Viral Respiratory Infections Flashcards
mechanisms used by respiratory tract pathogens to initiate disease
sufficient number of virus inhaled or acquired by direct contact
infectious particles are often airborne
infectious virus must remain alive and viable during transmission
virus must be deposited on susceptible tissue in the host
general approaches to prevention/treatment of respiratoory infections
genetically engineered or selected vaccines
passive antibodies - humanized, pooled, or human monoclonals
drugs against virus specific proteins or enzymes
hand washing - avoiding close contact
supportive care
orthomyxovirus
influenza A, B, and C
A infects both humans and animals
B and C only infect humans
influenza A most important - associated with epidemics and pandemics
particles are highly pleiomorphic - mostly pspherical or ovoid
components of the influenza A virion
host derived lipid bilayer that includes hemagglutinin (HA) and neuraminidase (NA)
inner shell is composed of matrix protein (M1)
nucleocapsid contains viral genome with eight unique segments, all are required to be infectious
H antigen
hemagglutinin
required for binding the influenza virus to the host cell
N antigen
neuraminidase
helps the mature virus escape from the cell
Describe the replication cycle of influenza.
Influenza binds to surface, endocytosed
Channel protein allows acidification of the vurlent particle
Release of genome into cell
Genome made in nucleus, transport into cytoplasm
Virus assembled and released
Two key steps - acidification step and the neuraminidase release step
classification of influenza
three types of H antigen
two types of N antigen
different combinations make different viruses
antigenic drift
changes in the discrete highly variable domains of the viral proteins through random mutations
antigenic shift
dramatic changes in virus by reassortment with another influenza virus
animals serve as a pool and where reassortment occurs due too infection with both animal and human viruses
epidemic flue
cyclic and usually caused by type B or type A
type A occur every 2 to 3 years, and type B occurs every 4 to 6 years
overall mortality rate is 1%
route and spread of influenza infection
entry via respiratory tract through inhalation
viral infection and spread is normally lmited to the epithelial cells of the respiratory tract
influenza pathogenesis
infects primarily upper and lower respiratory tract
influx of macrophages and lymphocytes
spectrum of disease ranges from asymptomatic infection to primary viral pneumonia
release of IL1 triggers fiver
release of interferon triggers aches and pains
humoral response is important for the control of these infections
replication of the virus causes desquamationof the ciliated epithelium, hyperplasia of transitoral cells, and increased secretions
inbucation time is 1 to 3 days
prevention/treatment of influenza
vaccinate those who are at risk
vaccines made from reassortment of egg-adapted strains that are then formalin inactivated
M2 protein
influenza protein channel that allows acidification for uncoating of the virus
permits flow of ions from the endosome into the virion center to disrupt interactions and release the viral genome
amantadine and rimantadine
drugs active against influenza A viruses
target is the M2 protein
prevents uncoating of the virus