
|
How is Hep A diagnosed?
|
Serology, IgM-anti HAV
|
|
|
What vaccines are available against Hep A?
|
HAVRIX & VAQTA are killed vaccines
Used for ppl traveling to endemic areas |
|
|
What diseases are caused Hep B virus?
|
Acute and chronic infections.
Viremia is common. |
|
|
What is the morphology of Hep B virus?
|
enveloped viruses
very pleomorphic |
|
|
What is the genome of Hep B virus?
|
dsDNA
At least 8 genotypes |
|
|
What variations are there w/different genotypes of Hep B virus?
|
Genotype B is associated w/less active liver disease & slower progression to cirrhosis
|
|
|
How does Hep B virus replicate?
|
1. DNA virus that replicates w/RNA intermediate using a reverse transcriptase
2. genome is gapped & must be completed |
|
|
Where does the Hep B virus replicate?
|
Viral DNA is transported to the nucleus of liver cells & exists as an episome
Viral mRNA is transcribed than transported to cytosol for RTase |
|
|
How does HBV cause infection?
|
Virus is hepatotropic
Replication can lead to XS amounts of viral proteins being released from infected cells. Autoimmune phenomena can occur |
|
|
Describe the development of immunity to HBV.
|
Epitopes on HBsAg induce protective immunity.
Presence of anti-HBsAg indicates immunity. |
|
|
What are key antigens of HBV?
|
S-protein (HBsAg)
C-protein (HBcAg) E-protein (HBeAg) |
|
|
What is the prime source for HBV?
|
Asymptomatic chronic carriers
|
|
|
Where is HBV found?
|
Blood & other bodily fluids
|
|
|
What makes up "chronic carrier status" of HBV?
|
Long-term absence (>6 mos) of anti-HBsAg antibody
|
|
|
What kind of treatment is available for HBV infection?
|
Antiviral therapy
Either nucleoside or nucleotide Used for chronic infections. |
|
|
Where can HBV be present?
|
Blood saliva semen vaginal secretions menstrual blood breast milk tears urine
|
|
|
What is the structure of HCV?
|
enveloped viruses
|
|
|
What is the genome of HCV?
|
ssRNA (+)
|
|
|
Where is HCV found?
|
Bodily fluids, including toothbrush rinse water
|
|
|
What antigens are used in commercial EIA tests for HCV dx?
|
NS3, NS4, and C antigens
|
|
|
What cells can HCV infect particularly that causes chronic infection?
|
B & T cells
|
|
|
What is used to dx active infection?
|
Serology, RT-PCR and RIBA
|
|
|
What treatments and prevention techniques are usable?
|
No vaccine
Alpha interferon therapy can help |
|
|
What is the structure of HDV?
|
Genome is covered by Delta protein & Delta protein is covered by HBsAg
|
|
|
What is the genome of HDV?
|
ss circular RNA (-)
|
|
|
How is HDV replicated?
|
Helper virus is required.
HOst cell RNA Pol II is involved w/transciription & replication |
|
|
How does HDV cause disease?
|
HDV infections can only occur w/a co-infection with HBV or a superinfection of HBV carriers
|
|
|
What antigens are produced by HDV?
|
Delta antigen
|
|
|
Where is the Delta virus found?
|
HDV
Worldwide |
|
|
How is HDV dx'ed?
|
Serology (EIA), RT-PCR & site-specific probes
|
|
|
How can HDV be prevented?
|
Vaccination against HBV
|
|
|
What is the structure of HEV?
|
non-enveloped
|
|
|
What is the genome of HEV?
|
ssRNA (+)
|
|
|
What types of disease are produced by HEV infection?
|
acute infections w/severe disease in pregnant women
|
|
|
How is HEV transmitted?
|
fecal contamination of water
shellfish |
|
|
Which 8 herpesviruses cause human disease?
|
Herpes simplex viruses 1 & 2
Varicella zoster virus (VZV) EBV Cytomegalovirus (CMV) Human herpesviruses types 6-8 |
|
|
What is the primary host of herpes simiae?
|
Monkey.
