Chapter 13: Virus and Prions Flashcards
Characteristics of viruses
-Obligate intracellular parasites that multiply in a living host
-Noncellular, filterable (can pass through bacteriological filter) agents
-Single type of nucleic acid ( (single type- some are DNA, some are RNA) surrounded by protein coat (capsid)
-Sensitive to interferons
Viral structure: virion
-ByMorphology (discovered through e- microscopy): helical viruses
-Hollow cylinder
-Coiled nucleic acid
-No envelope
-Enveloped helical virus
-Influenza virus
-Cylinder
-Morphology: polyhedral (Icosahedral) viruses
-Icosahedral capsid
-Many sided
-Morphology: complex viruses
-Bacteriophage
-Infects bacteria
-Tail fibers- adhere to receptor on bacterial cell
-Smallpox
-Contain several protein coats/capsids or undefined capsid/missing parts of capsid
Classification of viruses
-Herpesviridae (family)
-Herpesvirus
-Human herpes virus 1, HHV 2, HHV 3
-Retroviridae
-Lentivirus
-Human immunodeficiency Virus 1, HIV 2
Viral size
-Very small
-Smaller than diameter of RBC
-Seen w/ E- microscope
Growing bacteriophages
-Phages from plaques on a lawn of bacteria
-Called PFU’s- plaque forming unit
-Tryptic soy broth
-24hrs at 37 degrees celsius
-Clearings in lawn of bacterial growth
-Bacteria being lysed
Growing animal viruses
-Why are embryonated eggs used? (growing animal viruses)
-Inexpensive
-Multiple inoculation sites
-How influenza virus used to be grown for vaccine
-Cell (tissue) culture
-Animal and plant viruses may be grown in cell culture
1) a tissue is treated w/ enzymes to separate the cells
2) cells are suspended in culture medium
-Liquid nutrient
-plastic/glass dish
3) normal cells or primary cells grow in a monolayer across the plastic container.
-1 wk
Viral identification: cytopathic effect of viruses
-Visible effect or change in cells due to viral infections, that may result in host cell damage or death
-Infected cells: changes
-Cell fusion: cells moving closer together and fusion
-Nuclear changes (larger)
-Cell lysis
-Rounding up of cells
Viral identification: tests
-serology: direct or indirect (ELISA)
-DNA/RNA probes
-PCR-rapid test
-fluorescent antibody staining
Phage replication
-Lytic cycle- phage (when infecting cell) causes lysis and death of host cell
-Lysogenic cycle- Prophage DNA incorporated in host DNA (inserts it’s DNA into host’s DNA)
Multiplication of T-even bacteriophages (lytic cycle)
Chooses cycle if exposed to UV light or mutagens
1) Attachment
-DNA + sheath + tail fibers- attach to a receptor on bacterial cell wall
2) Penetration (entry)
-Phage/lysozyme- breaks down bacterial cell wall
-Sheath contracts and injects phage’s DNA into bacterial host’s cell
3) Biosynthesis
-Where replication occurs
1Production of viral parts
4) Maturation (assembly)
-Virion- Complete viral infectious particle
5) Release
-Lysozyme breaks down cell wall- lysed
-Virions free
-Can now infect other bacteria
Specialized transduction
-Contributes to some of antimicrobial drug resistance
-A special gene is being transferred from donor to host by means of a prophage
Multiplication of animal viruses
1) Attachment- viruses (may include spikes to help in adhere) attaches to cell membrane (where receptors (protein) are located)
2) Penetration (entry)- Entry by endocytosis (via a vescicle) or fusion
3) Uncoating- Enzymatic rem of capsid
-Not see w/ phages
-Unique to animal viruses
4) Biosynthesis- production of nucleic (viral) acid and proteins
5) Maturation (Assembly)- Nucleic acid and capsid proteins assemble into virion
6) Release- by budding (usually enveloped viruses) or rupture (usually naked viruses)
Viral entry (animal viruses): Penetration by fusion
enveloped viruses entering host cells by fusing their viral membrane with the host cell membrane, allowing the viral contents to enter the cell
-Envelope of viruses fuses w/ the host cell membrane
-Entrance by fusion
-After entrance, capsid is removed
Viral entry (animal virus): Penetration by endocytosis
process where the cell membrane engulfs the virus, to penetrate the cell.
