The Viruses: Introduction and Major Groups Flashcards
Viruses
- nucleic acids surrounded by protein coat
- only able to replicate inside cells
- not living organisms on their own
Origin of Viruses
- likely existed since beginning of life
- escaped nucleic acids
- co-evolved with cellular life
Viruses in Nature
- found everywhere, millions in just one ml of seawater
- 8% of human genome is from viruses
- expansion of early human viruses dependent on agricultural revolution, allowed easier transmission of first viruses
- many have arisen through contact with animals
Role of Viruses in Human History
- small pox
- defeat of Aztecs and Incas
- retreat of American troops from Quebec City
- influenza pandemics in 1918 and recently
- HIV currently a major viral ix in world
Viral Morphology
Icosahedral - 20 sided shape of equilateral triangles
Helical - linear nucleocapsid surrounds genome
Cone-shaped
Complex
Viral Genomes
- RNA vs. DNA
- ss vs. ds
- segmented vs continuous
DNA Viruses
Adenovirus Herpesvirus Hep B Smallpox Parvovirus B19
RNA Viruses
Polio HIV Influenza Rabies West Nile
Viral Replication
- Attachment - via receptors, determines specificity of virus
- Entry - vis endocytosis, fusion, direct penetration
- Uncoating - release of genome into cytoplasm
- Replication - using host cell machinery to make viral proteins
- Assembly - capsomeres assemble around genome
- Release - non-enveloped do so by host cell lysis, enveloped viruses bud out of cell
Viral Pathogenesis Determinants
- route of entry and viral tropism
- size of inoculum
- viral effects on host cells
- virulence of virus
Host Factors Determining Pathogenesis
- host immune system
- host genetics - expressing right receptors
- physiological state - age, metabolic state
Types of Viral Infections (6)
- Acute Ix eg. rhinovirus
- Acute Ix. w/ late complication eg. Measles and SSPE
- Latent Ix eg. Varicella and Zoster later in life
- Chronic Ix w/ shedding eg. HSV
- Chronic ix w/ late complication eg. Hep B and cancer
- Slow ix eg. CJD
Host Immune Response to Viruses
- physical barriers
- innate immune system - macrophages, NK cells
- adaptive immune system - B cells produce neutralizing antibodies, T cells produce cell mediated immunity against virally infected cells
Evasion of host immune system (5)
- modulate viral antigen expression, eg. downregulate expression or antigenic variation
- downregulate MHC expression
- integrate into genome
- infect cells that are not monitored by immune system (latent ix)
- infect cells of immune system
Persistent Viral Infections
Chronic ix’s - balance between viral replication and host immune response, persisted low level infection
Latent ix’s - viral genome replicated with daughter cells, either in genome or extrachromosomal, reactivates only when permissive environment
Norovirus
- non-enveloped
- icosahedral
- incubation 12-24 hr
- sx: watery diarrhea, vomiting, low grade fever, abdo cramps
- resolves in 12-72 hr
- viral shedding for 3 wks
Norovirus epidemiology
- # 2 most common viral ix in developed world
- # 1 most common non-bacterial gastroenteritis
- often occurs in long term care facilities and hospitals, cruise ships
Norovirus Transmission
- infectious dose 100 virions
- fecal oral transmission
- stable in environment for 24-48 hr
- resistant to alcohol and low levels of chlorine
Norovirus Pathogenesis
- asymptomatic and post-infectious shedders
- short term immunity to specific strains
- strong levels of antigenic drift and antigenic shift
- blood groups B and AB somewhat resistance to ix
- mutation in FUT2-alpha can confer resistance
Norovirus Diagnosis
- collect stool/vomitus for diagnostics
- RT-PCR is best, see highest viral load within 48-72 hrs of sx onset
- also EIA and electron microscopy (low sensitivity)
Varicella Zoster Virus
- Herpesviridae (HHV-3)
- dsDNA enveloped icosahedral virus
- causes both Varicella (chicken pox) and Herpes Zoster (shingles)
- highly infectious (most infectious Herpes virus)
- transmission via aerosols, droplets, contact
- Herpes Zoster is less infectious
- goes latent in nervous system (dorsal root ganglia)
Chickenpox Pathogenesis
- ix of URT, viremia, ix of reticuloendothelial system, second virema, rash appears
- rash is due to viral damage to host cells and host immune system (macules, papules, vesicles, pustules, crusting)
- rash spreads in centripetal pattern (head to trunk outward)
Pathogenesis of Shingles
- reactivation of VZV from sensory ganglia
- travel down neurons to epithelium, cause rash in single dermatome, resolves in 7-10 days
- associated with host factors (age, trauma, stress)
- can cause post herpetic neuralgia
VZV Diagnosis
- important to differentiate VZV and HSV
- aspirate fluid from vesicles
- PCR is best
- use serology to determine immune status
- important to know immune status for: health care workers, pregnant women, immunocompromised individuals who have been exposed
Chickenpox Management
- treatment: acyclovir, valacyclovir, famcyclovir
- post-exposure prophylaxis: vaccine within 3-5 days of exposure can reduce sx, immunoglobulin tx for newborns/high risk individuals
- live attenuated vaccine for children
Shingles Management
- treatment: antivirals reduce sx and post-herpetic neuralgia if given within 48-72 hrs of onset
- VZV vaccine for over 60