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List Viral Components
Virus Particle
Covering
Capsid (protein)
Envelope
Inner Core
Nucleic acid molecule (DNA or RNA)
Various Proteins (enzymes)
Identify Different Types of Viral Structure
Helical
Polyhedral
Spherical
Complex
Describe how viruses are classified
Named on capsid structure, chemical composition, and genome type
Virus Families
-viridae
Virus Genera
-virus
Describe and Order the steps of Animal Virus Replication
Adsorption
Penetration (Endocytosis or Fusion)
Uncoating
Production of Viral Components (Synthesis)
Assembly
Release (Budding, Exocytosis or Lysis)
Adsorption
The virus attaches to its host cell by specific binding of its spikes to cell receptors
Penetration
The virus is engulfed by the cell membrane into a vesicle or endosome and transported internally
Endocytosis
Viral particle engulfed into vesicle
Fusion
Viral particle’s cell envelope fuses with host’s cell membrane and nucleocapsid is released into the host
Uncoating
Conditions within the endosome cause fusion of the vesicle membrane with the viral envelope, followed by release of the viral capsid and RNA into the cytoplasm
Synthesis
Under the control of viral genes, the cell synthesizes the basic components of new viruses; RNA , capsomers, and spikes
Assembly
Viral spike proteins are inserted into the cell membrane for the viral envelope; nucleocapsid is formed from RNA and capsomers
Release
Enveloped viruses bud off of the membrane, carrying away an envelope with the spikes. This complete virus or virion is ready to infect another cell
Budding
Viral capsid pinches off covered in viral envelope
Exocytosis
1.Newly made viral proteins on rough ER transported to the Golgi Body
2.Membrane with viral proteins buds inside of golgi body while surrounding viral genome
Vesicle with virus inside
Vesicle fuses with cell membrane
Virus leaves cell
Lysis
Cell bursts with viral particles (deadly)
Describe 2 types of viral entry
Endocytosis & Fusion
Compare and Contrast 3 different types of Viral Release
Budding = enveloped viruses “steal” membrane while leaving cell alive.
Cell is enveloped
Cell membrane
Lysis = naked viruses burst cell open.
Cell dies
Exocytosis = enveloped viruses use vesicular trafficking to exit.
Cell usually enveloped
rough ER and Golgi Body
Describe and Identify 4 types of Viral Infections
Acute Infection
Latent Infection
Chronic Infection
Transformation into malignant cell
Acute Infection
Rapid multiplication
Cell death and virus release
Latent Infection
Viral components are present (e.g., viral genome) host is not harmed
leading to acute infection
Chronic Infection
Slow release of virus without cell death
Transformation into malignant cell
Activation of host proto-oncogene, insertion of oncogene, or inactivation of tumor suppressor protein
Define ‘plaque’
Virus replication lyses bacterial cells creating ‘plaques’
Essentially the absence of cells in a cell cultureDe
Describe 3 methods of viral propagation
Viruses are cultivated in ‘lawns’ of other cells
Cultivated in bird embryos (vitro)
Injected into live animals (mice)
Viral plaque culture injected
Explain 3 methods of Viral Detection
Infect Cell Culture and then look for plaques or cytopathic effects
Screen for parts of the virus
ex: DNA or RNA via quantitative PCR (molecular test)
ex: viral antigens via antibod-based tests (rapid test)
Screen for immune response
ex: antibodies against the virus (serological test)
Interpret results of Rapid Antigen test data
1. Microscopically contains a paper with antibodies that bind to virus (reporter antibodies)
2. Test line has antibodies that bind to virus
3. Control line has antibodies that bind to reporter antibodies
4. When sample (virus) is added, capillary flow will travel from reporter antibodies towards test line and control line
Positive Rapid test
Test line grabs COVID particles
Control line grabs reporter antibodies
Creates 2 lines
Negative Rapid Test
Test line grabs NOTHING
Control line grabs reporter antibodies
Creates ONE line for the test line since NOTHING is detected and one line for the control line since it detected the reporter antibodies
Understand Epidemiology (virus characteristics, disease signs, treatments, transmission) of skin and systemic viruses
Small Pox, HSV1, HSV2, Varicella-Zoster, Epstein-Barr, HPV, Measles, Mumps, and Rubella
Smallpox Characteristics
aka Variola Virus
DNA virus, eveloped
Hourglass capsid
Smallpox Tropism
Skin epithelial cells
Subcutaneous connective tissues
Smallpox Signs
Prodromal Stage: Fever, malaise
Eruptive stage: Pocks all over body
New pocks are pus filled
Healed pocks leave scars
Toxemia > Hemorrhaging
Smallpox treatment
Vaccinia virus (vaccine)
Smallpox Reservoirs / Transmission
Humans only reservoir
Inhalation of saliva droplets
Pock Crust
Fomites
Herpesvirus Characteristics
DNA, enveloped virus
All show latency and cause recurrent lytic infection
Herpesvirus Tropism
Varies between glands, lymph, and ganglia
Typees of Herpesvirus
Herpes Simplex 1 (HSV 1)
Herpes Simplex 2 (HSV 2)
Varicella-Zoster (Herpes 3) (AKA Chicken Pox)