Man is accident host. Also known as Herpes B |
|
|
What types of infections are caused by HSV-1 and HSV-2?
|
Mucocutaneous lesions
Pharyngitis Herpetic keratitis Herpetic whitlow Herpes galdiatorum Eczema herpeticum |
|
|
What type of infection is caused by VZV?
|
Chickenpox then becomes latent to reappear later as shingles (zoster)
|
|
|
What type of infection is caused by EBV?
|
Heterophile-positive IM and is associated with Burkitt's lymphoma and nasopharyngeal carcinoma
|
|
|
What is special about CMV?
|
Transplacental virus
Most common viral cause of congenital birth defects Can cause heterophile-negative IM |
|
|
Where were HHV-6, -7, and 8 first discovered?
|
Blood of AIDS patients.
|
|
|
What diseases does HHV-6 cause?
|
Childhood exanthem
Roseola infantum |
|
|
What diseases does HHV-7 cause?
|
Childhood exanthem
Roseola infantum |
|
|
What diseases is HHV-8 associated with?
|
Epidemic Kaposi's sarcoma
Primary effusion lymphoma |
|
|
What enzymes are encoded by herpesvirus genomes?
|
DNA Pol
Thymidine kinase Deoxyribonuclease Ribonucleotide reductase Protease |
|
|
What is the structure of the mature herpesvirus genome?
|
linear dsDNA
|
|
|
What facilitates the formation of genome isomers in herpesviruses?
|
The presents of repeated sequences within the genome
|
|
|
When are isomers generated in herpesviruses?
|
Replication
|
|
|
What is the structure of latent herpesvirus DNA?
|
circular or linear.
always bound in host cell histones replicated by host DNA pol |
|
|
Describe the process of viral transcription & protein synthesis in herpesviruses.
|
Coordinated cascade fashion.
Immediate early alpha mRNAs & proteins are made first. Early or beta mRNAs and beta proteins second. Late or gamma mRNAs and gamma proteins last |
|
|
How are alpha proteins of herpesviruses made?
|
Made on preexisting ribosomes b/c protein synthesis inhibitors added at the time of infection do not affect alpha protein synthesis.
|
|
|
What do beta proteins do?
|
Downregulate synthesis of alpha proteins & initiate synthesis of gamma proteins.
|
|
|
Waht do gamma proteins do in herpesviruses?
|
Downregulate beta protein synthesis
|
|
|
What does "early" mean in the context of viral replication?
|
Before viral DNA synthesis
|
|
|
What does "late" mean in the context of viral replication?
|
After viral DNA synthesis
|
|
|
What kinds of proteins are alpha proteins in herpesviruses?
|
Transcription factors
|
|
|
What kinds of proteins are beta proteins in herpesviruses?
|
Transcription factors & enzymes (including viral DNA pol)
|
|
|
What kinds of proteins are gamma proteins in herpes viruses?
|
Virus structural proteins, including capsid proteins
|
|
|
Where does viral DNA & capsid proteins assemble in herpesviruses?
|
In the nucleus
Acquire envelope by budding from nuclear membrane |
|
|
What happens to most herpesvirus infected cells?
|
Lysis
|
|
|
What is the hallmark of herpesviruses?
|
establishment of latency on primary infection
|
|
|
Which latent herpesviruses reside in cells of nervous tissues?
|
HSV
VZV |
|
|
Which latent herpesviruses reside in B cells?
|
EBV
HHV8 |
|
|
Which latent herpesviruses reside in mononuclear lymphocytes & stromal cells of bone marrow?
|
CMV
|
|
|
Which latent herpesviruses reside in endothelial cells or B cells?
|
HHV8
|
|
|
How do antiviral medications for herpesviruses work?
|
Inhibit DNA synthesis
|
|
|
What type of immunity develops to herpesviruses?
|
Unclear.
Most adults have antibodies to most herpesviruses. |
|
|
What is the morphology of papovaviruses?
|
non-enveloped w/icosahedral nucleocapsid symmetry
|
|
|
What is the form of the genome of papovaviruses?
|
dsDNA that is covalently-closed circular (CCC)
|
|
|
How do papilloma viruses induce an unscheduled S-phase?
|
Express early virus proteins E6 & E7 which bind to & inactivate host-cell encoded growth-suppressor genes p53 & p105RB
|
|
|
How do polyomaviruses induce an unschedule S-phase?
|
Express large T antigens which bind to & inactivate both p53 & p105RB
|
|
|
When can papovaviruses enter host cell?
|
S-phase only (need host replication machinery)
|
|
|
What genes are encoded by HPV genomes?
|
8 early genes (E1-E8)
2 late (L1 & L2) genes Contains a non-coding ori |
|
|
Which strand of the genome do all HPV transcripts come from?
