Exam 3 Super Review Flashcards
- Archaea and bacteria are the only domains present
Pre-Eukaryotes. Over 2 Billion Years Ago
- Mostly anaerobes, but some microaerobes.
Pre-Eukaryotes. Over 2 Billion Years Ago
- Facultative and Aerobic cells appear
a. With (superoxide dismustase and catalase)
Pre-Eukaryotes. Over 2 Billion Years Ago
- Some oxygenic photosynthesis via Cyanobacteria
Pre-Eukaryotes. Over 2 Billion Years Ago
- 1% atmospheric oxygen can support aerobic cellular respiration
Pre-Eukaryotes. Over 2 Billion Years Ago
- Some predation
Pre-Eukaryotes. Over 2 Billion Years Ago
ii. Eukaryotic first appeared with the advent of enough (What element?) in the atmosphere to support cellular respiration and be a threat to anaerobic and microaerobic bacteria
Oxygen
iii. Eukarya believed to be resulted from
1. __________, recombination
a. NOT mutation
Symbiosis
- Anaerobic Archaea phagocytized aerobic bacteria that resembled _______
Rickettsia!
Phagocytized aerobic bacteria became ____, which provided Archaea with enzymes (catalase!) while the larger Archaea provided a safe haven + nutrients
Endosymbionts
b. After giving-up its genes to Archaea the endosymbionts became first ______ and then became the first membrane bound _____
Enslaved
Organelle
- Photosynthetic bacteria (similar to cyanobacteria) are also engulfed; they develop into _______
chloroplasts
Mitochondria function
Energy Production
Energy Producer
Outer membrane has G- like proteins
Mitochondria
Energy Producer
Inner Membrane with folds
Mitochondria
- Hold the enzymes/electron carriers for aerobic respiration
Cristae
Inner Membrane
Mitochondria
- Divide independently of cell
a. Binary fission reproduction *
Mitochondria
Eukarya organelle, but
- Contains
a. Circular DNA stored *
b. 70s Prokaryotic ribosomes (!!!) *
mitochondria
Eukarya organelle
- Function
a. Convert the energy of sunlight into chemical energy through photosynthesis
Chloroplast
- Found
a. In algae and plant cells
Chloroplast
- Consists of
a. Outer membrane which covers
b. Inner membrane, folded into sacs
c. Thylakoids, stacked into grana
Chloroplast
Primary producers of organic nutrients for other organisms
Chloroplast
How it’s derived from G- prokaryotic cells **
a. G- outer membrane proteins
b. 70s ribosomes
c. Circular DNA strand
d. Divides by binary fission
Chloroplast
a. All Eukarya are such because they have
mitochondria
i. Are mosaic of genes from both Archaea and bacteria
Eukarya
i. Protista is the kingdom that came ____ wth the Acquisition of Undulipodia
last
a. Derived from centrioles that strongly resemble Spirochetes
Undulipodia
synonymous with flagella
undulipodia
i. Member of Protista at some point phagocytized and ultimately enslaved a photosynthetic bacterium such as cyanobacteria
- origin of ____
Plants
- This photosynthetic bacteria became a
chloroplast
- Photosynthetic protisa became the subkingdom (phyla)
algae
Plants appear to have evolved from
green algae
ii. Protista that did not contain photosynthetic bacteria became the subkingdom (phyla) _____
protozoa
i. No Undulipodia
1. Fungi
a. Unicellular
i. Yeast
Animal cells?
Algae phyla are derivative of ____ kingdom
Protista
i. Photosynthetic organisms
Algae
Protista Kingdom
Eukarya
- Unicellular
- Colonial
- Filamentous
Algae
Protista Kingdom
Eukarya
iv. Contains
1. Chloroplasts with
a. Chlorophyll and other pigments
Algae
Protista Kingdom
Eukarya
- Cell wall
a. Made of cellulose
Algae
Protista Kingdom
Eukarya
- May or may not have
a. Undulipodia
Algae
Protista Kingdom
Eukarya
Has
a. Ribosomes
b. Flagellum
c. Mitochondrion
d. Nucleus
e. Nucleolus
f. Chloroplast
g. Golgi Apparatus
h. Cytoplasm
i. Cell membrane
j. Starch Vacuoles
k. Cell Wall
Algae
Protista Kingdom
Eukarya
i. May have
1. Undulipodia
ii. Do NOT have
1. Chloroplasts
2. Cell wall
Protozoa
Protista Kingdom
Eukarya
iii. Does have
1. Flagellum
2. Ribosomes
3. Mitochondrion
4. ER
5. Nucleus
6. Pellicle
7. Nucleolus
8. Cell membrane
9. Golgi Apparatus
10. Water vacuole
11. Centrioles
12. Cell membrane
13. Glycocalyx
Protozoa
Protista Kingdom
Eukarya
iv. Most have locomotor structures
1. Flagella
2. Cilia
3. Pseudopods
Protozoa
Protista Kingdom
Eukarya
v. Single celled eukarya, along with algae
Protozoa
Protista Kingdom
Eukarya
vi. Often demonstrate polymorphism (multiple life forms)
1. Trophozoite
2. Cyst
3. Other class specific
Protozoa
Protista Kingdom
Eukarya
a. Motile, feeding stage
i. Forms in response to moistures, restored nutrients
Trophozoite stage
Protozoa
Protista Kingdom
Eukarya
a. Many can enter into a dormant resting stage when conditions are unfavorable for growth and feeding
Cyst stage
Protozoa
Protista Kingdom
Eukarya
All reproduce
- Asexually
a. Mitosis
b. Or Multiple fission - Sexually
a. Conjugation
Protozoa
Protista Kingdom
Eukarya
viii. Respiration
1. Usually aerobic (cellular respiration)
2. Chemoheterotrophs
Protozoa
Protista Kingdom
Eukarya
a. Mastigophora
b. Sarcodina
c. Ciliata
d. Sporozoa
Classifications
Protozoa
Protista Kingdom
Eukarya
- Found in soil and water
2. Parasites of multicellular organisms
Classifications
Protozoa
Protista Kingdom
Eukarya
- Most are consumers and some are decomposers
4. Sporozoa cause 50% of deaths before the age of 5
Classifications
Protozoa
Protista Kingdom
Eukarya
Which has
Mitochondrion?
Protozoa or Algae?
Both
Which has
Chloroplasts
Protozoa or Algae?
Algae
Which has
Cell wall? Composition?
Protozoa or Algae?
