Vital composition
-Viral capsid-Viral envelopes-Viral spikes
What is a single virus called?
virion
What is in a virion
The capsid and genetic material
Viral capsids
-Protein Shells that protect the viral genome-3 shapes: helical, icosahedral, complex
Viral envelopes
-Lipid coating surrounding the capsid formed from budding from host cell and taking part of its lipid membrane in process
Naked virions
-unenveloped-Lyse cells. Do not pick up hosts membrane when they leave
Viral spikes
- Glycoprotein extension that ID and bind to host well- mutating genomes can change spikes-gives virus specificity. Can only bind to cell that has corresponding "lock
Viral genomes
- genes encode proteins & viral protein- necessary for capsomere, structures (like spikes), and enzyme replication- viruses have small genomes but have alot of variation- has less than 300 genes
double stranded DNA viruses
Transcribed straight into mRNA then to viral protein
Single stranded DNA viruses
complementary DNA is built—> then transcribed into mRNA—> which then becomes a viral protein
Single stranded RNA+
- mRNA like genome immediately ready for translation to viral protein
Single stranded RNA-
-Genome is complementary to mRNA—> transcribed by viral RNA-dependent RNA polymerases—> mRNA —> viral protein
Double stranded RNA viruses
-Genome is double stranded RNA—> transcribed by RNA-dependent RNA polymerases —> mRNA —> viral protein.
Retrovivuses
- mRNA like genome is converted to DNA form—> reverse transcription—> dsDNA integrates into host genome —> transcription —> mRNA—> viral protein
Retroviruses contain viral enzymes that allow them ...
To convert their DNA into RNA
dsRNA viruses must be...
Unwound before it can be transcribed due to its double stranded nature
Examples of ssRNA+ viruses
PolioRubellaWest Nile Encephalitis
Examples of ssRNA- viruses
InfluenzaMeaslesEbolaRabies
examples of retroviruses
HIV/AIDS
Examples of dsRNA viruses
Rotavirus
6 steps to viral replication
1. attachment or adsorption > binds to host cell surface2. penetration > enters host cell3. uncoating > release nucleic acid4. replication or synthese of virus > replicate new acid & caspid5. assembly > caspid surrounds nucleic acid6. release from host cell > replicates somewhere else
Viral replication
Uses host cells resources (amino acids, nucleotides, enzymes, and organelles) to make new visions
Viral replication step 1: attachment
To host cell via capsid proteins for naked viruses or spike proteins
Viral replication step 2: Entry
Endocytosis or membrane fusion (for animal viruses)- direct (only used by bacteriophages)
Viral replication step 3: uncoating
Break down of the capsid to release viral proteins and genome
Viral replication step 4: replication
Synthesize its genome and transcribe mRNA to translate to viral proteins
Viral replication step 5: assembly
Capsids form another viral genome to produce new visions
Viral replication step 6: release
Visions either bud off host cell creating their own envelope or lyse the cell creating naked visions
Encapsulated
The spike protein has to recognize a particular protein or target on the host cell for the virion to attach- No target found = No infection
Naked
Protein of capsomere that makes up the capsid is binding to the host membrane to attach to the cell
Tropism
Attachments and specificity of a virus to attach to a host cell- some viruses have narrow tropism= can only bind to specific kind of cell or tissue in host.- others have broad tropism = can attach& infect many types of cells and tissue
Replication:
Depending on the virus, this can take place in diff locations of the well.- DNA viruses can take DNA into nucleus to be replicated- RNA viruses can work in the Cytoplasm
Release
Virus will pick up the hosts membrane any of the hosts surrounding proteins. Now the virus will look like the host itself- a naked cell would burst the cell and therefore not taking any host cell components.
3 types of infections
Acute, Latent and chronic
Acute infections
referred to as Acute non-persistentLasts days
Latent infections
Referred to as latent persistent- infection peaks, then decreases, but the host cannot clear it. Infection stays in body & persists- lasts days, months, years-time where varian replication is low is referred to as quiet perio
Chronic infections
referred chronic persistent - when host is infected the replication is quite low, may stay low so the host doesn't know it has an infection- during this quiet period, the host may still be infectious- HIVis chronic persistent. Not until years later will it start to affect the immune system
Structure of bacteriophages
- Capsid = icosahedral. • collar-Sheath- base plate- tail fibers
Bacteriophage replication uses which pathway
The Lytic Replication Pathway = Lyses and kills host cells- phases referred to a "T" and an even # use this pathway
5 steps of bacteriophage replication (Lytic Replication Pathway)
Step 1: Attachment; phage binds to bacterial cellStep 2: Entry; phage injects genome into mostStep 3: Replication; protein synthesis makes phage partsStep 4: Assembly; phage structures assembledStep 5: Release; bacterial cell lyses and new phages are released.
