Viruses Flashcards
basic unit from which capsids are built
structural unit
protomer
surface structures seen by EM
morphological unit
capsomer
protein shell surrounding the nucleic acid genome
capsid
coat
lipid bilayer derived from host membrane carrying viral glycoprotein
envelop
viral membrane
complete infectious virus particle
virion
nucleic acid core (genome), core proteins, and capsid (protein coat)
nucleocapsid
capsid type
assembly of nucleocapsid requires the presence of nucleic acid
each protomer interacts directly with nucleic acid
size of the nucleocapsid is limited by the amount of nucleic acid enclosed
helical capsids
capsid type
nucleic acid is notneeded for capsid formation (empty capsid forms)
size of the capsid limits the amount of nucleic acid enclosed
multiple proteins are usually involved in forming the capsid
icosahedral capsid
capsid type
poxviruses
DNA viruses carries machineries for cytoplasmic replication (replication enzymes)
virions are very sable (6 months) even when desiccated and at room temperature
complex virion
viral genome directly translatable into protein, acts as mRNA
Positive sense RNA genome
viral genome from which mRNA is made and translated into proteins
Negative sense RNA genome
pattern of viral disease
infection and complete recovery
acute infection
pattern of viral disease
final disease is different from initial disease
acute infection, rare late complication
pattern of viral disease
second disease episode is the same as the first; no infectious virus between episodes
latent infection
pattern of viral disease
following initial disease episode, virus is shed without overt disease
chronic infection
pattern of viral disease
virus is produced and shed for long period before disease manifests
chronic infection, late disease
amount of virus increases over time until sufficient level is reached to cause disease
slow infection
virus family 10-12 segments in dsRNA genome non-enveloped, icosahedral capsid Coltivirus - Colorado Tick Fever Rotavirus
Reoviruses
most important cause of severe diarrhea in children under 5 worldwide (most common in 6-24 months)
outbreaks in child care centers, nosocomial infections in children’s hospitals
increased viral survival at higher humidity, peak incidence in cooler months
resists inactivation by concentration of chlorine used in treating sewage and drinking water
fever/vomiting for 2-3 days, progress to diarrhea for 4-8 days
watery profuse diarrhea, abdominal pain, severe volume depletion (dehydration)
seizures with aspiration of vomitus
chronic diarrhea in the immunocompromised
clinical diagnosis; ELISA, stool viral culture, stool EM, Latex agglutination, PCR
supportive care, no antivirals, hygiene, inactivation with 95% ethanol
RotaShield = oral, live attenuated vaccine, no longer available, causes intussusception
RotaTeq and Ratarix = oral, live attenutated vaccine, small risk of intussusception
non-enveloped, iscosahedral
11 dsRNA segments
triple layer structure: outercapsid (VP4, VP7), middle capsid (VP6, target of Ab), inner capsid (VP2, structure)
polymerase (VP1, transcription), guanyltransferase (VP3, RNA capping)
7 antigenic groups (Group A causes most human disease)
fecal-oral transmission; sloughing of enterocytes in stool results from receptor mediated endocytosis causing enterocyte infection and conversion to dual layer structure; viral replication produces new dual layer structures that obtain the third layer in the ER; progeny released by cell lysis
Rotavirus
virus family
nonsegmented +ssRNA genome
non-enveloped, icosahedral
worldwide distribution, affects all ages
occurs year round but is more common in less humid months/winter
associated with epidemic outbreaks of waterborne, foodborne, and shellfish-associated gastroenteritis
Norovirus
Caliciviridae
leading cause of food-borne disease outbreaks worldwide
Genetic mutation and recombination contribute to broad heterogeneity and emergence of new strains resulting in antigenic drift (especially genotype II)
Immunity is incomplete and temporary
Genotype GII.4 is responsible for 70-80% of outbreaks worldwide
VP1 is the major capsid protein; receptor binding region and major site of antigenic variation
Individual human susceptibility is related to the presence of specific histo-blood group antigens (secretor status); these are glycans on the surface of gut epithelial cells (polymorphic fucosyltransferase genes)
O negative individuals are resistant to infection
Frequently reported on ocean liners; transmission is linked to sewage contamination, poor water storage/ filtration/ chlorination, food handler carriage, food preparation/storage; also seen in hospitals, military camps, jails, and schools
rapid onset of symptoms and brief clinical course
Fever, anorexia, explosive watery diarrhea, forceful vomiting
Respiratory symptoms in 1/3 of children
Illness begins 12hr to 4 days after exposure and lasts 3-7 days
Diagnosis by clinical manifestations and PCR of stool, treatment is supportive
Norovirus
Norwalk virus
virus family linear ssRNA genome icosahedral, non-enveloped stable at pH 3-10 (survive stomach acid) replicate in the GIT and pharynx resistant to chloroform and alcohol shed from GIT more than URT cause minor and major viremia Enteroviruses
Picornaviridae
Enterovirus
Three serotypes; humans are the only natural host
life-long immunity, no cross-immunity with other serotypes
fecal-oral transmission
replication in the gut, dissemination to the RER via minor viremia, rare major viremia spread to other organs (muscle and brain)
biphasic
90-95% of infections are asymptomatic
abortive infection: fever, headache, sore throat, anorexia, indistinguishable from other viral infections
non-paralytic infection: aseptic meningitis similar to other enteroviruses, signs of meningeal irritation
paralytic infection: flaccid paralysis resulting from lower motor neuron damage; asymmetric, proximal muscles most affected, loss of reflexes but sensation intact; residual deficit in most