- Algae
2. Cellulose
Protozoa responsible for Amebic Dysentery
Entamoeba Histolytica (Sarcodina) Amebic Dysentery
- 4th most common protozoan infection
Entamoeba Histolytica (Sarcodina) Amebic Dysentery
a. food and waterborne illness
b. Ingested cysts hatch into trophozoites in intestine
Entamoeba Histolytica (Sarcodina) Amebic Dysentery
c. Trophozoites produce pore toxin
i. Lyses epithelia cells of intestines
1. Causes ulceration and bloody diarrhea
2. Bloody diarrhea = dysentery
Entamoeba Histolytica (Sarcodina) Amebic Dysentery
ii. Can penetrate broken blood vessels and invade other organs
1. Lungs
2. Liver
3. Brain
iii. Cause life threatening abcesses
Entamoeba Histolytica (Sarcodina) Amebic Dysentery
- Asymptomatic in 90% of patients
5. Ameba may secrete enzymes that dissolve tissues and penetrate deeper layers of the mucosa
Entamoeba Histolytica (Sarcodina) Amebic Dysentery
- It Causes
a. Dysentery
b. Abdominal pain
c. Fever
d. Diarrhea
e. Weight loss
Entamoeba Histolytica (Sarcodina) Amebic Dysentery
- Carried by 10% of world population
8. Mortality is 100,000 per year worldwide
Entamoeba Histolytica (Sarcodina) Amebic Dysentery
- Treatment
a. Commonly Metronidazole = Flagyl
b. Works in anaerobic conditions
Entamoeba Histolytica (Sarcodina) Amebic Dysentery
Protozoa responsible for Giardiasis
i. 2 nuclei
ii. No mitochondria
iii. Adhesive discs – trophozoites
Giardia Lamblia (Mastigophora) Giardiasis
- Second to E. Coli as most common source of chronic diarrhea picked up while traveling
Giardia Lamblia (Mastigophora) Giardiasis
a. Found in 97% of surface water
Giardia Lamblia (Mastigophora) Giardiasis
i. Problem for
1. Campers
2. Hikers
3. Daycare centers
4. Among gay men
Giardia Lamblia (Mastigophora) Giardiasis
ii. Beavers, muskrats are the primary reservoirs
Giardia Lamblia (Mastigophora) Giardiasis
- Cysts are food and waterborne
Giardia Lamblia (Mastigophora) Giardiasis
a. The microbe attaches to lining of small intestine with adhesive discs
Giardia Lamblia (Mastigophora) Giardiasis
b. Incubation
i. 12-20 days
Giardia Lamblia (Mastigophora) Giardiasis
c. Heavy infestation causes inflammation that inhibits absorption of nutrients
Giardia Lamblia (Mastigophora) Giardiasis
- Diagnosis
a. Difficult
i. Organism shed in feces - intermittenly
Giardia Lamblia (Mastigophora) Giardiasis
- Symptoms include (last for 2-6 weeks)
a. Fever
b. Cramps
c. Diarrhea
d. Nausea
e. Weight loss
Giardia Lamblia (Mastigophora) Giardiasis
b. Chlorinating water
i. This does not kill cysts
Giardia Lamblia (Mastigophora) Giardiasis
- Prevention
a. Filtering water before boiling
b. Chlorinating water
c. Ozonating city water supplies
Giardia Lamblia (Mastigophora) Giardiasis
- Treatment
a. Metronidazole
Giardia Lamblia (Mastigophora) Giardiasis
Causes Cryptosporidiosis
b. Intestinal pathogen
Cryptosporidium Protozoa
Cryptosporidiosis
- Leading cause of diarrheal disease by protozoan in the world, since 1982 (beginning of AIDS epidemic)
Cryptosporidium Protozoa
Cryptosporidiosis
- Acquired via
a. Fecal-oral route from
b. Threatens our water supply
Cryptosporidium Protozoa
Cryptosporidiosis
a. Fecal-oral route from
i. Kittens
ii. Puppies
iii. Livestock
iv. Deer
v. Person to person
1. Daycare centers
2. Hospitals
vi. Ponds
vii. Lakes
Cryptosporidium Protozoa
Cryptosporidiosis
a. =Discovered after 1970
=Emerging Disease
Cryptosporidium Protozoa
Cryptosporidiosis
b. 1993 – Milwaukee, WI
i. 370,000 cases due to
1. Contaminated water
2. Filtration required for removal
a. Chlorination will not work
Cryptosporidium Protozoa
Cryptosporidiosis
a. Ingestion of oocysts gives rise to
i. Sporozoites that
1. Penetrate intestinal epithelial cells
a. Give rise to merozoites
i. Which re-infect the epithelial of intestinal lining, develop oocysts that are excretted
Stages in Development
Cryptosporidium Protozoa
Cryptosporidiosis
b. Within 12-14 hours
i. Gastroenteritis
ii. Headache
iii. Sweating
iv. Vomiting
v. Abdominal cramps
vi. Extremely watery Diarrhea
Cryptosporidium Protozoa
Cryptosporidiosis
c. May persist for weeks
d. AIDs patients may suffere chronic persistent diarrhea
Cryptosporidium Protozoa
Cryptosporidiosis
- Treatment
a. No effective drugs
Cryptosporidium Protozoa
Cryptosporidiosis
- Self limiting in uncompromised victims
- Opportunistic in immunocompromised victims and may persist indefinitely
a. AIDS patients
b. The young
Cryptosporidium Protozoa
Cryptosporidiosis
a. 1 of top 3 killers in world
b. 300-500 million new cases in world each year
Plasmodium
Malaria
c. 40% of the world population
d. Mortality
i. 1-2 million deaths, primarily children
Plasmodium
Malaria
a. Reemerging disease caused by several species of _________
Plasmodium
Malaria
Re Emerging
i. First emerged about 40,000 years ago
Plasmodium
Malaria
_________ causes 95% of malarial deaths
i. Children and fetuses deprived of O2 from infected mother
Plasmodium Falciparum
Malaria
c. Obligate intracellular sporozoan
Plasmodium
Malaria
i. P. malariae
ii. P. vivax
iii. P. falciparum
iv. P. ovale
Plasmodium
Malaria
- Historicially most common and widespread
- Can emerge from liver in stages causing relapses (1-30 years)
- 95% of Africans have mutation (Duffy negative)
a. Blocks merozoites from infecting RBC’s
ii. P. vivax
Plasmodium
Malaria
- Not as widespread
- More deadly
- No relapses
- All merozoites emerge from liver at same time
- Sickle cell heterozygous people protected
- 80-90% of infections in Africa
- 90% of deaths
- HIV infection increases malarial deaths
P. Falciparum
Plasmodium
Malaria
a. Female Anopheles mosquito
b. Blood transfusions
c. Mother to fetus
Vectors
Plasmodium
Malaria
- Life Cycle
a. Asexual Phase – Human host
b. Sexual phase – mosquito host
Plasmodium
Malaria
i. Infected mosquito injects asexual sporozoite
Asexual Phase
Plasmodium
Malaria
- Localizes in liver
Asexual Phase
Plasmodium
Malaria
- Undergoes division generating numerous merozoites, which enter circulation in 5-16 days depending on species