|
+ strand
|
|
|
Where in the body does HPV replicate?
|
Squamous epithelium of skin and/or mucous membranes
|
|
|
What does HPV do during maturation?
|
Moves from basal layer to upper layer (squamous epithelium) of the skin.
|
|
|
Where is mature HPV found?
|
Elevated keratin layer of skin (wart)
|
|
|
Which HPV strands cause dysplasia?
|
HPV-16 and HPV-18
|
|
|
What causes cervical dysplasia due to HPV?
|
inactivation of p53 & p105RB
|
|
|
What is the name given to genital warts?
|
Condyloma acuminatum
|
|
|
Which HPV strains cause 90% of genital and anorectal warts?
|
HPV-6 and HPV-11
|
|
|
Which strains does the HPV vaccine protect against?
|
6, 11, 16, 18
|
|
|
What type of vaccine is the HPV vaccine?
|
Tetravalent prepared from capsid proteins
|
|
|
What are the two polyoma viruses that infect humans?
|
BK and JC
|
|
|
What is SV40?
|
Simian (monkey) virus 40
40th polyomavirus to be identified Propagates in vitro |
|
|
What are the hosts for BK and JC viruses?
|
Man is only host.
|
|
|
Describe the order of transcription of polyoma proteins.
|
Nonstructural early T antigens are transcribed from on strand of the viral genome.
Late virus proteins (VP1, VP2, VP3) are transcribed from the other (complementary) strand. |
|
|
Where does replication of SV40 DNA take place in the cell?
|
Nucleus following entry into the cell.
|
|
|
What are the functions of SV40 T antigens?
|
1. bind to viral ori & initiate early & late gene transcription + viral DNA synthesis
2. bind p53 & p105RB to induce unscheduled S phase |
|
|
How are BK & JC viruses acquired?
|
respiratory tract infections
|
|
|
Where is BK virus latent?
|
Kidney cells.
|
|
|
Where is JC virus latent?
|
Kidneys, B cells, and monocyte-lineage cells
|
|
|
When do BK and/or JC viruses become active?
|
Immunocompromised individuals
|
|
|
Which polyoma virus may cause severe UTIs?
|
BK virus
|
|
|
Which polyoma virus can result in viremia & CNS infection?
|
Latent JC virus
|
|
|
Which virus can cause PML?
|
JC virus
|
|
|
What is PML?
|
Progressive multifocal leukoencephalopathy
Produced when JC crosses BBB. Subacute demyelinating disease in immunocompromised individuals Diagnosed by finding foci of demyelination |
|
|
What infections are considered in the perinatal period?
|
Infections acquired in utero, at the time of delivery, and in the immediate newborn period
|
|
|
What is the neonatal period?
|
first month/28 days of life
|
|
|
What are the two primary means of acquiring intrauterine infections?
|
1. Transplacentally
2. Ascending from vagina |
|
|
Why are perinatal infections different from infections in adults?
|
It takes a few months for an infant's immune system to mature to the adult level.
|
|
|
How does the repertoire of clinical signs of infection in neonates compare to that of the adult?
|
Much more limited.
|
|
|
What is the most common congenital infection?
|
CMV
|
|
|
How is CMV transmitted to the fetus?
|
Primary maternal infection during pregnancy w/viremia
Passage of infected maternal leukocytes across placent (primary or latent infection) Attachment of placenta to uterine tissue latently infected w/CMV |
|
|
What is the manifestation of congenital CMV at birth?
|
95% are asymptomatic at birth
The remaining 5% exhibit congenital CMV syndrome (psychomotor retardation, hearing deficit, petechiae, etc.) |
|
|
When are long term sequelae of congenital CMV more likely to appear?
|
If maternal infection during pregnancy is primary or when infants are symptomatic at birth
|
|
|
How is congenital CMV diagnosed?
|
Ideally: Isolation/ID of virus during 1st 2 weeks of life (urine, resp. secretions)-->must be prior to 2wks of age.
