virology week 3: rna viruses Flashcards
structureof picornaviruses
stable at pH between 3-10; satablein heat and detergents, resist lipid solvents, ether, chloroform andalcohol, inactivated at temperatures >50ºC; infectious at refrigerator room temp
picornaviridae includes:
picornaviruses include: enterovirus, coxsackie A, coxsaskie B, polioviruses, rhinovirus, hepatovirus
replication process 2steps for picornaviruses
-virus via VP1 bindsto ICAM-I then -VP4 is realeased upon binding
which cells are affected when virus via VP1 binds to ICAM-I
epithelial, fibroblast, endothelial cells,
which VP4 is released upon binding (3 sub processes)
Genome injected across cell membrane; Channel creatd by VP1 protein (pleconaril blocks binding); replication within 3-4 hours (what happens is the viral RNA genome binds to ribosomes, 5’cap structure isn’t needed , - RNA strand synthesized ,viral production rapid, inhibits cell function: protein synthesis, transcription, permeability changes
pathogenesis and immunity of picornaviruses
Virus DOES NOT cause enteric disease, enteric and URT portals of entry , resistant to GI Acids, enzymes, bile acids, enteric adn URT replication and shredding; viremia 2 stages
viremia 1st phase of picornaviruses
virus sprads to receptor bearing target tissues: reticuloendothelial cells,lymph nodes, spleen, liver
viremia 2nd phase of picornaviruses
symptoms, viral productio nand shredding (30 days), immunoglobulins (protective); T cell respone augments pathogenesis.
epidemiology of picornaviruses
transmision via (fecal-oral route), inhalaion, contaminated food/water ; asymtpmatic shedding, virus resistant to enviornmental conditions
clinical syndromes of poliovirus infection
(type of picornaviruses) asymptomatic illness, abortive poliomyelitis, nonparalytic poliomyelitis, paralytic polio, bulbar poliomyelitis, post-polio syndrome
fact about poliovirus
wild-type poliovirus has been eliminated from the western hemisphere
clinical syndromes of coxsackie A virus
herpangina(mouth blisters), hand-foot-mouth disease,
coxsackie B virus
pleurodynia, myocardial and pericardial infections, echovirus, viral (aseptic) menningitis
note about coxsackievirus and echonirus
can cause fever rash and flu-like symptoms
Clinical syndromes of coxsackie A virus
Herpangina which include: fever, sore throat, vomiting, vesicular lesions on soft palate ; or Hand foot and mouth disease: vesicular exanthema, hands, feet, mouth
clinical syndromes of cossack B virus
pleurodynia (bornholm disease) - known as devil’s grip: fever, pleuritic chest pain, abdominal pain
laboratory diagnosis of picornavirus
Cerebral spinal fluid: lymphocytic pleocytosis, non-specfic; culture: polio virus grows in culture, coxsackie virus does not grow in culture; ELISA RT-PCR
treatment of Polio
inactivated polio vaccine (IPV): virus shed for weeks, virus convert to virulent form, can infect immunocompromised OR attenuated oral polio vaccine (OPV) which replicates inintestinal tract and oropharynx,, cannot infect neurnal cells
treatment of coxsackie A and B
no vaccines but supportive care
characteristics of rhinoviruses
cause the common cold, 100 serotypes, uses ICAM-I receptor for entry
pathogenesis of rhinoviruses
unaleto replicated in GI tract, infection initated by 1 viral particle , peak point of illness is nasal secretions contain 1k>virions/mL ; infection initiated in URTY/throat
immunity of rhinoviruses
bradykinnin/histamine from infected cells (runny nose) ; interferons limit progression of infection (too many serotypes of immunity)
agents causing flu like symptoms
rhinovirus, enterovirus, adenovirusm, parainfluenza, coronavirus
transmission of rhinovirus
respiratory droplet and fomites : hands/major vector ; virus is stable:mouth, nost, etes ; peak occurrence in early authum; asymptomatic ppl can shred and infect (clinical symptoms on seen in 1/2 that’s infected) ; *rates hightes in infants and children