Asexual Phase
Plasmodium
Malaria
a. Invade red blood cells, convert to trophozoites, and multiply
Asexual Phase
Plasmodium
Malaria
b. 48 hour cycle burst, release more merozoites, eventually differentiate into gametes. (3-5 years later)
Asexual Phase
Plasmodium
Malaria
i. Mosquito draws infected RBC’s when nomming on blood
Sexual Phase
Plasmodium
Malaria
ii. Gametes fertilize, form diploid cell
Sexual Phase
Plasmodium
Malaria
iii. Forms sporozoites in stomach of mosquito
Sexual Phase
Plasmodium
Malaria
iv. Sporozoites lodge in salivary glands
1. Available to infect the human host
Sexual Phase
Plasmodium
Malaria
- Symptoms
a. Episodes of chills-fever-sweating
b. Anemia
c. Liver and spleen enlargement and brain damage
i. Due to clots and hypoxia
d. Occur at 48-72 hour intervals as RBC’s rupture
e. Interval depends on species
Plasmodium
Malaria
- Diagnosis
a. Presence of trophozoite in RBC’s, symptoms
Plasmodium
Malaria
- Increasing drug resistance
Plasmodium
Malaria
- Therapy
a. Fansidar cocktail with Chloroquine
b. Hospitalization for 5 days with quinine
c. Mefloquine
d. ACT Artemisinin Combination Therapy
e. Nothing
i. Rely on continuous infection and immune response
Plasmodium
Malaria
- Prevention
a. Destroy mostquito
i. Breeding grounds
b. Vaccine
i. Goal: eliminate mortality; not necessarily infection
c. Insectiside treated nets
d. Fansidar
i. For pregnant women
Plasmodium
Malaria
i. No undulipodia – “True Fungi”
Fungi
General Characteristics
ii. Terrestrial, but require moisture
Fungi
General Characteristics
iii. Develop from spores
Fungi
General Characteristics
iv. Eukaryotes with rigid cell wall consisting mostly of chitin
Fungi
General Characteristics
- Unicellular
a. Yeast - Multicellular - hyphae
a. Molds
Fungi
General Characteristics
vi. Decomposers
1. Chemoheterotrophs
Fungi
General Characteristics
a. Acquires nutrients via
i. Diffusion after exoenzymes break down their food source
Fungi
General Characteristics
- Sometimes parasites
a. Never obligate
Fungi
General Characteristics
multicellular forms can change to unicellular forms in the host body; yeast may change to the hypha form
Dimorphic
Fungi
General Characteristics
viii. Are the single most important cause of disease in plants
Fungi
General Characteristics
Does it have undulipodia? (Fungi)
NO
Do Fungi have cell wall? made of?
YES.
CHITIN.
i. Soft, uniform texture and appearance
ii. Single celled fungi
Yeast Phyla
Fungi Kingdom
iii. Grow in colonies
iv. Produce exoenzymes
Yeast Phyla
Fungi Kingdom
v. Can form biofilms
Yeast Phyla
Fungi Kingdom
vi. Contain
1. Plasmids
Yeast Phyla
Fungi Kingdom
- Best understood eukarya
a. 1st mapped genome
b. Stripped down version of human cell
Yeast Phyla
Fungi Kingdom
vii. Reproduce
1. Asexually
a. Via mitosis
b. Generate BUDS
2. Sexually
a. Via Ascospores + Basidiospores
Yeast Phyla
Fungi Kingdom
- The ability to ferment and generate
a. Beer
b. Wine
c. Vinegar
d. Ethyl alcohol
Yeast Phyla
Fungi Kingdom
- Use of their plasmids for genetic engineering
a. Advantage
i. Don’t produce toxins
Yeast Phyla
Fungi Kingdom
i. Consist of hyphae forming a mycelium (mat)
ii. Form the thallus (body) of the mold
Mold Phyla
Fungi Kingdom
- Production of
a. Commercial acids
b. Enzymes
c. Antibiotics
Mold Phyla
Fungi Kingdom
disease caused by a fungi
=mycoses
Mold Phyla
Fungi Kingdom
b. Many begin as lung infections
i. Result from inhaling spores
ii. Wind makes the spores airborne where they can
Mycoses
Mold Phyla
Fungi Kingdom
c. Often result in TB – symptoms
i. Cough
1. Droplets
ii. Aches
iii. Fevers
Mycoses
Mold Phyla
Fungi Kingdom
d. Treatment
i. Amphotericin B
Mycoses
Mold Phyla
Fungi Kingdom
iv. Usually self limiting if person has normal immune system
v. FRUITING BODIES
Mold Phyla
Fungi Kingdom
Which:
is unicellular
Yeast or Molds?
both
Which:
multicellular
Yeast or Molds?
molds
Which:
has plasmids?
Yeast or Molds?
yeasts
Which:
made of hypha
Yeast or Molds?
molds
Which:
generate fruiting bodies?
Yeast or Molds?
molds
Yeast that causes Candidiasis
Candida Albicans
Candidiasis
a. Normally found in intestinal tract
i. Causes opportunistic infections of
1. Skin
2. Mouth
3. Vagina
Candida Albicans
Candidiasis
- Accounts for 70% of nosocomial fungal infections
a. Mycoses
Candida Albicans
Candidiasis
- Opportunistic
a. For immunocompromised individuals
Candida Albicans
Candidiasis
- Risk Factors
a. Taking antibitoics
b. High Blood Sugar
Candida Albicans
Candidiasis
- Virulence Factors
a. Adhesins
b. Can convert to the hyphal form in the human body
i. Stimulates production of blood blots
c. Secretion of proteases and phospholipases
Candida Albicans
Candidiasis
- Thrush
a. Thick
b. White
c. Adherent growth on mucous membranes of mouth and throat
Candida Albicans
Candidiasis
- Vulvovaginal yeast infection
a. Painful
b. Inflammatory condition that causes ulceration and discharge
Candida Albicans
Candidiasis
- Cutaneous candidiasis
a. Occurs in chronically moist areas of skin and in burn patients
Candida Albicans
Candidiasis
- Treatment
a. Amphotericin B
Candida Albicans
Candidiasis
Dermatophyte
Tinea
Ringworm
- =tinea capitis, affects calp and hair-bearing region of head
- Hair may be lost
of Scalp
Ringworm
- =tinea barbae
- Affects the chin and beard of adult males
- Contracted mainly from animals
of Beard
Ringworm
- =Tinea corporis
2. Occurs as inflamed, red ring lesions anywhere on smooth skin.
of Body
Ringworm
a. Discovered in 1898
Viruses
Hypothesized Source
b. Most Abundant Agent on earth
i. A billion billion trillion (10^30)
ii. Attacks ALL cells
Viruses
Hypothesized Source
c. Non-Cellular
i. Not alive
ii. Can’t actively maintain themselves
iii. No cell membrane
iv. No organelles
Viruses
Hypothesized Source
v. Do
1. Have a genome
2. Evolve/adapt faster than anything else on the planet
Viruses
Hypothesized Source
d. Suspected to be
i. Genes that got “loose”
ii. Transposons?