Lytic Replication Pathway step 1: Attachment
- phage binds to bacterial cell wall- tail fibers make contact w/ host cell. TF interact w/ specific proteins on bacterial membrane— this gives specificity to cell type phage can infect- phase cannot move so they randomly encounter host
Lytic Replication Pathway step 2: Entry
-phage injects its genome into host; empty capsids remain outside the cell.-TF bend and lower the baseplate towards the surface of the cell. -the sheath contracts and nucleic acids are injected into the host cell. -the phage itself stays outside the cell and only the genome enters.-this is referred to as direct entry
Lytic Replication Pathway step 3: Replication
-protein synthesis makes phage parts and genome is replicated; host cell DNA is broken down by bacteriophage DNAases-phage genome also gets transcribed and translated to produce components to make new phage particle
Lytic Replication Pathway step 4: Assembly
-genome packed into capsid and phage structures assembled. -the genome, the capsid, the sheath and TF. hundreds to thousands of phages can be made
Lytic Replication Pathway step 5: Release
-bacterial cell lyses and new phages are released. -lysis is made possible by protein encoded by the phage called Lysozyme, and it breaks down cell walls. phages are release
Lysogenic replication pathway is used by ...
Temperate phages
Lysogenic Replication Pathway (steps)
Step 1: Attachment Step 2: EntryStep 3: IntegrationStep 4: Cell DivisionStep 5: Lytic cycle
What is the Lysogenic Pathway
-after entry, the phase genome is integrated into the host cell's genome and the bacterial cell will replicate and copy the phages genome
What is Prophage
Phage DNA integrated into host cell's genome
Lysogenic Replication Pathway Step 3: Integration
Phage DNA integrates into host genome forming a prophage
Lysogenic Replication Pathway Step 4: Cell Division
-Host and phage genomes are copied before cell division; -Despite a single infection event, multiple cells now carry the phage genome
Lysogenic Replication Pathway Step 5: Lytic Cycle
- Phage my enter Lytic cycle if host is stressed
Culturing Bacteriophages
can be done in either liquid or solid media
What is Turbidity
a measure of the cloudiness of a solution
What is the Viral Titer
the viral load OR the amount of viral particles present in sample
How do we measure the Viral Titer
the turbidity of a mixture-Really cloudy = lots of bacterial cells -Not cloudy/ clear = Fewer bacterial cells bc phages are lysing cells
How is turbidity measured?
spectrophotometer
What is a lesion
any observable change or abnormality
What is a rash
widespread outbreak of lesions
Vesicle/Vesicular rash
small, elevated lesion filled with clear fluid (ex: chickenpox)
Macule
flat, discolored area of the skin; doesn't alter thickness or texture of the skin (ex: freckles)
papule (papular rash)
raised solid lesion (not fluid filled); may be discolored; has distinct borders; less than 0.5 cm in diameter (ex: warts)
Pustule
raised lesion with pus below the surface (ex: inflammatory acne)
Maculopapular rash
small slightly raised papule lesions that overlay or are interspersed with macules (ex: rubella, rubeola)
Rubella (German Measles)
-Virus: Togaviridae---Enveloped, single-stranded RNA-Transmission: aerosols from respiratory tract 1 week before and after the rash appears-Signs/Symptoms: Pink maculopapular rash starts at face and travels downward last 3-7 days, fever, swollen lymph nodes, muscle/joint aches, runny/stuffy nose----Rare but encephalitis is a possible symptoms. -Treatment/Prevention: MMR (Measles, Mumps, Rubella vaccine)
Major Complication of Rubella
-Congenital Rubella Syndrome (CRS)---when women contract the infection within the first few weeks on conception---Virus can be transmitted to the fetus via placenta ---CRS can lead to miscarriages and stillbirths ---Children born with CRS can have multiple defects to multiple organ systems. ---can lead to blindness, deafness, heart defects and growth or cognitive problems in the infant
Measles (Rubeola)
-Virus: Paramyxoviridae---Envelope single-stranded RNA virus-Eipidemiology: Extremely contagious. 1 person infected can infect 12-18 people-Transmission: Respiratory Droplets-Signs/Symptoms: Fever, sore throat, cough, Koplik's spots, maculopapular rash----Can lead to Pink eye, ear infections and bacterial pneumonia-Treatment/prevention: MMR vaccine
Measles treatment
-MMR vaccine--CDC found that 25% of infected need to be hospitalized--1/1,000 have encephalitis (brain swelling). which is fatal in 10% of cases---Side effects of Vaccine: fever, rash, swelling at injection sight. more serious effects = joint pain, convulsions, and allergic reactions but occur less than in 1 million doses given
Mumps (epidemic parotitis)
-Virus: Paramyxovirus---Enveloped, Linear, Single-stranded RNA-Epidemiology: Endemic in areas with low MMP vaccination (africa, south asia. middle east)-Transmission: Respiratory droplets and saliva -Signs/Symptoms: Non-specific viral symptoms (low fever, fatigue), swelling of parotid salivary glands, orchitis, and meningitis---primarily respiratory in 50% of patients---orchitis is seen in about 50% of infected sexually mature men-Treatments/Preventions: MMR vaccine
What is orchitis?