CMV-specific IgM can be used but is not good. |
|
|
Is there any treatment for congenital CMV?
|
No.
|
|
|
Where do cases of rubella appear in the US?
|
In isolated populations w/low immunization rates.
|
|
|
What is the pathogenesis of rubella infection?
|
maternal resp. infection-->placental infection-->fetal infection
|
|
|
When is there the highest risk of clinically evident congenital infection of rubella?
|
First & second months.
|
|
|
What is included in classical congenital rubella syndrome?
|
Intrauterine growth retardation
Eye defects Deafness Cardiac defect CNS defects Hepatomegaly |
|
|
How is congenital rubella diagnosed?
|
Isloation of rubella virus from resp. tract-->tricky, unavailable
Most common: rubella-specifc IgM in infants serum Persistance of rubella-specific IgG abs ib lood after 6 mos |
|
|
How can rubella be prevented?
|
Vaccination (2 doses)
Lifelong immunity |
|
|
What is the pathogenesis of intrauterine toxoplasmosis?
|
Acute primary maternal gestational infection-->parasitemia-->subsequent placental & fetal infection.
Transmission does not occur w/chronic latent infection |
|
|
Does transmission of toxoplasmosis occur in presence of maternal antibodies to Toxoplasma?
|
NO
|
|
|
What percentage of infants who are infected w/Toxoplasma in utero are asymptomatic at birth?
|
70%
|
|
|
What are the clinical manifestations of congenital toxoplasmosis syndrome?
|
Chorioretinitis
abnormal CSF (pleocytosis) Seizures Generalized intracranal calcification |
|
|
How is congenital toxoplasmosis syndrome diagnosed prenatally?
|
Detection of parasite in fetal blood or amniotic fluid
Detecting Toxoplasma IgM or IgA antibodies or Toxoplasma DNA in fetal or maternal blood |
|
|
How is congenital toxoplasmosis syndrome diagnosed postnatally?
|
Detection of parasites in placenta
Toxoplasma DNA by PCR on buffy coat Toxoplasma IgM or IgA |
|
|
How is congenital toxoplasmosis syndrome treated?
|
Pyrimethamine plus sulfadiazine (and Spiramycin)
|
|
|
How can congenital toxoplasmosis syndrome be prevented?
|
Heat meat
Avoid uncooked eggs and feline feces |
|
|
Which HSV is more common?
|
HSV-2
|
|
|
What is the most common transmission method for perinatal herpes simplex?
|
Natal transmission during birth
|
|
|
How does intrauterine transmission of perinatal HSV occur?
|
Ascending w/ or w/o rupture of membranes
Viremia |
|
|
What herpes simplex virus is most commonly acquired post-natally?
|
HSV-1
Usually acquired from oral HSV infection |
|
|
What are clinical manifestations of neonatal HSV?
|
Vesicular skin lesions (absent at initial presentation, occur in crops of multiple vesicles)
Seizures Conjunctivitis |
|
|
How might neonatal HSV be diagnosed?
|
Identification of HSV by virus culture or PCR
Tzank prep of vesicle Immunofluorescens of skin lesions |
|
|
What is the treatment for neonatal HSV?
|
Acyclovir 60mg/kg/day
|
|
|
Describe the spectrum of perinatal HIV infections.
|
Asymptomatic
Acute illness following primary infection (seroconversion syndrome) Symptomatic w/lymphadenopathy, wasting syndrome |
|
|
What are the methods of transmission of HIV?
|
Intrauterine
Natal Postnatal Sexual abuse Most common: late in pregnancy or labor |
|
|
How can HIV be diagnosed in the newborn?
|
HIV antibody
HIV DNA by PCR HIV RNA by PCR Viral culture of blood HIV p24 antigen |
|
|
How can HIV be managed during pregnancy?
|
Zidovudine as a single antiretroviral agent can decrease mother-to-infant transmission by 70%
|
|
|
What is the most important feature of neonatal bacterial infections?
|
Can be rapidly fatal even w/early institution of treatment
|
|
|
What is the rate of neonatal sepsis?
|
1-5/1000 births
|
|
|
What is a sepsis work-up in perinatal infections?
|
Bacterial cultures of the blood (2)
CSF Urine Gram stain of urine & CSF Cell counts glucose and protein determination X-ray |
|
|
What is the most common regimen (empiric) for neonatal sepsis?
|
1 of the penicillins (ampicillin) + 1 of the aminoglycosides
|
|
|
What is reflected in the empiric antibiotic regimen for neonatal bacterial infections?
|
The most common causes of nenonatal sepsis:
group B beta-hemolytic strep E. coli |
|
|
What is particular commonly associated with neonatal sepsis?
|
concurrent meningitis
|
|
|
What are some differences in the immune systems of neonates from those of adults?
|
Neonatal PMNs have impaired chemotactic & phagocytic capacity
Decreased bone marrow reserve of neutrophil precursors Less circulating IgM, complement components |
|
|
How are organisms causing early onset sepsis usually acquired?
