Viruses
Virus
obligate intracellular parasite that sub-microscopic and has a specific rang of hosts
Viral structure
Nucleic acid
DNA
RNA
Capsid
outer protein cover protecting genetic material
basic protein subunits
capsomeres
protect nucleic acid
interact with host cell surface
facilitate nucleic acid penetration into cell
Capsids determine shape
icosahedron symmetry
Some viruses have
Envelope
Lipids and proteins
helps with entry
does not protect
Spikes
proteins in envelope that assist in recognition and attachment of host cells
do not penetrate
Classifying Viruses
Type of host
animal viruses, human viruses
Nucleic acid content
Viral genomes include single stranded RNA, single stranded DNA, double strand RNA, single strand RNA
Envelope presence
Enveloped viruses
Naked viruses
non-enveloped viruses
Infection type
lytic, persistent
Steps in Replication
Attachment
use capsids or envelope spikes to attach to host cell receptors
outside host cell
virion
Entry/penetration
virus injects genetic info into host cell
envelope is lost
Uncoating
capsid sheds
synthesis/replication
viral genome is replicated and capsid proteins produced
hijack host genetic machinery
Single Strand DNA
use host enzymes to make a complementary strand
Double strand DNA
replicated in the nucleus
Positive sense single strand RNA
genomes acting directly as mRNA
negative sense single strand RNA
Double stranded RNA
use host enzymes to make proteins from positive-sense stands
Retroviruses
use reverse transcriptase
Assembly
Assembling protein capsid around the nucleic acid core
Release
Replicated viruses are released
budding-enveloped
lysis-naked
Viruses acquire the envelope during the release stage
Retroviruses
Retrovirus
replicated by converting its single stranded RNA genome to double stranded DNA and integrating into host genome
contain genes producing reverse transcriptase
Reverse Transcriptase
DNA-RNA hybrid forms
RNA is removed
DNA stand templates and makes DS DNA
Integrase integrates dna
Provirus/Prophage
HIV is a retrovirus
Viral Pathogenicity
Cell penetration ability
wounds, insect bites, mucous membranes
mucosal immunity
Intracellular growth ability
Defense mechanism resistance
Host damage ability
lysis
tranforming genome
etc
How Viruses Enter Human body
Mucous membrane
respiratory most common
alveolar macrophages
important immune cells fighting infection in alveoli and protecting against pathogens
genital, conjunctiva (Eyelids)
Skin
parenteral route
non oral infection
insect bites, surgical trauma
Key points
Entry point is not the infection site
Entry point is not the exit point
Fecal-0ral route
entering via mouth exiting via feces
Characteristic entry patterns exist
How Viruses spread
Local spread over epithelial surface
Neurotrophic viruses
nervous system cells
Blood-brain barrier
Lymphotropic viruses
spread through lymphatic system
Viremia
viruses present in blood
Skin penetration
Congenital disease
viruses pass mother to fetus via placent
How Viruses Shed
Virus shedding
virus exit methods
Consequences of a viral infection
Types of viral infections
lytic infection
standard viral infection
enter, hijack, destroys via lysis
Abortive
Enter but The virus cannot replicate
Productive
Virus can replicate
Persistent Infecvtion
The virus does not immediately kill the hosts
Host cells continue to produce
result in chronic infections
Latent infections
Viruses remain dormant until triggers activate replication
Cold sores
Transforming infections
viruses affect host genetics, causing mutations
oncogenes, which cause cancer
Virus-Induced changes in cells
Cytopathic effects refer to microscope-visible effects of viral infections
Viral plaque formation
visible areas in Petri dishes where viruses destroyed infected cells in culture
Synctia
formation involves the creation of a single cell with multiple nuclei
One Step Growth Cycle
A
Attachment and penetration
receptor-mediated endocytosis
Forming endosomes
Low ph causes uncoating and fusion of the virus to an endosome
B
Eclipse
No detectable viruses exist, but components are produced
B
Yield/maturation
Burst/Rise
Infectious viruses increase as assembly begins
C
release
Viral particle numbers remain high
viruses liberated through budding or lysis
Viral Syndromes
Syndrome
Collection of signs and symptoms
Signs
objective manifestations
ie rashes
Symptoms
internal manifestations
Viral signs and symptoms
oral infections, RT infection, rashes, eye infections, fevers, hepatitis, STDS, etc
Mechanisms for Viral Reproduction
Lytic Cycle
Type of phage replication cycle resulting in the release of new phages by lysis (and death) of the host cell
Mechanism
Phage binds to surface receptor, injects DNA
DNA of host is degraded
Host’s metabolic machinery makes DNA and protein of the phage
The phage produces lysozymes, cell lyses
new phages are released
Lysogenic cycle
Integration of the bacteriophage’s nucleic acid into host genome
no cell death
Phage binds to receptor
DNA of phage takes a round shape
Prophage
Induction
environmental cue causes the prophage to synthesize new phages
new phages enter lytic and kill host
Temperate Phage
Phage capable of establishing lysogeny
Lysogen
bacterium that contains a virus
Lysogenic conversion
Bacterial host acquires a new trait as a direct result of expression of a gene or lysogen
How Viruses are Grown in Lab
Viruses can be cultured in
cell culture
lab animals
Primary culture
group of cells removed from an organism and placed in suitable environment
Monolayer
Layer or homogenized cells growing side by side of one another
embryonated eggs
Quantifying viruses
Plaque Assay Technique
place a few drops of host cells on agar plate
Allow host cells to grow
Infect bacteria with virus
Count number of plaques, or clear areas where the virus has killed a group of cells through lysis
Hemagglutination Assay
Hemagglutinin causes red blood cells to agglutinate, or clump up
Expose solution of viruses to cells and observed agglutination
Tissue culture assay technique
uses human or animal cells
Viruses and Cancer
Viruses have the ability to cause cancer
Hep B/C
liver cancer
HPV
cervical
Neoplasia
Any new abnormal cell growth/reproduction due to loss of regulation of cell cycle
Neoplasia leads to formation of tumors
Tumors can become dangerous when they metastasize
Anaplasia
loss of cell differentiation that allows cancer to spread
Carcinogenesis
Process by which can forms
Oncogenes
cancer causing genes
Prions
Infectious proteins
BSE/Mad cow
Scrapie (sheep)
Creutzfeldt-Jakob
Proteins have PrP
Disease causing protein turns PrP into disease causing protein
Viroids
Infectious agents consisting of closed, single-stranded RNA
Require host cell to replicate
Cause diseases in plants