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81 Cards in this Set

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Adenovirus
Nonenveloped
Icosahedral
ds-DNA
Transmission
respiratory (upper respiratory tract infections)
Affects
acute (upper and lower) respiratory infection
All Herpes Viruses
Enveloped
Icosahedral
ds-DNA
Common viruses
Can cause latent phase infection after earlier acute infection.
Viral DNA hides in the nerve close to infection
Latent disease stimulated by . . .
Fever
Abrasion
UV light
Stress
Human Herpes 1 Herpes Simplex Virus 1
Causes mucosal eruptions
Eruptions on lips are called fever blisters or cold sores
Found on genitalia also
Latency usually follows acute infection
Viral DNA is produced inside nerve cells
Exposure by direct contact with infected person may induce immunity
Human Herpes 2 : Herpes Simplex Virus 2
Genital eruptions due to (primarily) sexual contact
Latency usually follows w/ viral DNA in nerve cells
Sheds particles 75% of the time even when lesions are absent
Neonatal infections are common and may be fatal – neurological defects – spontaneous abortion
Associated w/ cervical cancer (unsure of the cause)
Associated with HIV
Human Herpes 3 : Varicella-Zoster Virus or Chicken Pox Virus
VERY contagious
Primary infection is “Chicken Pox”
Eruptions of fluid filled-vesicles over entire skin
Spread by aerosol (respiratory)
very contagious
Reactivation is called Zoster or SHINGLES
Occurs in the area of the infected nerve (unilateral)
VERY PAINFUL
Human Herpes Virus 4: Epstein-Barr Virus (EBV)
Causes many conditions:
Infectious Mononucleosis
Sore throat
Fever
Swollen lymph nodes
Increase in mononuclear cells
Common in teens “kissing disease”
Self-limiting
Rarely fatal
enlarged spleen
Most patients are able to return to work within 3 to 4 weeks
Burkett’s Lymphoma
Tumors on jaw and central organs develop (full of viral capsid protein)
Found in Africa
Rare in US
A connection to Chronic Fatigue Syndrome
Human Herpes Virus 5
Cytomegalovirus CMV
Common
Most asymptomatic
Mucous transmission
Giant cell is characteristic
Problems with fetuses and newborns
Enlarged liver and spleen, neurological damage
Possible hearing visually inpaired
Possibly fatal
Human Herpes 6:
T-lymphotropic virus
Replicated in T-lymphocytes, macrophages, salivary and gland cells
Linked to
Fever in infants (105oF) and rash
Multiple sclerosis
70% of MS pts test positive
Brain lesions contain the virus
Hodgkin lymphoma
Oral carcinoma
Some T-Cell lymphoma
Variola
Causes “Smallpox”
Large brick-shaped enveloped virus
ds-DNA
Symptoms
Severe fever
Prostration
Rash (starts 2-3 days later)
Papules (bumps)
Vesicles (fluid bumps)
Pustules (cloudy fluid bumps)
Deep scar
Causes severe disfigurement and was very deadly
5-10% die
Eradicated through universal immunization
1966
10-15 million die world wide
1967
WHO begins eradication
1977
last case in Somalia
1980
Eradicated
Papovavirus
Includes Papillomavirus (HPV)
Papillomavirus (HPV)
40 types of wart-causing viruses such as “genital warts”
Nonenveloped
Icosahedral
circular ds-DNA
All are associated with human tumors
Tumors are usually benign
Some cause cervical cancer
Picornavirus
Morphological characteristics
Very small
ss-RNA
Enveloped
Includes
Enterovirus (gastro-intestinal) i.e. Coxsackie virus
Rhinovirus (common cold)
> 100 types
And…
Hepatitis A (more later)
Poliovirus is a
Picornavirus
Spread by fecal-oral transfer
Most infections are asymptomatic and limited to GI tract.
However, it can invade Central Nervous System (CNS) tissues causing . . .