|
Maternal birth canal
|
|
|
How are organisms causing late onset sepsis usually acquired?
|
maternal birth canal or other sources (nosocomial, community)
|
|
|
What is the transmission method most commonly associated with early onset sepsis?
|
vertical
|
|
|
What constitutes early onset sepsis?
|
birth-7 days
|
|
|
What constitutes late onset sepsis?
|
7 days-1 month
|
|
|
What clinical manifestations of early onset sepsis?
|
Early onset of apnea
Respiratory distress w/ or w/o shock |
|
|
What are clinical manifestations of late onset sepsis?
|
Fever
Irritability |
|
|
For what groups is intrapartum chemoprophylaxis recommended for GBS?
|
1. Women w/asymptomatic or symptomatic GBS bacteruria at any time during current pregnancy
2. Women w/prior infant w/invasive GBS 3. Positive GBS screening during current pregnancy |
|
|
What is included in intrapartum prophylaxis regimens?
|
Penicillin
Ampicillin PCN-allergic: cephalosporin, clindamycin |
|
|
Influenza viruses types A, B, and C are why type of virus?
|
orthomyxoviridae
|
|
|
What three types of influenza viruses cause illness in humans?
|
A, B, C.
|
|
|
How are influenza types determined?
|
by epitopes located on a ribonucleoprotein complex
|
|
|
Which influenza types are zoonoses?
|
A & B
|
|
|
What is the structure of influenza viruses?
|
Enveloped w/spikes or peplomers.
|
|
|
What is the function of the spikes on influenza viruses?
|
Determinants of virulence-->targets for immunization
|
|
|
What is the genome of influenza viruses?
|
Multipartite
7 or 8 ssRNA segments |
|
|
What is the importance of the hemagglutinin spike of the influenza virus?
|
used for attachment of virus to host cells.
HA polypeptide is cleaved to form two polypeptide chains, HA1 and HA2. HA1= viral attachment HA2= fuses viral & host cell membranes |
|
|
If HA is not cleaved to form HA1 and HA2, what is the result?
|
HA2 is nonfunctional and membranes cannot fuse-->virus in noninfective.
But HA1 function is intact. |
|
|
What has the epitopes that determine the subtype of the orthomyxoviridae?
|
HA
|
|
|
What is neuramidase (NA)?
|
Envelope spike consisting of a stalk and head similar to a mushroom.
NA allows the virus to escape after binding to mucins present in respiratory tract. |
|
|
What is the function of NA?
|
Has a role in viral release-->slow spread if there is an Ab to NA
Cleaves sialic acid on virion proteins & prevents/reduces viral clumping |
|
|
What characterizes the envelope of influenza viruses?
|
M1 protein (matrix) has type-specific epitopes
M2 appears to be needed for viral release from endosomes |
|
|
What is the function of NS1 protein in influenza viruses?
|
Inhibits cellular mRNA translation
Virulence factor--> can bind dsDNA |
|
|
Describe the replication of influenza viruses.
|
Dependent on host cell nuclear fxns.
Parental viral RNA is transported to nucleus where viral RNA-transcriptase complex transcribes parental (-) RNA into mRNA Viral transcriptase captures newly synthesized host cell mRNA |
|
|
How does influenza cause diseases?
|
infects & kills cells of the respiratory tract-->temporal loss of local primary defense mechanism
|
|
|
When was H5N1 identified?
|
1997
|
|
|
What are the two terms for antigenic variation?
|
Antigenic drift-minor
Antigenic shift- major |
|
|
What is the difference between antigenic shift and antigenic drift?
|
Drift=point mutations
Shift=intro of new or different RNA segment by genetic reassortment |
|
|
What is the preferred method of specimen collection for influenza virus testing?
|
Nasopharyngeal aspiration
|
|
|
What is a new innovation in flu vaccine technology?
|
FluMist
Live vaccine nasal spray Only for 2-49yo |
|
|
What is Morbillivirus?
|
Measles virus
a paramyxovirus |
|
|
What is pneumovirus?
|
Respiratory syncytial virus
a paramyxovirus |
|
|
What is henipavirus?
|
Hendra virus and Nipah virus
a paramyxovirus |
|
|
What is Respirovirus?
|
Parainfluenza viruses types 1 & 3
paramyxovirus |
|
|
What is Rubulavirus?