-Ex. Herpes simplex virus
-Forms vesicle around virus
Animal virus: Release of enveloped virus by budding
Enveloped viruses release themselves from host cells through a process called budding, where the viral core, enriched with viral membrane proteins, buds out from the host cell membrane, acquiring a lipid envelope in the process.
-Bud becomes part of the envelope
-Ex. HIV
Bacteriophage
-Attachment: tail fibers attach to cell wall proteins
-Entry: viral DNA is injected into host cell
-Uncoating: not required
-Biosynthesis: in cytoplasm
-Chronic infection: lysogeny
-Release: Host cell is lysed
Animal viruses
-Attachment: attachment sites are plasma membrane proteins and glycoproteins
-Entry: Capsid enters by receptor-mediated endocytosis or fusion
-Uncoating: enzymatic rem of capsid proteins
-Biosynthesis: in nucleus (DNA viruses) or cytoplasm (RNA viruses
-Chronic infection: latency, slow viral infections; cancer (Ex. HPV linked to cervical or male genital cancer- due to latency)
-Release: enveloped viruses bud out; nonenveloped viruses rupture plasma membrane
Separating of viral nucleic acid from its protein coat is:
Uncoating- only occurs w/ animal virus replication
Papovaviridae
-2x stranded DNA, noneveloped viruses
-Causes warts- benign growth
-Anywhere on body
-HPC type 16 and 18 causes cancer
-Transmission: Direct contract; sexual contact; perinatal route
-Morphology: polyhedral- naked
-Latency- viruses integrate genome into host cell, dormant, then can be reactivated by stress or decrease in immune system
-Papillomavirus
-Signs and symptoms: pain, (plantars) warts
-Treatment: cryotherapy
-Genital warts
-Papillomavirus type 16 and 18
-Dx:
-physical exam- observe wart (benign wart)
-DNA probes/ molecular method
-Pap Smear
-Sample looked under microscope
-Ex. of infection- double-nucleated cells
-Treatment:
-Cryotherapy
-Podofilox (cream), Imiquimod
-Hysterectomy, Radiation (HPV 16, 18), chemotherapy
-Prevention
-Gardasil 9- HPV 6 and 11 (genital warts), HPV 16 and 18
Double stranded, enveloped viruses
SImplex virus (HHV- 1 (cold sores) and 2 (genital herpes)
Varicella(chicken pox)-zoster (Shingles) virus
Cytomegalovirus
Epstein-Barr virus
-herpesvividae
Herpesvivirdae
-DNA, enveloped
-Transmitted through infected secretion (ex. Through sexual contact)
-Hallmark characteristic of latency
-Recurrence or reactivation
-Dx: viral cell culture*- most accurate, takes weeks, antigen testing, nucleic acid amplification test (NAAT)- PCR
-cold sores, genital herpes, stromal keratitis, cancer, meningitis and encephalitis
Herpes simplex type 1: latency (cold sore)
-The initial infection occurs in 3-5 yrs children and symptoms include cold sores or fever blisters. The virus then moves up the trigeminal nerve where it remains latent in the sensor ganglia of the nerve
-Becomes latent in trigeminal nerve (along cheek)- symptoms go away
Latency
virus remains in host cell for a long period of time, away from immune system, no signs or symptoms for long period of time, not detected as foreign, then reactivated by stress or weakened immune system
Bacteria vs virus
Virus:
-Binary fission: no
-Intracellular parasite; yes
-Plasma membrane: no
-Passes through bacteriological filters: yes
-Posses both DNA and RNA: no
-ATP-generating metabolism: no
-Ribosomes: no
-Sensitive to antibiotics: no
-Sensitive to interferons: yes
-Treated w/ antivirals
Bacteria:
-Binary fission: yes
-Intracellular parasite: no
-Plasma membrane: yes
-Passes through bacteriological filters: no
-Posses both DNA and RNA: yes
-ATP-generating metabolism: yes
-Ribosomes: yes
-Sensitive to antibiotics: yes
-Sensitive to interferons: no
-Treated w/ antibiotics