inflammation/swelling of the testes
Chickenpox (Varicella)
Virus: Varicella-zoster. Herpesviridae family---Enveloped, double-stranded DNA genome. -Epidemiology: humans are only reservoir; highly contagious; incubation = 14-16 days-Transmission: respiratory droplets/direct contact w lesions-Prevention: routine childhood vaccine-Signs/symptoms: fever w itchy vesicular rash-Diagnosis: lesion appearance and medical history. no cure, calamine lotion and oatmeal baths reduce itch
Shingles (related to chicken pox)
Virus: Varicella-zoster. Herpesviridae family---Enveloped, double-stranded DNA genome.-Epidemiology: reactivation of chickenpox virus, variable incubation period-Transmission: reactivation of dormant virus; prevented by Zostavax vaccine for older adults-Signs/symptoms: headache, flulike symptoms wo fever, painful vesicular rash on one side of body-Diagnosis: lesion appearance and medical history. no cure, calamine lotion and oatmeal baths reduce itch
Chickenpox vaccinations
-Live Attenuated Vaccines---Active virus or live bacterium are weakened to lose pathogenicity-Attenuated Vaccines: active virus or live bacterium rendered non-pathogenic
Small Pox
-Virus: orthopoxvirus: Variola major and minor---Linear, Double-stranded enveloped DNA virus---Epidemiology: highly contagious with 30% death rate. Eradicated in 1980---Transmission: respiratory droplets or contact with fomites (contaminated objects)---Signs/Symptoms: Fever, fatigue, rash on palms and soles then tend to be on appendages-----The rash became raised bumps filled with a thick, opaque fluid that would eventually form scabs. Once the scabs fell off, it often left marks on the skin resembling pitted scars-Diagnosis/Treatment: Vaccination
Polio (poliomyelitis)
-Virus: Picornaviridae ---Single-stranded, non-enveloped RNA virus (it will lyse host cells as part of its replication process)---Most significant small virus (30nm)---Because polio destroys host cells, its considered a cytolytic virus. -Epidemiology: endemic in Afghanistan and Pakistan -Transmission: Respiratory droplets and fecal-oral route-Signs/Symptoms: flu-like symptoms (sore-throat, fever, fatigue, nausea/stomach pain, headache), small portion have paresthesia, meningitis and paralysis-Diagnosis and treatment/prevention: vaccination
what does Polio effect
virus can attack the central nervous system and damage motor neurons which can cause paralysis or death.
Conditions caused by Polio
-Asymptomatic infection-Minor polio -Non-paralytic polio -Paralytic polio-Post- Polio syndrome
Asymptomatic infection caused by Polio
affects 90% of those infected
Minor Polio caused by Polio
effects 5% of those infected (fever, headache, malaise, sore-throat, gastroenteritis)
Non-paralytic Polio caused by Polio
effects 2% of infected (minor polio symptoms with muscle spasms and back pain)
Paralytic Polio caused by Polio
- effects 2% of those infected (paralysis and bulbar poliomyelitis) ---most cases resolve over time but some are life long---when the respiratory muscles are involved, it can be deadly.
bulbar poliomyelitis
when the respiratory muscles are involved in the muscles affected by paralytic polio This can be deadly
Post-polio syndrome caused by polio
--experienced by 80%. typically happens about 30-40 years after the original infection.--patients report further deterioration of their muscles
two types of polio vaccines
Salk Vaccine: Inactivated polio vaccineSabin vaccine: Oral Polio Vaccine. Both require a booster for life long immunity.
Influenza virus
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