|
Parainfluenza viruses types 2 & 4
Mumps virus paramyxovirus |
|
|
Which paramyxoviruses can manifest manifest as croup?
|
Parainfluenza virus type 1 & 2
|
|
|
Which paramyxoviruses cause zoonosis?
|
Hendra
Nipah Menangle virus |
|
|
Do paramyxoviruses undergo major antigenic changes?
|
No.
|
|
|
What is the viral structure of paramyxoviruses?
|
Pleomorphic enveloped viruses w/spikes that emanate from the envelope.
|
|
|
What is the nucleic acid of paramyxoviruses?
|
ssRNA (-) strand
Nonsegmented |
|
|
What determines the virulence of paramyxoviridae?
|
Two spikes
|
|
|
What spike is common to all paramyxoviridae?
|
F protein
|
|
|
What is the function of the F protein?
|
Fusion protein.
Binds to membranes and catalyzes membrane fusion. Similar to orthomyxoviridae HA. Does not act as adsorption. Must be cleaved to become active. Essential for infectivity |
|
|
What is HN protein?
|
As adsorption protein of parainfluenza viruses.
Binds to neuraminic acid, agglutinates erythrocytes. Has both hemagglutinin AND neuraminidase activity. |
|
|
What is H protein?
|
Morbillivirus adsorption protein
Acts only as hemagglutinin |
|
|
What is G protein?
|
Adsorption protein of pneumovirus
Has neither hemagglutinating nor neuraminidase activity |
|
|
Where does paramyxovirus replication occur?
|
Cytoplasm
|
|
|
Describe the replication process of paramyxoviruses.
|
viral mRNA is generated from viral RNA.
Gene expression is temporarily regulated (3' before 5' on RNA) leads to cell-to-cell fusion-->syncytium formation |
|
|
What types of infections are caused by parainfluenza viruses?
|
Colds, pharyngitis, laryngitis, croup, bronchitis, bronchiolitis, pneumonia, croup
|
|
|
How can RSV be transmitted?
|
Direct contact between infected infants & non-infected individuals is significant.
Also respiratory droplets. |
|
|
Croup is a manifestation of what virus?
|
Parainfluenza viruses types 1 & 2
|
|
|
What are the most common severe manifestations of RSV?
|
Lower respiratory tract infections (bronchiolitis & pneumonia)
|
|
|
What is the clinical manifestation of metapneumovirus?
|
Similar to that of RSV
Newly discovered. Often found in SARS patients |
|
|
Where were Hendra & Menangle viruses identified?
|
Australia in the mid 1990's
|
|
|
What type of disease is caused by Hendra virus?
|
Flu-like illness + encephalitis
|
|
|
Where (other than humans) has Hendra virus been found?
|
Bats
|
|
|
What type of disease is caused by Menangle virus?
|
Flu-like illness
|
|
|
Where (other than humans) has Menangle virus been found?
|
Bats + swine
|
|
|
Where was the Nipah virus identified?
|
Malaysia in 1999
|
|
|
What type of immunity is found with paramyxoviridae?
|
Parainfluenza + RSV = incomplete (natural infection does not prevent reinfection but reinfection is less severe)
measles and mumps= lifelong |
|
|
How are parainfluenza viruses detected?
|
Heamadsorbing viruses in tissue
|
|
|
How is RSV detected?
|
Giant cell formed in culture
|
|
|
What is ribavirin?
|
Guanosine analog antiviral treatment for severe RSV infections.
|
|
|
What is respigam?
|
neutralizing antibodies from pooled adult plasma for treatment of premature-born childrne <24mos. that have RSV
|
|
|
What is synagis?
|
mab used to treat RSV
|
|
|
What does picornavirus stand for?
|
small RNA viruses
|
|
|
What is the structure of picornaviruses?
|
Non-enveloped
|
|
|
What is the form of the genome of picornaviridae?
|
(+) ssRNA
|
|
|
What is IRES?
|
Internal Ribosome Entry Site
Initiation of translation by internal binding of mRNA to ribosomse. located at 5' end of genome |
|
|
What is the importance of IRES?
|
Important for picornavirus translation after virus shuts down host cell translation b/c it degrades host cap-binding-complex (CBC).
|
|
|
What pH inactivates rhinoviuses?
|
<5.0
|
|
|
Where does picorniavirus replication occur?
|
Cytoplasm
|
|
|
Describe picornavirus replication process.
|
Single translation product is made=polyprotein
VPg is required for replication (antiviral target) |
|
|
What types of receptors are used by picornaviruses?
|
ICAM=rhinovirus
LDLR=rhinovirus (minor) CD49b/CD29=enterovirus DAF-CD55=enterovirus |
|
|
What is the clinical manifestation of enterovirus infection?
|
Diseases involving skin, muscle, CNS, liver, heart, pancreas, GI tract, eye, etc.
