2 Virus: Entry and Transmission Flashcards
Viral Tropism
→ meaning / defintion (1/1P)
→ Mechanisms of tropism (2P+)
Meaning
shape/response
Defintion:
the way a virus responds to host factors in order to enter and infect a cell
Mechanisms of tropism
Binding and entry
→ different cellular receptor expression leads to different susceptibility of cells
Post Entry factors
→ Transcription/Translation machinery compatible with VIC
→ Innate immune system
overcome e.g. by counteracting viral proteins (interferon antagonist)
→ Adaptive immune system overcome e.g. by counteracting viral proteins (immune evasion)
Permissibility of cell type for viral replication
3 different types of tropism and example
Cellular
HIV infects macrophages but no neurons
Tissue
Influenza infects respiratory tract but no brain tissue
Host
Myxoma Virus infects rabbits but no humans
Mucosal surfaces (3P) + location (4P)
→ line all body cavities
→ wet enviroment (mucus)
→ epithelial cells that form physical barrier via tight junctions
Location:
eye, Respiratory, GI, UG
Breach of epithelial layer (3P)
Breach of tight juctions
Direct infections of cells
Endo/Exocytosis
Immune priviliged sites (3P)
→ definition and kind of infections as a result + e.g.
Eye, brain, reproductive tract
immune priviliged sites
→ devoid of some initiators and effectors of immune systeme because a strong immune response would be bad for host
→ persistent infection of these organs is common, e.g. Ebola in ocular fluid or semen
Eyes
RT
UTI
GIT
Skin
Eyes
Systemic: HSV
Localized: Adenovirus
- *GIT**
systemic: Enterococcus
localized: Rotavirus
RT
localized upper: Rhinovirus
localized lower: Influenza, RSV
systemic: Rubella
- *UTIs**
localized: Paillomavirus
systemic: HBV
Skin
anthropod: Bunya
Needle: HCV, HIV
Bite: Rhabdovirus
How does infection spread in host
→ Localized
→ Dissemination
→ 3 types of dissemination
After replication at entry site, virus may remain localized
→ spread only within epithelium + contained by immune response
But some viruses disseminate and if multiple organs infected is it called systemic infection, this requires breaching of endothelial cells as well
3 types of dissemination
→ lympahtic
→ hematogenous
→ neural
Endothelial vs Epithelial cells
Endothelial
→ specialised type pf epithelial cells that line the internal surfaces of the components of circulatory system like blood vessels
Epithelial
→ line internal and external surfaces of the body
Lymphatic dissemination with example
→ e.g Dengue Virus that infect DCs in lymphatic capillary via anthropod bite → lymphatic dissemination
Dengue Virus
→ route of infection
→ Disease
→ genome, family, serotypes
→ ADE and vaccine limitations
route of infection
→ mosquito bite, virus infects DCs into dermis, they migrate to regional lmyph nodes through lymphatic capillary along with their maturation process
disease
→ Dengue Fever
→ mild, flu like symtoms up to 1 week
→ 2-4% severe → 1-2% fatal
→ Hemorrhagic fever
→ Dengue Shock syndrome
genome, family + serotypes
→ +ssRNA, Flaviviridae
→ DENV1-4(5)
ADE
= Ab dependent Enhancement
→ no antibodies → mild infection
→ high affinity antibodies lead to neutralization
→ low affinity antibody leads to severe disease because no neutralization occurs and these antibibodies also enhance entry into DCs and lead to severe cases including DHF and DSS
→ vaccine needs to be protective against all 4 serotypes, otherwise even vaccination can be reason for severe case
Passive, primary and secondary Viremia
→ characteristics, titers, time
Passive
→ without need for replication, e.g. direct inoculation via mosquito
→ 1 day, decent titer
Primary
→ initial spread of virus in blood stream from the first infection site
→ 2 days, low titers
→ e.g. Hepatitis B, HIV
Secondary Viremia
→ occurs when primary Viremia already has resulted in infection of additional tissue, in which virus multiplicated and from there entered the bloodstream again
→ 1-2 weeks, high virus titers
→ Rabies, first muscle tissue, then via secondary Viremia CNS
Measles
→ e.g. for …..
→ family, genome, R0, hosts
→ serotypes
→ Transmission
→ contagiousness
→ symtoms
→ Complications
→ SSPE
e.g.
for hematogenous dissemination
family, genome, R0, host
→Paramyxoviridae, enveloped -ssRNA, R0= 15-20, humans
serotype
→ 1 serotype = life long protection
Transmission
→ Transmission via inhalation of respiratory secretions
Contagiousness
→ contagiousness max 2-3 days before rash
Symptoms
Fever, Cough, Conjunctivitis, Skin rash
Complications:
→ Immunosuppresion leading to secondary infections sometimes fatal
→ Acute post infection encephalitis
SSPE
Subacute sclerosing pan encephalitis (SSPE) that is 100% fatal, 6-8 years pst measles infection
Neural dissemination
→ e.g.
→ how ?
→ low neurovirulence examples
→ 2 different ways of spreading
→ Neurotropic, neuroinvasive, neurovirulent definitions + e.g.
→ BBB
e.g.
Rabies, Herpes
how?
spreading from primary site via entering local nerve endings to get avvess to CNS
nerve ending towards cell = retrograde
low neurovirulence
→ Polio, Reovirus
2 ways to spread
→ spread from nerve ending towards cell = retrograde spread
→ spread from cell towards nerve ending = anterograde spread
Neurotropic
can infect neural cells, infection by neural or hematogenous spread
Neuroinvasive
→ can enter CNS after infection of peripheral site
Neurovirulent
→ can cazse disease in neural tissue
HSV = low neuroinvasiveness, high neurovirulence
Mumps = high neuroinvasiveness, low neurovirulence
Rabies = high neurovirulence, high neuroinvasiveness
BBB
→ blood brain barrier that is a high selective permeability barrier that seperates circulating blood from brain and extracellular fluid in CNS, breaching of blood brain junction needed to infect brain tissue
Aerosols vs Droplets
Aerosols
→ can contain virus particles
→ may travel long distances
→ can be inhaled → mucosal surfaces
→ e.g. Corona
Droplets
→ can contain virus particles
→ larger → up to 1.5 distance
→ e.g Ebola
How can infection by persistent?
examples
Primary infection is not cleared by adaptive immune response
immunopriviliged sites, Immunemodulation to prevent clearance, latency to prevent detection
HCV blocks inate immune response
EBV resides in non proliferating memory B lymphocytes
HSV viral genome persists in neutron cell, no new virus but genome replicates, reactivation possible