iii. 90% of genes don’t match genes from any modern source
Viruses
Hypothesized Source
e. Genome
i. Either DNA or RNA
1. Vast majority are RNA
Viruses
Hypothesized Source
a. Genome
i. Have genes that code for protein but
1. No Transcription
2. No Ribosomes
a. No Translation
3. The host cell MUST express any viral genes
Viruses
Hypothesized Source
Always intracellular parasites
Viruses
Hypothesized Source
i. Bear no resemblance to cells
1. Lack protein-synthesizing machinery
Virus Structure
ii. Contain only the parts needed to
1. Invade a cell
2. Control a host cell
Virus Structure
- Nucleic acid molecules (either D or R, not both)
- Matrix Proteins enzymes
a. optional
Central core
Virus Structure
i. Usually double stranded (ds) but may be single stranded (ss)
ii. Ds usually attack
1. Animal cells
DNA core
Virus Structure
i. Usually ss, but may be ds
ii. Ss small, usually attack
1. Animal or
2. Plant cells
RNA core
Virus Structure
viruses that attack bacteria
=bacteriophage
Virus Structure
b. provides
i. protection for the core
ii. way to transmit viral core to host cell
Capsid
Coverings
Virus Structure
c. All viruses have these
Capsid
Coverings
Virus Structure
d. =protein coats that enclose and protect their nucleic acid
Capsid
Coverings
Virus Structure
ia. Closed shell
ib. Helical
ii. Complex
Capsid
Coverings
Virus Structure
- Capsomeres arranged into shapes
2. EX: isometric, cubc, polyhedral, icosahedra (20 sided)
Closed shell Capsid
Coverings
Virus Structure
- Continuous helix of capsomers
- Forming a cylinder
- Has two “lids” open to the world.
Helical Capsid
Coverings
Virus Structure
- Combination of helical + closed shell arrangements, heads and/or tails
- Have polyhedral capsid
a. +helical tail
b. +attachment fibers
c. Ex: bacteriophage - Atypical
Complex Capsid
Coverings
Virus Structure
g. May have ____ to assist in attaching and penetration of a cell.
i. Assist in adsorption + penetration of host cell
Spikes
Coverings
Virus Structure
Optional
a. Mostly animal viruses
Envelope
Coverings
Virus Structure
b. Derived from
i. Cell membrane
ii. When virus leaves the host cell
Envelope
Coverings
Virus Structure
c. Helps
i. Escape host cell
ii. Penetrate a new cell
Envelope
Coverings
Virus Structure
d. Spikes
i. Exposed glycoproteins on the outside of envelope
1. Essential for attachment of virus to the host cell
Envelope
Coverings
Virus Structure
i. H
1. Associated with flu viruses
a. 16 different types
2. Facilitate attachment of the viruses to host cell
a. Binds to sialic acid in host cell membrane
=hemagglutinin spikes
Envelope
Coverings
Virus Structure
i. N
1. these spikes Disrupts sialic acid of the host cell membrane and facilitates the flu virus ESCAPE from the host cell
2. Cuts bud free to escape from the host cell
=Neuraminidase spikes
Envelope
Coverings
Virus Structure
i. Neuraminidase INHIBITOR that is used to treat people with the flu
TamifFlu
Envelope
Coverings
Virus Structure
- Spikes to bind to receptors on APC’s (HIV)
a. CCR5 receptors on macrophages
b. CD4 receptors on T Cells
Gp120 spikes
Envelope
Coverings
Virus Structure
e. Bilayered membrane composed of
i. Phospholipid
ii. Protein
iii. Carbohydrate
Envelope
Coverings
Virus Structure
without envelope
Naked
Envelope
Coverings
Virus Structure
i. Represents the different kinds of organisms a virus can infect
Range
i. Refers to what kinds of cells a virus can infect
Specificity
- Determined by whether or not virus can attach to a cell
a. Whether it can be replicated by cell
b. Whether it can escape from the host cell - Some limited to infecting one kind of host cell, while others can infect many types of cells.
a. Ex: Poliovirus infects intestinal AND nerve cells
b. Ex: Hepatitis B infects liver cells
Specificity
i. =the viruses binds to the receptors on the surface of the host cell using spikes or receptors on its capsid and/or envelope
a. Adsorption
i. =the virus or just the viral genome enters the host cell
Penetration
- Bacteriophage
a. Will release lysozyme
i. Weakens the bacterial cell wall
ii. Then injects genome through the wall
Penetration
- Virus attacking plant cell
a. Will enter only if there has been mechanical damage to the plant
Penetration
i. Once inside host cell
ii. = uncoating the virus may occur
iii. Capsid will be digested to release the core
iv. Frees the viral genome
Uncoating
i. = viral parts (genomes and capsids) are produced
Including
- Capsomeres
- Enzymes
- spikes
Synthesis
- Destroy, inhibit, or lysogenize the host DNA
2. Use own DNA as template used to transcribe viral mRNA
DNA Virus
Synthesis
- Use the host’s tRNA + ribosomes to translate viral mRNA into viral proteins
- Use their DNA as template for generating more viral cores
DNA Virus
Synthesis
i. Nucleoside mimic of Guanine
ii. DNA Polymerase of host cell is competitively inhibited by drugs
Acyclovir
DNA Virus
Synthesis
- When it’s added to growing chain of DNA nucleotides
a. No attachment point for next nucleotide
b. Viral DNA replication is terminated
Acyclovir
DNA Virus
Synthesis
iii. Selective because enzyme needed to convert it to a single phosphate nucleotide is only found in infected cells.