Includes poliomyelitis Most infections are subclinical |
|
|
What type of paralysis is caused by poliomyelitis?
|
Flaccid muscle paralysis
|
|
|
What cells are destroyed by poliovirus?
|
Anterior horn cells of the spinal cord & neurons in the motor cortex of the brain
|
|
|
What is the clinical manifestation of rhinoviruses?
|
Common cold
|
|
|
What type of immunity may be associated with picornaviruses?
|
Neutralizing antibody.
No corss-protection between serotypes |
|
|
How are picornaviruses spread?
|
Fecal-oral
Fomites |
|
|
How are picornaviruses dx'ed?
|
viral isolation
RT-PCR serology |
|
|
Why might a killed vaccine be better than a live attenuated poliomyelitis vaccine?
|
A live vaccine can revert to virulence.
|
|
|
How does the live polio vaccine revert to virulence?
|
Mutations in 5' end
|
|
|
What are some antivirals used with picornaviruses?
|
Pleconaril-inhibits uncoating
Protease inhibitors |
|
|
Which polio vaccine was developed first?
|
Salk killed vaccine
|
|
|
Describe the prodromal stage of measles.
|
CCCF + Koplik's spots
Cough(severe)CoryzaConjunctivitisFever |
|
|
When is measles most infectious?
|
Before the rash appears.
|
|
|
Koplik's spots are indicative of what disease?
|
Measles
|
|
|
What are Koplik's spots?
|
Small white dots on the throat
|
|
|
Describe the Morbilliform rash.
|
Diffuse, erythematous, maculopapular
Confluent With late desquamation Begins at head and moves down |
|
|
Describe the fever progression of measles.
|
Begins with cough and peaks @ appearance of rash and continues for 5 daysish
|
|
|
What are complications of measles?
|
Respiratory tract complications!!!!
Also diarrhea (issue in dev. countries) Encephalitis |
|
|
How is measles diagnosed?
|
Clinical picture
IgG antibody |
|
|
What is the treatment for measles?
|
Supportive care
Vitamin A |
|
|
How can measles be prevented?
|
Vaccination: 2 doses
In outbreak: unvaccinated can get 1 does w/in 72 hours of exposure |
|
|
How long is the prodromal stage of measles?
|
3 days (avg)
|
|
|
What is the family of Parvovirus B19?
|
Parvovirus
Genus: Erythrovirus |
|
|
What is the genome of parvovirus B19?
|
ssDNA
|
|
|
In what cell does parvovirus B19 replicate in?
|
Erythrocyte precursors
|
|
|
How can parvovirus B19 be transmitted?
|
Respiratory secretions
Blood & blood products Vertical (mother-->fetus) |
|
|
What type of infections are caused by parvovirus B19?
|
Asymptomatic infections are most common
50% of adolescents have had the virus |
|
|
When is the peak incidence of parvovirus B19?
|
Spring
|
|
|
What clinical diseases are associated with parvovirus B19 infection?
|
Fifth disease (erythema infectiosum)
Polyarthropathy (female adults) Transient aplastic crisis (sickle cell) Chronic anemia (immunocompromised) Hydrops fetalis (fetus) |
|
|
Describe erythema infectiosum.
|
Mild to no fever.
Slapped cheeks appearance 2 days before rash Rash: erythematous, lacy, itchy, worse on extremities that comes & goes based on temperature |
|
|
What is the risk of fetal death due to parvovirus B19?
|
<1%
|
|
|
Transient aplastic crisis is associated with what disease?
|
Parvovirus B19 in individuals w/hemolytic crisis
|
|
|
What is transient aplastic crisis?
|
Transient: reticulocytopenia
Contagious in blood & saliva |
|
|
Describe polyarthropathy syndrome.
|
Arthralgia and & arthritis-->symmetrical
Due to parvovirus B19 usually resolves in a few weeks |
|
|
What happens with parvovirus B19 in immunocompromised individuals?
|
Chronic anemia for 1-2 years
|
|
|
How is parvovirus B19 diagnosed?