Meningitis (mild form in the CNS)
Post-Polio Syndrome
Had polio but learned to use different muscles
Lose these muscles in old age
Paralysis occurs
Bulbar-Spinal Poliomyelitis is a Picornavirus
Worse case
Brain stem attacked
Rhabdovirus
Helical virus w/ protein spikes, bullet shaped
ss-RNA
Causes Rabies
Spread usually by a bite of dog, rabbit, squirrel, cattle, horses, etc.,(rarely inhalation of dust with bat droppings)
Virus moves along peripheral nerves to CNS
May take 2 weeks to several months. Average is 8 weeks before symptoms:
Difficult swallowing
Nervousness
Excitation
Headache nausea
Untreated is usually fatal in humans (only 2 exceptions in history)
Hepatitis
Five viruses that cause liver disease and/or cancer
Fibrosis
virus infects liver cells and damages them producing scar tissue. This scar tissue replaces the liver cells.
Cirrhosis
a build up of fibrous tissue. Liver becomes hard and bumpy. Blood flow is blocked. Get back pressure in the veins (can’t get nutrients from stomach and intestine to needed cells). Varicose veins form in stomach and esophagus can burst . . . vomiting blood or passing black stools.
Liver Cancer
5,000 people die in the US each year related to Hepatitis B and C
Hepatitis A
A picornavirus (small)
ss-RNA
enveloped
CDC estimates:
150,000 people in US are infected each year
1/3 of US population have been infected
Most recover within 6 months w/out serious health problems
Transmitted:
Water, food w/ fecal material (enterovirus)
Fecal matter has high conc. of viruses compared to saliva or other fluids
Shellfish a big problem
Direct contact w/ infected person
Kissing
Anal sex
IV needles
> 40% cases are unknown causes
Symptoms
None or asymptomatic
Symptomatic
Fatigue
Nausea
Vomiting
Liver area pain
Dark urine
Light colored stools
Fever
Jaundice due to liver damage
Prevention
Sanitation
Hygiene
Vaccine (attenuated)
High risk areas
Middle East
South America
Eastern Europe
Central America
Africa
Southeast Asia
A few areas in US with poor sanitation
Day care
Military
Institutions for the disabled
Hepatitis B
Icosahedral
ds DNA
Enveloped
CDC estimates:
125,000 contract the liver disease each year.
90 – 95% ADULTS fight off infection off themselves . . . develop immunity.
Will always test positive & can’t give blood even though it’s cleared.
5%-10% infected are carriers (currently, ~1 million are carriers in US)
Carry virus in blood > 6 mos.
Usually no symptoms
May clear virus on their own . . . most don’t!
Have a higher risk of liver failure or cancer
chronic liver disease and cancer
Transmitted
More infectious than HIV
Direct contact w/ infected person
Biting
Sex
IV needles
Blood
Body fluids
Semen
Vaginal secretions
Saliva
Open sores
3%-40% unknown (diff. due to pts. not wanting to admit)
Has been found in, but not transmitted by sweat, tears, breast milk, urine, and feces
Symptoms
None or asymptomatic (approximately 40%, blood donation test is 1st indication
Symptomatic
Fatigue (lasting weeks or months)
Nausea
Vomiting
Liver area pain
Dark urine
Light colored stools
Fever
Jaundice due to liver damage
Prevention
Vaccine . . . 2 + 1 booster
Lasts 13 years (after that . . . ?)
Hepatitis B Immune Globulin (HBIG)
Pooled human plasma w/ Ab’s to Hep.B.
Given right after exposure (sex, needle sticks)
Successful in 70%-75%
Condoms
Wear gloves
Cleaning blood
Clean blood contaminated area w/ Bleach
Don’t share razors, toothbrushes, pierced earrings
Don’t share gum or pre-chew for a baby
Use caution w/ body piercing & tattooing
High risk
Work w/ blood & blood products
First aid EMT
Mortician
Police
Dentist /hygienist
Medical personnel
Etc.,
Live in the same house with an infected person
Have sex with chronically infected or carrier
IV drug user
> 1 sex partner
Blood transfusion prior to 1975 (screen was developed at this time)
Hemophilia
Pt. in a long-term care facility (nursing home)
Incarcerated person
Bitten by infected/carrier
Travel to countries w/ high incidence
Treatment
Interferon
Hepatitis C
ssRNA, icosahedral, enveloped
Causes a current epidemic
CDC estimates
Four million cases in the US (1/8 the population)
It is expected to triple in the next decade (partly due to increased screening)
#1 reason for Liver Transplants
Previously, it wasn’t regularly screened for
Can’t test liver enzymes due to fluctuations
Was first named and fully identified in 1989 (before then it was called “Non-A & Non B Hepatitis).