Acyclovir
DNA Virus
Synthesis
iv. Selectively attacks herpes virus
1. Particularly genital
Acyclovir
DNA Virus
Synthesis
v. Beneficial against chickenpox and shingles
Acyclovir
DNA Virus
Synthesis
a. Viral DNA
b. Viral mRNA
i. Viral Proteins
c. Transcription
i. Via RNA Polymerase
d. Maturation
e. Replicated viral DNA can be lysogenized into host DNA
DNA Virus
Synthesis
- Use their genome directly as mRNA that is transcribed by host ribosomes into viral protein
RNA Virus
Synthesis
- Use their genome as a template for generating more viral cores
RNA Virus
Synthesis
a. Nucleoside mimic
i. A or G
b. Used to treat RNA viral infections
i. Hepatitis C
Ribarvirin
RNA Virus
Synthesis
- Viral RNA polymerase replicates RNA
a. Poor proofreading
b. More mistakes and more mutations
RNA Virus
Synthesis
- Makes (-) strand first which is used as a template to make the new (+) strands
RNA Virus
Synthesis
- Translation of ssRNA makes proteins
a. Includes viral RNA Polymerase
RNA Virus
Synthesis
- Use reverse transcriptase to transcribe their ssRNA into a ssDNA
a. The worst proofreading
Retrovirus
Synthesis
- ssDNA then coped to create dsDNA
3. DNA enteres nucleus to be transcribed, or
Retrovirus
Synthesis
- The viral DNA then uses integrase to lysogenize the host DNA
- Viral DNA transcribed into viral mRNA host ribosome
a. Ex: HIV
i. 2 single strands that are identical
Retrovirus
Synthesis
- Have ssRRNA
7. Viral protein generated
Retrovirus
Synthesis
- Viral protease cuts viral proteins to the correct length
9. Viral DNA used as template for generating core
Retrovirus
Synthesis
a. =azidothymidine
AZT
Retrovirus
Synthesis
b. Competitively inhibits reverse transcriptaste in retroviruses
i. Ex: HIV
AZT
Retrovirus
Synthesis
c. Is nucleoside mimic of Thymine
d. Terminates DNA elongation like Acyclovir
AZT
Retrovirus
Synthesis
e. Can penetrate Blood Brain Barrier
AZT
Retrovirus
Synthesis
f. Also has affinity for DNA Polymerase
i. Adversely affects host cell replication
ii. Ex: formation of Red blood cells
AZT
Retrovirus
Synthesis
i. Virus components (capside/core etc.) are assembled into viruses
Assembly/Maturation
i. Refers to the escape of virus from the host cell
1. Lysis (the host cell dies)
2. Enveloped Virus
Release
a. Animal cells filled with viruses lose the integrity of their cell membrane
b. Bacteriophages
i. Have holing to pierce the cell membrane and
ii. endolysin to digest peptidoglycan
Lysis
Release
a. Exit via budding
i. Acquire envelope as they emerge
ii. Exocytosis
1. Nucleocapsid binds to membrane which pinches off and sheds the viruses gradually;
iii. Cell is not immediately destroyed
Enveloped Virus
Release
- Used to stop the release of flu viruses
- Block their neuraminidase spikes
- Ex
a. Tamiflu
b. Relenza
ii. Neuraminidasae Inhibitors
Release
- Synthesis of DNA from RNA
2. AIDS virus
i. Reverse transcriptase
- Lysogenizes the viral DNA into host DNA
ii. Integrase
- To cut viral proteins
Protease
- Digests peptidoglycan of cell wall
Lysozyme
- Transcribes DNA to mRNA
RNA Pol
Transcribes DNA from DNA
DNA Pol
you can damage the
1. Envelope with
a. Anything that disrupts cell membranes
you can damage the
2. Capsid with
a. Anything that denatures proteins
you can damage the
3. Core with
a. Anything that damages nucleic acids
b. Radiation
you can damage the
4. Replication process with
selective antiviral drugs
i. Nucleoside mimic of Guanine
Acyclovir
ii. DNA Polymerase of host cell is competitively inhibited by drugs
1. When it’s added to growing chain of DNA nucleotides
a. No attachment point for next nucleotide
b. Viral DNA replication is terminated
Acyclovir
iii. Selective because enzyme needed to convert it to a single phosphate nucleotide is only found in infected cells.
Acyclovir
iv. Selectively attacks herpes virus
1. Particularly genital
Acyclovir
v. Beneficial against chickenpox and shingles
Acyclovir
i. =azidothymidine
AZT
ii. Competitively inhibits reverse transcriptaste in retroviruses
1. Ex: HIV
AZT
iii. Is nucleoside mimic of Thymine
AZT
iv. Terminates DNA elongation like Acyclovir
AZT
v. Can penetrate Blood Brain Barrier
AZT
vi. Also has affinity for DNA Polymerase
1. Adversely affects host cell replication
2. Ex: formation of Red blood cells
AZT
i. TAMIFLU
1. Neuraminidase INHIBITOR that is used to treat people with the flu
ii. Keeps the virus from budding out of already infected host cell
i. TAMIFLU
1. Neuraminidase INHIBITOR that is used to treat people with the flu
ii. Keeps the virus from budding out of already infected host cell
i. Inhibit viral enzymes in HIV: reverse transcriptase (AZT), protease, integrase (Raltegravir)
e. Raltegravir
i. Nucleoside mimic
1. A or G
ii. Used to treat RNA viral infections
1. Hepatitis C
f. Ribavirin
i. Blocks viral uncoating
g. Amantadine
i. Used to stop the release of flu viruses
ii. Block their neuraminidase spikes
iii. Ex
1. Tamiflu
2. Relenza
h. Neuraminidasae Inhibitors
i. Generate so many viruses that the hot cell bursts
ii. Spread rapidly to new host cells
iii. Treatment must start early to interrupt a step in the replication cycle
Lytic
iv. Examples
1. Cold
2. Polio
Lytic
i. Involves a virus that isn’t replicating; follows a lytic cycle, where virus enters dormant phase
ii. Often involves lysogeny
Latent
- =A stable long term relationship between a host cell and virus
- The DNA of the virus is incorporated into the host DNA and replicates at the same rate
a. Inactive viral DNA = prophage
Lysogeny
Latent
iii. Virus not initially replicated instead inactive viral DNA (prophage) incorporated into host DNA and copied.
iv. If something interferes with host DNA replication a lytic infection may develop.
Latent
i. Releases new viruses gradually
ii. May continue for months or years or a lifetime without causing overt disease
iii. The virus can’t be attacked unless it begins a lytic cycle
iv. A sort of “carrier state” where new viruses are released gradually.
v. Can continue for months or years without causing overt disease.
Persistent
vi. Examples
1. Hepatitis B
2. Measles
Persistent
i. Virus periodically reactivates
ii. Examples
1. Herpes viruses
Chronic Latent
i. Virus is detectable in tissue samples
ii. Multiplying at a slow rate
iii. Symptoms mild or absent
Chronic
i. Direct contact via
1. Skin
2. Mucous membranes
ii. Lysogenize host cell
IMportant DNA VIruses
iii. Chronic Latent Infections
1. Infections become more severe with age or conditions that compromise immune system, i.e. AIDS
Chronic latent
- Include
a. Herpes Virus
b. Papillomavirus
c. Hepatitis B
Chronic latent
A stable long term relationship between a host cell and virus
Lysogeny
ii. The DNA of the virus is incorporated into the host DNA and replicates at the same rate
1. Inactive viral DNA = prophage
iii. Occurs most frequently when a host cell is infected with more than one virus
Lysogeny
Lysogeny - who does it?
i. DNA and Retroviruses
- Cell/tissue cultures
- Bird embryos
- Live animal inoculation
Ways to Cultivate Animal Viruses
i. Large Family, 8 infect humans
Herpesvirus
ii. Enter the host cell via pinocytosis and fusion of the envelope with the cell membrane and nuclear membrane
Herpesvirus
iii. Can remain latent (usually in neurons) and then reappear
Herpesvirus
- Usually lesions on the oropharynx, cold sores, fever blisters
a. Occurs in early childhood
Herpes Simplex Virus 1 - HSV-1
Herpesvirus
– lesions on the genitalia, possibly oral
- Occurs in age 14-29
- Can be spread without visible lesions
Herpes Simplex Virus 2 - HSV-2
Herpesvirus
- Direct exposure to secretions containing the virus
2. Active lesions most significant source
Transmission
Herpesvirus
- Genital herpes can be transmitted in the absence of lesions
- HSV multiplies in sensory neurons, moves to ganglia
a. HSV 1 enters 5th cranial nerve
b. HSV 2 enters lumbosacral spinal nerve trunk ganglia
Transmission
Herpesvirus
- Recurrent infection is triggered by various stimuli
a. Fever
b. UV radiation
c. Stress
d. Mechanical injury
Epidemiology
Herpesvirus
- Newly formed viruses migrate to body surface
a. Producing local skin/membrane lesion
Epidemiology
Herpesvirus
- Symptoms
a. Blisters
b. Itching
c. Tingling
d. Outbreaks decrease in number and severity as time goes on.