|
Serologic testing
PCR |
|
|
How is parvovirus B19 treated?
|
Symptomatic treatment
Intrauterine blood transfusions for hydrops fetalis |
|
|
How is HHV-6 transmitted?
|
Asympatomic shedding in saliva of family members
Almost everyone has had it by 3years |
|
|
How long does HHV-6 viral presence last?
|
Life.
|
|
|
When is HHV-6 infection most common?
|
6 months-2/3 years
|
|
|
What is roseola?
|
HHV-6
"Exanthem subitum" High fever: 3-4 days Rash appears when fever is gone Post-occipital lymphadenopathy Seizures |
|
|
What does the roseola rash look like?
|
Papules w/fine pinkish rash
|
|
|
What are complications of HHV-6?
|
Seizures
Encephalitis Inssuscpetion |
|
|
How is HHV-6 diagnosed?
|
CLINICAL PICTURE
HHV-6 DNA by PCR |
|
|
How is HHV-6 treated?
|
Supportive care
Ganciclovir or foscarnet for severe disease in immunocompromised. |
|
|
How can VZV be transmitted?
|
Chickenpox: airborne or contact w/lesions.
Shingles: contact with lesions only |
|
|
What is the mode of entry of VZV into the body?
|
Upper respiratory tract or conjunctiva
|
|
|
How long is VZV contagious for?
|
1-2 days before onset of rash and until all lesions have crusted.
|
|
|
What are the clinical manifestations of varicella?
|
Fever
Rash Crops of lesions in different stages of development Mucous membranes may be involved |
|
|
When does the fever peak in varicella?
|
Right before the peak of the crops of lesions.
|
|
|
What are the clinical manifestations of shingles?
|
Crops of vesicles following 1-3 contiguous dermatomes
Pruritus Post-herpetic neuralgia (worse in adults) |
|
|
What is shingles?
|
Re-activation of virus from dorsal root ganglion
|
|
|
What are complications of varicella?
|
Skin infections (Strep & staph)!!!!
Thrombocytopenia Pneumonia Reye syndrome Hemorrhagic varicella (low platelet ct.) Congenital varicella syndrome |
|
|
What can happen in congenital varicella syndrome?
|
Developmental abnormalities
Severe Retardation Small limbs Unequal eyes |
|
|
How is VZV infection diagnosed?
|
CLINICAL PICTURE
PCR |
|
|
How can VZV be prevented?
|
Passive immuneprophylaxis-->rare
Active immunization: 2 doses |
|
|
How can VZV be treated?
|
Acyclovir
|
|
|
What is Kawasaki disease?
|
Acute, self-limited diffuse vasculitis
Fever Bilateral conjunctivitis Changes in oral mucosa & lips Rash Cervical lymphadenopathy Extremity changes CA aneurysms |
|
|
What are the oral mucosa changes in KD?
|
veryveryvery red lips & tongue
"strawberry" tongue |
|
|
What is the rash like in KD?
|
Measles-like
|
|
|
What kind of extremity changes can be found in KD?
|
Swelling & bright red color of palms & soles of feet.
Peels late. |
|
|
What kind of lymphadenopathy is found in KD?
|
Unilateral cervical lymphadenopathy
|
|
|
How can KD be diagnosed?
|
>5 days of fever and >4 features
Features: rash, lymphadenopathy, mucous membrane changes, conjunctivits, extremity changes |
|
|
How is KD treated?
|
Large does of aspirin.
High-dose IVIG for 6-8 weeks w/in 10 days of onset of symptoms |
|
|
What is key in the treatment of RMSF?
|
treat before a confirmation of the diagnosis
|
|
|
What is associated w/RMSF?
|
Rickettsia (bacteria)
Diffuse vasculitis!!!! |
|
|
What are the clinical manifestations of RMSF?
|
Fever
Severe headaches, myalgia, nausea, confusion, Rsh |
|
|
What is the RMSF rash like?
|
Begins at wrists and ankles & spreads to trunk.
Erythematous maculopapular & petechial rash that does not blanch on touch. |
|
|
What are complications of RMSF?
|
Renal, hepatic, CNS, GI involvement
DIC Shock Limb amputation due to hemorrhage under skin & swelling |
|
|
How is RMSF diagnosed?
|
Lab tests: leukopenia, thrombocytopenia, hyponatremia
Serology |
|
|
How is RMSF treated?
|
Doxycycline (even in young kids)
Chloramphenicol |