replication in the anterior horn cells of the spinal cord leads to spinal infection
involvement of the medulla and brain stem causes bulbar infection that leads to cranial nerve paralysis
involvement of the cortex causes encephalitic infection
Respiratory failure is responsible for most deaths (weakness of diaphragm and intercostals, involvement of respiratory center in brainstem, CN infection)
Post-infection syndrome is a late manifestation of acute paralytic infection in childhood; characterized by muscle pain and exacerbation of paralysis resulting from late attrition of oversized motor units that developed in the recovery process
Dx: viral isolation from throat, feces; serology
Occurred most often in the summer and fall in the US but can occur year round in tropic areas
Pre-industrial era: milder endemic form in infants protected by maternal antibodies
20th century: improved hygiene, epidemics in older children peaked in 1952; vaccine in 1955 resulted in sharp decline
Salk vaccine: (IPV) inactivated virus; mix of three types inactivated by formalin; currently used in most of Europe, US, and Canada
Sabin vaccine: (OPV) oral, leads to the additional development of mucosal immunity; used in developing countries; vaccine derived infection (if population is underimmunized, cVDPV)
Problems with eradication: subclinical cases, vaccine associated infections, changes in world populations/politics, long duration of eradication programs
Vaccine derived viruses can cause paralytic infection, potential for sustained circulation; can cause outbreaks in areas with low OPV coverage; OPV replaced with IPV in US; new cases in only 2 countries (Pakistan, Afghanistan)
Poliovirus
Non-polio enterovirus
Acquired by ingestion of virus shed in feces or URT
Replication in lymphoid tissues of the ileum gives rise to transient minor viremia and RES involvement
Major viremia seeds other target organs (CNS [meningitis], heart [myocarditis], skin [viral exanthema])
Infants and young children have the highest rates of infection and disease
Most infections are asymptomatic but some develop nonspecific febrile illness (lethargy, poor feeding, vomiting, and diarrhea)
Exanthema = rash resembling measles and rubella;
herpangina, hand-foot-mouth disease, acute hemorrhage conjunctivitis
Diagnosis by viral isolation in cell culture and PCR; serology can be done but there is cross-reactivity
Infection is usually self-limited and do not require treatment; in severe infection, Ig therapy has been used
Coxsackie viruses A
Non-polio enterovirus
Acquired by ingestion of virus shed in feces or URT
Replication in lymphoid tissues of the ileum gives rise to transient minor viremia and RES involvement
Major viremia seeds other target organs (CNS [meningitis], heart [myocarditis], skin [viral exanthema])
Infants and young children have the highest rates of infection and disease
Most infections are asymptomatic but some develop nonspecific febrile illness (lethargy, poor feeding, vomiting, and diarrhea)
Exanthema = rash resembling measles and rubella;
Aseptic meningitis, myocarditis and pleurodynia
Diagnosis by viral isolation in cell culture and PCR; serology can be done but there is cross-reactivity
Infection is usually self-limited and do not require treatment; in severe infection, Ig therapy has been used
Coxsackie virus B
virus family
enveloped ssRNA genome
bud from cell surface with embedded surface proteins
attachment to cell surface glycoproteins via hemagglutinin-neuraminidase, hemagglutinin, or G proteins
F protein mediated fusion of virus to host cell
Parainfluenza, mumps, measles, respiratory syncytial virus, metaneumovirus
Paramyxovirus
Morbillivirus; ssRNA virus
Hemagglutinin attaches to cell surface
predominantly a childhood illness, humans are the only hosts
seen worldwide, mostly in winter/spring
US cases largely due to importation
highly contagious, droplet spread by infected nasopharyngeal secretions
infects epithelial cells of respiratory tract, spread by viremia to RES, followed by secondary viremia
replication in conjunctiva, respiratory tract, GI, GU, lymphatics, blood vessels, and CNS
disease manifestations due to T-cell response to virus infected cells lining capillaries
multi-nucleated giant cells in skin, mucosa
Koplik’s spots = mucosal enenthem
maculopapular rash initially on face, spreads to trunk and limbs; confluent
complications: pneumonia, bacterial superinfection, encephaltits, subacute sclerosing panencephalitis
Dx: clinical appearance, serology, PCR
Tx: supportive, vitamin A
vaccine: MMR, two doses
Measles
Rubeola
endemic worldwide
US outbreaks related to importation from UK
humans are the only host
transmitted by direct contact, droplets, fomites
prodromal low grade fever, malaise, headache (flu-like)
progresses to earache and tenderness with parotid palpation
bilateral parotid enlargement
post-pubertal epididymo-orhcitis, meningitis, encelphalitis are possible
vaccine preventable (MMR), some evidence of lost immunity with time
Mumps
major cause of lower respiratory tract infection in young children; also seen in immunocompromised adults
primarily in winter and spring
outbreaks last up to 20 weeks
all children are infected in the first few years of life
inoculation through nose or eye (mouth is less effective)
Bronchiolitis (lymphocytic peribronchiolar infiltration): endothelial sloughing, mucus secretion, airflow obstruction
pneumonia with mononuclear cell infiltration
acute complications: apnes, increased risk of infant aspiration
chronic complications: recurrent wheezing, bronchiectasis
pneumonia in immunocompromised
tx: ribavirin, bronchodilators, corticosteroids
prevention: infection control, IVIG for high risk infants
Respiratory Syncytial Virus
RSV
attaches via G protein, structure similar to RSV
infects all ages, most children are infected by age 5
infection mostly in winter
upper respiratory infection, bronchiolitis, pneumonia
co-infection with RSV and/or influenza possible
Metapneumovirus
MNV