Epidemiology
Herpesvirus
- Acyclovir used to inhibit viral replication
Epidemiology
Herpesvirus
i. Caused by Varicella-Zoster Virus (VZV)
Varicella-Zoster Virus (VZV)
Chickenpox/Shingles
ii. Range – humans the only natural host
Varicella-Zoster Virus (VZV)
Chickenpox/Shingles
iii. Transmitted by
1. Respiratory droplets and contact
Varicella-Zoster Virus (VZV)
Chickenpox/Shingles
iv. Primary Infection – chickpox
1. Characteristic vesciles
Varicella-Zoster Virus (VZV)
Chickenpox/Shingles
v. Specificity
1. Virus enters neurons and remains latent
Varicella-Zoster Virus (VZV)
Chickenpox/Shingles
vi. 20% reactivates later to become shingles
1. With vesicles localized to distinctive areas on the dermatomes
Varicella-Zoster Virus (VZV)
Chickenpox/Shingles
More common in older patients
Varicella-Zoster Virus (VZV)
Chickenpox/Shingles
vii. Treatment
1. Treat symptoms in uncomplicated infections
2. Acyclovir
Varicella-Zoster Virus (VZV)
Chickenpox/Shingles
i. Vaccine
ii. Live attenuated vaccine for chickenpox and shingles
1. 80-85%
Varicella-Zoster Virus (VZV)
Chickenpox/Shingles
Caused by Epstein-Barr Virus
Epstein-Barr Virus (EPV
Mononucleosis
ii. Ubiquitous virus; lysogenizes B lymphocytes
Epstein-Barr Virus (EPV
Mononucleosis
iii. Transmission
1. Direct, oral contact +
2. Contamination with saliva
Epstein-Barr Virus (EPV
Mononucleosis
iv. In industrialized countries, college-age population is vulnerable to infectious mononucleosis
1. “mono” or kissing disease
Epstein-Barr Virus (EPV
Mononucleosis
v. By mid-life, 90-95% of all people are infected
Epstein-Barr Virus (EPV
Mononucleosis
vi. Anyone with an immune deficiency is highly susceptible to
Epstein-Barr Virus (EPV
Mononucleosis
vii. Is a direct contact disease transmitted by saliva via the respiratory tract (airborne droplets) and via fomites)
Epstein-Barr Virus (EPV
Mononucleosis
- Sore throat
- High fever
- Swollen lymph nodes
- (what we think of when people get the disease)
- Headache
- Weakness
- Develop after 3-50 day incubation
Infectious Mononucleosis
Epstein-Barr Virus (EPV
Mononucleosis
ix. Dormancy in B cells
x. Reactivated
xi. May be asymptomatic
Epstein-Barr Virus (EPV
Mononucleosis
i. 200 serotypes with 15 high risk for cancer; 2 account for 70% of metastatic tumors
1. E.g. cervical
Human Papillomavirus
ii. Infects epithelial cells of the skin and mucous membranes
Human Papillomavirus
- Oropharynx
a. 60% head and neck cancers due to
Human Papillomavirus
- Esophagus
Human Papillomavirus
- Genitals
a. Carcinoma 9 Cervical cancer
b. Warts
i. Spread via Sloughing
Human Papillomavirus
- Virus inactivates tumor repressor gene p53
Human Papillomavirus
iii. Transmissible through d
1. Direct contact OR
2. Contaminated fomites
Human Papillomavirus
iv. Incubation
1. 2 weeks to more than a year
Human Papillomavirus
v. Warts can recur
Human Papillomavirus
vi. Early Detection
1. Pap Smears
Human Papillomavirus
vii. Two effective vaccines
1. Gardasil
a. - HPV protein genetically engineered in a yeast
b. -Assembled into a capsid without a core
c. -Contains 2 viruses responsible for most cases of cervical cancer (#16 and #18) and 2 viruses that cause genital warts
d. -3 doses over 6 months (95% efficacy)
e. -Currently given to females 11-26
f. -Approved for boys 9-26 in 2009
g. -Currently mandated in 24 states
h. -Pap smears still required
Human Papillomavirus
i. = inflammatory disease of liver cells that may result from several viruses
Hepatitis
ii. Interferes with liver’s excretion of bile pigments,
Hepatitis
iii. bilirubin accumulates in blood and tissues
1. causing jaundice,
a. = a yellow tinge in skin and eyes
Hepatitis
- DNA Virus
Hepatitis B
- =serum hepatitis
3. Caused by Hepatitis B virus
Hepatitis B
- Virus enters through break in
a. skin or
b. mucous membrane
c. or by injection into bloodstream
i. contaminated needles, transfusions, sexually
Hepatitis B
- Reaches liver cells,
- multiplies,
- and releases viruses into blood;
Hepatitis B
- and releases viruses into blood;
a. average 7 week incubation
b. Most exhibit few overt symptoms and eventually develop HBV immunity
Hepatitis B
- Some experience
a. malaise,
b. fever,
c. chills,
d. anorexia,
e. abdominal discomfort,
f. and diarrhea
Hepatitis B
- Fever, jaundice, rash, and arthritis in more severe disease cases
Hepatitis B
- Small number of patients develop chronic liver disease –
a. Necrosis and cirrhosis
Hepatitis B
- 300 mil carriers
Hepatitis B
- 6 mo incubation period with about 90% recovery
Hepatitis B
- Vaccine now available
14. Gamma globulins given as prevention and treatment
Hepatitis B
These types of hepatitis are both RNA viruses
-i.e. do NOT lysogenize
Hep A and C
from i. Rhabdovirus
Rhabdovirus
Rabies
ii. Slow, progressive
iii. zoonotic
1. (transmitted from animals) disease
Rhabdovirus
Rabies
iv. Primary reservoirs are
1. wild mammals
Rhabdovirus
Rabies
v. it can be spread by
1. both wild and domestic mammals by
a. bites,
b. scratches,
c. and inhalation of
i. droplets,
ii. transplants
d. skunk/foxes/coyotes/raccoons
e. Washington bats
f. Worldwide dogs are the most important vector
Rhabdovirus
Rabies
vi. Deaths
1. 55,000 to 70,000 per year
2. Cardiac arrest or respiratory collapse
Rhabdovirus
Rabies
viii. Incubation period
1. 5 weeks to 6 mos
Rhabdovirus
Rabies
viii. Specificity
1. Sensory and motor neurons
Rhabdovirus
Rabies
ix. Signs and Symptoms
1. Paralysis
2. Numbing
3. Aggression
Rhabdovirus
Rabies
x. Often diagnosed at autopsy
xi. Can’t be treated after nervous system symptoms develop
Rhabdovirus
Rabies
xii. Treatment – passive and active postexposure immunization
Rhabdovirus
Rabies
- Infuse the wound with human rabies antibodies;
vaccination with human diploid cell vaccine (HDCV), an inactivated vaccine given in 6 doses with 2 boosters
Rhabdovirus
Rabies
- 100% efficacy in rabies prevention unless person is immunocompromised or doesn’t follow protocol.