Epstein-Barr (Herpes 4)
HSV 1 types of infection
Herpes labialis (cold sore)
Ocular Herpes
Neonatal encephalitis
HSV-1 Site of Latency
Trigeminal Ganglia
HSV-1 treatment/prevention
Acyclovir, Valacyclovir (NOT A CURE)
HSV 2
Genital Herpes
HSV-2 Transmission
Direct contact ESPECIALLY SEXUAL CONTACT
HSV 2 Types of infection
Herpes Gentalis
Neonatal ecephalitis
HSV-2 Site of latency
Sacral Ganglia
HSV2 Treatment / Prevention
Barriers (i.e., condoms)
Acyclovir, Valacyclovir (NOT A CURE)
Varicella Zoster Virus
Herpes 3 / Chicken Pox
Varcella Zoster Transmission
Direct Contact, respiratory droplets
Varicella Zoster Signs/Symptoms
Asymptomatic in respiratory tract
Incubation period 10-20 days
Rash > blisters on face and torso
Herpesvirus 4 (Epstein-Barr Virus)
Infectious mononucleosis
‘mono’
Varicella-Zoster Site of Latency
Ganglia
Varicella Zoster Treatment / Prevention
Acyclovir
Varivax Vaccine or MMR-V
Varicella Zoster primary infection
Chicken pox
Varicella Zoster recurrent infection
Shingles
Shingles signs/symptoms
Pain
Rash > blisters on face and torso
Epstein-Barr virus site of latency
B cells
Epstein-Barr primary infection
Infectious Mononucleosis
Epstein-Barr signs/symptoms
High fever
Swollen lymph nodes
Extreme Fatigue
Epstein-bar transmission
Direct contact (via saliva)
Epstein-Barr treatment
DNA Synthesis inhibiting anti-viral drugs (Acyclovir, Famcyclovir, Valacyclovir)
Explain how Acyclovir inhibits herpes replication
Acyclovir looks like a nucleotide, but another nucleotide cannot be added to it during DNA synthesis thus blocking viral DNA synthesis
Explain why Acyclovir cannot cure herpesvirus infections
Stops DNA synthesis of the virus, the virus is already present. Prevents its production. Reduces time that blisters appear
Reduces risk of transmission does NOT remove latently infected cells
Human Papillomavirus
HPV
HPV Characteristics
DNA virus
Non-enveloped
Oncogenic
100+ strains
HPV Tropism
Epithelial cells
Seed wart
Painless, elevated, rough, growth on hands and fingers
Plantar Wart
Depp, painful growth on soles of foot
Genital warts
Common STI, various morphologies (tiny and flat to cauliflower-like growth)
HPV types of Disease
Warts
Cancer
HPV treatment / prevention
Physical Removal
Cauterization
Freezing
Laser
Chemical Treatment: Gardasil, Cervarix
HPV transmission
Direct contact and fomites
List 2 strains of HPV with highest cancer risk
HPV 16 and HPV 18
Measles, Mumps, Rubella
MMR
All childhood diseases, preventable with one effective vaccine
MMR Characteristics
RNA
enveloped viruses
MMR Transmission
Via respiratory droplets
Measles aka
Rubeola
Measles caused by
Morbillivirus
Measles signs/symptoms
Systemic skin rash, oral lesions, high fever
Measles major complications
Pneumonia
Ecephalitis
Rubella aka
German measles
Rubella caused by
Rubivirus
Teratogenic
Teratogenic
Can cross the placenta
Rubella signs/symptoms
Systemic skin rash
Rubella Major complications
Miscarriage
Various birth defects
Mumps aka
Epidemic Parotitis
Mumps caused by
Orthorubulavirus
Mumps signs/symptoms
40% of cases asymptomatic
Painful swelling of salivary glands
Mumps major complications
Deafness, infertility (inflammation of gonads)
Define latency
dormant state of viral infection in which the virus remains present within host cells but does not actively replicate or produce new viral particles.
Compare and contrast Gentalis vs labialis herpes
Herpes labialis is HSV-1, coldsores, triggered by stress, spread through oral contact, treatment is majorly acyclovir
Herpes gentalis is HSV-2, genital herpes, random recurrances, spread through sexual contact specifically genital area, treatment is barriers and acyclovir
Describe differences between chicken pox vs shingles
Chicken pox is the primary infection of Varicella Zoster, demographics are majorly children, asymptomatic in respiratory tract, incubation 10-20 days,
Shingles is the recurrent infection of Varicella Zoster, demographics are majorly elderly
Same prevention, acyclovir and varivax vaccine. Both leads to rashes/blisters on face and torso
Name 1 Oncogenic DNA virus
HPV-16 leads to a lot of cancers like cervical cancers, anal cancers most prevalent in men
Name 1 teratogenic virus
Rubella aka German measles
Differentiate between measles, mumps, and rubella
All caused by different viruses
Measles - morbillivirus
Mumps - orthorubulavirus
Rubella - rubivirus
Measles can cause fevers
Mumps is most unique with swelling of salivary glands
Rubella is majorly systemic skin rashes
Measles major complications are pnuemonia and ecephalitis
Mumps major complications are deafness and infertility
Rubella major complications are miscarriage, various birth defects
Define MMR Vaccine
Primarily given during childhood to prevent Measles, Mumps, Rubella and all childhood diseases
Understand Epidemiology (disease triangle) of Enteric- and/or Neuro- tropic Infections
Hepatitis A
Hepatitis B
Hepatitis C
Norwalk virus (norovirus)
Poliovirus
Hepatitis Viruses
Very different viruses but all have liver tropism
Hep A
Hep B
Hep C
Hepatitis A characteristics
RNA, non-enveloped virus
Hepatitis A caused by
Enterovirus 72