Transmission
Mostly we don’t know
What we do know
We carry virus in blood
Can live in dried caked blood
Body piercing
Tattoos
Acupuncture
Nasal cocaine use
Symptoms
Asymptomatic
usually the case
Symptomatic
Most infections are acute/ not chronic
May have headache and fatigue (vague . . . no biggie)
Affects mostly 20 – 40 year olds
Prevention:
see other hepatitis viruses
gloves
Treatment:
Interferon
Hepatitis D
Transmission by contaminated blood and syringes
Hepatitis E and Hepatitis F
Transmission by contaminated water . . . oral-fecal route
Hepatitis G
Unknown
Hantavirus
Pulmonary Disease - Pulmonary Syndrome
Transmission
In the urine and feces of field mice
First found in NW corner of NM in 1993.
Now has been identified in 21 states
Symptoms
Flu-like in healthy adults
Fever
Abdominal pain
Shortness of breath
Fatal in 30% – 60% cases that proceed to later stages if the disease.
Human Immunodeficiency Virus (HIV)
Retrovirus
Subfamily “Lentiviruses” contains HIV-1 and HIV-2
These viruses differ genomically and biologically
HIV-1 is the more aggressive disease
Icosahedral
enveloped with spikes
ss RNA
Capsid contains:
ss RNA
3 + genes
env – envelope
gag – inner core protein
pol – polymerase
Enzymes
Reverse Transcriptase - functions as . . .
All around DNA polymerase
Protease
Cuts new viral proteins to their proper size .
Integrase
allows the viral DNA intermediate to be incorporated into host cell chromosomal DNA.
Cycle
HIV Replication:
Attachment
Spikes (w/ gp41) are specific and attaches to:
CD4 proteins on
Helper T-lymphocytes
Macrophages
Monocytes
Dendritic cells
Uncoating
Viral RNA is exposed
Viral reverse transcriptase makes dsDNA (replicative intermediate)
Viral dsDNA may then be integrated into the host DNA (integrase)
Virus may remain latent or produce more viral particles
Progeny virus RNA and mRNA are made by host cell RNA polymerase from the dsDNA intermediate.
Viral proteins originate from the mRNA.
Assembly of the proteins with viral RNA produces new viruses except for the envelope which is acquired when the viruses leave the host cell.
Release
Buds out of the host cell
Outcome
Helper T-lyphocytes become depleted and pt. progresses towards immunodeficiency
May take as long as 10 years to develop into AIDS
Acquired Immunodeficiency Syndrome

Transmission
Sexual contact
Homosexual
Heterosexual
Easier transmission with anal intercourse or with ulcerous V.D.
Contaminated blood
Blood products
Injection equipment
In utero Infected mothers pass on virus to children
Symptoms
Lymphadenopathy
Weight loss
Fatigue
Other
Opportunistic pathogens
Cryptococcus neoformans
fungi from pigeons/soil
pulmonary infection-pneumonia
brain/meninges - meningitis
Candida albicans
Pneumoncystis carinii
Fungi cysts/spores?
Normal in lungs
Others
Dementia
Kaposi’s sarcoma (cutaneous neoplasm)

Lab identification
Low lymphocyte count
Ab’s to HIV – Western Blot
Others
Prevention and Treatment
Monitor blood for contamination
“safe sex” whatever!
Abstinence … good luck!
Nucleic Acid analogs
Azidothymidine (AZT)
Dideoxyinosine (ddi)
Reverse transcriptase inhibitors
Protease inhibitors
Integrase inhibitors
Combination of nucleic acid analogs and integrase inhibitors appear promising
SARS - Severe Acute Respiratory Syndrome
Coronavirus
ssRNA
enveloped
Helical/Pleomorphic
Respiratory
Colds
Low grade fever
Common in animals
Orthomyxoviridae
Enveloped; pleomorphic and filamentous forms occur; spherical, or filamentous;
Divided into two genera:
Influenza A  viruses
In humans, pigs, birds, and horses.