Rhabdovirus
Rabies
- Transplants
a. Cornea
b. Heart
c. Liver
d. kidneys
Rhabdovirus
Rabies
poliomyelitis (polio), caused by Picornavirus
Polio
poliomyelitis/Picornavirus
- acute enteroviral infection of the spinal cord that can cause neuromuscular paralysis
Polio
poliomyelitis/Picornavirus
naked capsid;
2. resistant to acid, bile, and detergents; can survive stomach acids when ingested
Poliovirus
poliomyelitis/Picornavirus
iii. Worldwide vaccination programs have reduced the number of cases; eradication is expected
Polio
poliomyelitis/Picornavirus
a. Dead virus
b. Multiple doses needed
c. Life long immunity
Salk vaccine
Polio
poliomyelitis/Picornavirus
a. Live attenuated
b. Causes polio in 10-15 people/year
i. Mutation in virus
ii. Immune deficiency in recipient
Sabin vaccine
Polio
poliomyelitis/Picornavirus
- Transmitted by
a. fecal-oral route
Polio
poliomyelitis/Picornavirus
a. adhere to receptors of mucosal cells in oropharynx and intestine,
b. multiply in number and
c. shed in throat and feces,
d. some leak into blood
Polioviruses
poliomyelitis/Picornavirus
- Most infections are short-term, mild viremia
Polio
poliomyelitis/Picornavirus
- Some develop mild nonspecific symptoms of
a. fever,
b. headache,
c. nausea,
d. sore throat,
e. and myalgia
Polio
poliomyelitis/Picornavirus
- If viremia persists,
a. virus spreads to
i. spinal cord
ii. and brain
Polio
poliomyelitis/Picornavirus
- If nervous tissue is infected but not destroyed –
a. muscle pain and spasm,
b. meningeal inflammation, and
c. vague hypersensitivity
Polio
poliomyelitis/Picornavirus
- Invasion of motor neurons causes
a. flaccid paralysis
Polio
poliomyelitis/Picornavirus
Decades later
a. – progressive muscle deterioration;
b. occurs in 25-50% of patients infected with polioviruses in childhood
Post Polio Syndrome (PPS)
Polio
poliomyelitis/Picornavirus
- Treatment is largely supportive for pain and suffering; respiratory failure may require artificial ventilation; physical therapy may be needed
Treatment
Polio
poliomyelitis/Picornavirus
- Prevention is vaccination:
a. Inactivated polio vaccine (IPV) Salk vaccine
i. -available 1955
ii. -multiple doses required
Polio
poliomyelitis/Picornavirus
- Oral polio vaccine (OPV) Sabin vaccine, attenuated virus – no longer recommended in the U.S.
a. -easier to administer
b. -causes polio in 10-15 people per year
Polio
poliomyelitis/Picornavirus
- -2011 Endemic in Nigeria, Pakistan and Afghanistan
- No new cases in India for 9+ months
- Epidemic in 17 countries
Polio
poliomyelitis/Picornavirus
- Conflicts/war
- Remote locations
- Unwilling to accept vaccines from outsiders due to mistaken beliefs (infertility, illness (HIV))
- Money (Gates foundation has given $65 million to eradicate polio)
Eradication Issues
Polio
poliomyelitis/Picornavirus
a. AIDS pandemic
i. Recognized in 1981
HIV/AIDS
i. Incidence
1. 5 million worldwide
2. 40,000 in US
HIV/AIDS
ii. Prevalence
1. Up to 37 million worldwide
2. Up to 1 million + in the US
HIV/AIDS
- UP to 3 million/yr
2. US 20,000 per year
HIV/AIDS
i. Is a retrovirus
Human Immunodeficiency Virus (HIV)
- Has a core consisting of 2 identical strands of positive sense (+) RNA
Human Immunodeficiency Virus (HIV)
- Carries HIV specific enzymes made by its previous host
a. Reverse transcriptase
b. Integrase
c. Protease
Human Immunodeficiency Virus (HIV)
i. Enzymes that transcribes viral RNA into viral DNA
a. Reverse transcriptase
Human Immunodeficiency Virus (HIV)
i. Enzymes that inserts the viral DNA into the host genome
ii. Lysogenize
b. Integrase
Human Immunodeficiency Virus (HIV)
i. The enzyme that cuts newly generated viral proteins to the correct length
c. Protease
Human Immunodeficiency Virus (HIV)
ii. Range: Humans
Human Immunodeficiency Virus (HIV)
- Facilitated by an extremely long incubation period
- Is primarily direct contact via heterosexual sex
a. Semen
b. Vaginal secretions a
c. And/or blood
Human Immunodeficiency Virus (HIV)
- Easier for man to give it to woman than for woman to receive from man
- Frequently via inoculation with contaminated needles
a. 1/3 of all US AIDS cases
Human Immunodeficiency Virus (HIV)
- Occurs across the placenta via mother’s milk
- Loss of its ability to infect occurs
a. When HIV envelope exposed to air
i. Dries
b. UV light
c. Heat or bleach
d. Loss of gp120 spikes
Human Immunodeficiency Virus (HIV)
- Healthcare workers take precautions
a. Double glove, etc.
b. When handling any and all body fluids as all body fluids are ultimately derived from blood
Human Immunodeficiency Virus (HIV)
i. Initially attaches to macrophages
ii. Dendritic cells &
iii. Monocytes
Adsorption
Replication
Human Immunodeficiency Virus (HIV)
iv. HIV adsorbs via its gp120 spikes to cells with CD4 and CCR-5 receptors
v. Penetrates via envelope fusion or endocytosis
Adsorption
Replication
Human Immunodeficiency Virus (HIV)
vi. Lysogenizes the cells and may replicate for decades
1. Cellular reservoir
vii. After replicating and mutating
1. Each of its 9 genes mutates ever 24 hours
2. For average of ten years,
Adsorption
Replication
Human Immunodeficiency Virus (HIV)
viii. Acquires mutation that allows it to attach to
1. Helper T lymphocytes with receptor combo CD4 + CXCR-4
Adsorption
Replication
Human Immunodeficiency Virus (HIV)
i. Replication of the HIV genome uses reverse transcriptase to transcribe viral RNA into viral DNA that can lysogenize the host DNA
1. No proofreading
2. Mutations constant
Synthesis
Replication
Human Immunodeficiency Virus (HIV)
ii. The lysogenized DNA generates viral mRNA
Synthesis
Replication
Human Immunodeficiency Virus (HIV)
iii. mRNA goes to
1. host ribosomes to be translated into viral proteins
2. also represent a source of new viral core
Synthesis
Replication
Human Immunodeficiency Virus (HIV)
i. Involves assembly of the viral capsid and core
Maturation
Replication
Human Immunodeficiency Virus (HIV)
i. Accomplished via new viruses “budding” from infected cells
Release
Replication
Human Immunodeficiency Virus (HIV)
i. Occurs when people are
1. HOMOZYGOUS for 2 CCR-5 genes with deletions
a. 10% of Caucasians of European descent
Natural Resistance
Human Immunodeficiency Virus (HIV)
ii. Thought to be after the Black Plague
1. Since the bacteria that caused it also invaded CD4 cells via CCR-5 receptors
Natural Resistance
Human Immunodeficiency Virus (HIV)
a. HIV
i. Usually no signs or symptoms
ii. The “Incubation” period
Signs and Symptoms
Human Immunodeficiency Virus (HIV)
b. 3 months
i. Virus begins to rapidly replicate and the host mounts a significant immune response causing
1. Flu-like symptoms
Signs and Symptoms
Human Immunodeficiency Virus (HIV)
c. Death of T Helper Lymphocytes
Signs and Symptoms
Human Immunodeficiency Virus (HIV)
d. Conversion to AIDs
i. Helper T cell count below 200/ul of blood
Signs and Symptoms
Human Immunodeficiency Virus (HIV)
ii. Symptoms
1. Chronically swollen lymph nodes
2. Recurrent fevers
3. Weight loss
4. Failure to thrive
5. AIDs dementia complex
Signs and Symptoms
Human Immunodeficiency Virus (HIV)
iii. TB accounts for 1/3 of all AIDs death
Signs and Symptoms
Human Immunodeficiency Virus (HIV)
a. AZT
b. Integrase Inhibitor
c. HAART
Treatment
Human Immunodeficiency Virus (HIV)
i. Reverse transcriptase inhibitor
ii. Nucleotide mimic
iii. Prevents HIV replication
1. Competitively inhibits reverse transcriptase and therby halting the conversion of viral RNA to viral DNA
AZT
iv. Are powerless against HIV that has already lysogenized the host cell
v. Toxic
1. Interferes with host DNA synthesis
2. Aplastic anemia
vi. HIV resistance often appears within 18 mos of initial treatment
AZT
i. To block the lysogeny of the hose cell DNA
ii. =Raltegravir
Integrase Inhibitor
i. =Highly Actie AntiRetroviral Therapy
1. Given a cocktail of antiviral drugs
2. Reduces load of HIV in blood to undetectable levels
3. Cannot eliminate it from body
4. Only 30% of AIDs victims respond to ths
a. Makes most patients too sick to continue
b. Non-compliance has resulted in resistance
5. Can extend lifespan by 13 years
HAART
collapsed circles of ssRNA, no protein coat.
Viroid
ii. Can cut other RNA molecules.
Viroid
- Identified in plant infections
2. - Causes Hepatitis D
Viroid
a. - Cell must be double infected with
i. Hepatitis D viroid and
ii. Hepatitis B virus at same time
Hepatitis D
Viroid
b. As Hep B virus assembles the Hep Dviroid will enter and travel inside the capsid to infect liver cells.
Hepatitis D
Viroid
i. Replicates via host RNA Polymerase
ii. Enters a new Hep B virus when the viral capsid self-assembles
Hepatitis D
Viroid
deviant form of a misfolded proteins (pleated), contain no nucleic acid
Prions
ii. Abnormal form is pleated
1. Insoluble in water
2. Digestible via protease
Prions
iii. Cause conversion of normal proteins into the deviant form
Prions
iv. Extremely resistant to usual sterilization techniques
1. (proteases,
2. chemicals,
3. heat)
Prions
v. Do not elicit an immune response
Prions
vi. Cause transmissible spongiform encephalopathies –
1. fatal neurodegenerative diseases
a. (Alzheimers,
b. Parkinsons,
c. ALS)
Prions
vii. Acquired via
1. Mutation or mutation and event (ie. Head trauma)
2. Transmitted via food or by intimate contact with infected tissue.
Prions
viii. Reproduce by effecting the folding of normal proteins.
ix. Target the brain and spinal cord, lymph organs.
Prions
x. Long incubation period, months to years.
Prions
xi. Transmission
1. Through foods containing contaminated animal p roducts
2. Via transplants
3. Growth hormone from cadavers
4. Intimate contact with infected tissues/secretions
5. Spontaneous/inherited mutation
Prions
- Progressive
2. Long incubation period
Prion Diseases
- Associated with amyloid production
a. Precursor protein that is the cellular isoform of the prio protein
i. Undergoes a conformational change to the abnormal amyloidogenic form
Prion Diseases
- Neurodegerneration causes brain to become riddled with holes
Spongiform Encephalopathies
Prion Diseases
- Sheep and goats
- May be the original source of other communicable prion diseases
- May be spread via contaminated urine to other sheep/goats
Scrapie
Prion Diseases
- Acquired via supplements derived from infected sheep tissue
Mad Cow Disease
Prion Diseases
- Emerged in US in 1967
- Moose
- Deer
- Elk
- That may have had contact with infected
a. Beef
b. Sheep
c. Goats - Of concern to HUNTERS in the US
Chronic Wasting Disease
Prion Diseases
- Human form of mad Cow disease
- Acquired via
a. Contact with contaminated beef products
iv. Varient Creutzfeldt-Jacob disease
Prion Diseases
a. The Fore people of New Guinea
b. Transmitted through
i. Cultural practice
1. Eating brains of deceased family members
c. Variant of Creutzfeldt-Jakob disease from eating infected beef.
Kuru
Infectious
Human Prion Diseases
i. Which agent has membrane bound organelles?
- Molds
- Protozoa
- Yeast
ii. Which agent is non cellular with no organelles?
Viruses
iii. Which agent is always single cellular
- Bacteria
- Protozoa
- yeast
iv. Which agent usually has peptidoglycan in its cell wall?
Bacteria
v. Which cellular agent has no cell wall?
Protozoa
vi. Which agent has chitin in its cell wall?
- Molds
2. yeast
vii. Which agent can have lipopolysaccharide in its cell wall?
- bacteria
viii. Which agent is put into classes by how their trophozoites move?
protozoa
ix. Which agent is classified by the spores they generate in fruiting bodies?
molds
x. Which agent produces endospores?
bacteria
xi. Which agent produces cysts?
protozoa
xii. The genome of this agent can be either DNA or RNA
- viruses
xiii. Which agent has a nucleoid consisting of one circular chromosome?
- bacteria
xiv. Which agent has plasmids?
- Bacteria
2. yeast
xv. Which agent would have at least a capsid and a core?
Viruses
xvi. Which agent is always an intracellular parasite?
Viruses
xvii. Which agent produces antibiotics?
- Bacteria
2. molds
xviii. Which agent is compose of hyphae?
mold
xix. Which agent would use spikes to attach to their host cell?
- viruses
xx. Which agent would use fimbriae to attach to a host cell?
bacteria