Haemagglutinin (HA) – the larger protein is an essential virulence factor
Neuraminidase (NA) – the smaller protein is responsible for the transport of the virus into and out of cells.
Influenza B viruses
Only humans
Influenza C viruses
Only humans
Human Influenza
Transmitted
Respiratory Disease
Contagious 1 day before symptoms
Symptoms
fever (usually high)
headache
extreme tiredness
dry cough
sore throat
runny or stuffy nose
muscle aches
Stomach symptoms, such as nausea, vomiting, and diarrhea, also can occur but are more common in children than adults
~5% to 20% of the population gets the flu
More than 200,000 people are hospitalized from flu complications
~36,000 people die from flu.
CDC, September 28 , 2005
Prevention/Treatment
Antivirals approved for treatment of influenza A viruses
Amantadine,
Rimantadine
Zanamivir
first neuraminidase inhibitor available for clinical use and is effective against both influenza A and B.
Oseltamivir
Neurominidase inhibitor
Vaccine
Sigh!
Spanish Flu
First Wave
Spring 1817
infants and aged
Second/Thirst Wave
Spring 1818
20 yrs - 40yrs
Mortality rate was 2.5% - 5%
previous influenza epidemics are usually less than 0.1%
20% affected
Symptoms
Cyanosis
Severe obstruction of the lungs
Coughing up blood
Hemorrhaging suffocation
Some military doctors injected severely afflicted patients with blood or blood plasma from people who had recovered from the flu
Human Influenza A
RNA genome (genetic material) split into 8 segments.
If two different viral types infect the same cell, then segments from both types can get jumbled together (they reassort) as the new virus particles are assembled.
Antigenic Shift (antigenic drift is minor changes)
The new viral strain can emerge that contain a mixture of the parental genes and has the potential to spread rapidly.
Avian influenza, influenza A (H5N1)
Morphology
Enveloped,
Spherical helical
8 stranded RNA
Jumped species
Thailand November 2003.
Chicken cholera?
South Korea December 2003,
avian flu’.
Thailand January 23, 2004
first human case of ‘avian-flu’ confirmed
Vietnam followed, 2004,
Symptoms
Fever, malaise, myalgia, sore, throat and cough are found in most of the patients
Persistent high fever is an useful sign.
Life threatening
viral pneumonia and respiratory distress syndrome
multiorgan failure
65% mortality (1.6 billion)
Treatment
Amantadine (rapid viral resistance)
Rimantadine (rapid viral resistance)
Zanamivir (approved for treatment of persons aged >7 years)
first neuraminidase inhibitor available for clinical use and is effective against both influenza A and B.
Oseltamivir (approved for treatment of persons aged >1 year)
neuraminidase inhibitor
Tamilflu
Neuropsychiatric events
Noroviruses
Like Norwalk
genus Norovirus, family Caliciviridae
single-stranded RNA
nonenveloped viruses
cause acute gastroenteritis in humans
incubation period is between 24 and 48 hours
transmitted primarily through the fecal-oral route
Symptoms
a change in body function
Syndrome
a collection of symptoms that accompany a disease
Etiology
the cause of the disease
Epidemiology
the study of when and where disease occurs
Incidence
number of people in a population at a particular time who develop a disease
Prevalence
total number of people in a population who have developed the disease (both old and new cases)
Sporadic disease
occurs occasionally
Endemic disease
a disease consistently in a particular area (malaria, cold)
Epidemic disease
many people in a population acquire the disease during a short period of time (flu epidemic)
Pandemic disease
an epidemic disease occurring worldwide
Extent of Host Involvement
Subclinical Infection vs. Clinical Infection
Localized Infection
Generalized Infection (systemic or disseminated infection)
Bacteremia
Presence of bacteria in the blood
Septicemia
Bacterial are multiplying in the blood
Viremia
Presence of viruses in the blood
Toxemia
Presence of toxins in the blood
Primary Illness
Acute infection
Secondary Illness
Opportunistic infection
Nosocomial infection
Infection acquired during a hospital stay
Microbe availability
Compromised hosts (patients)
Easily transmitted by staff
Zoonotic
A disease transmitted between animals and humans
Contact Transmission of Disease
Fomite
Normal Microbiota(Flora)
Transient Microbiota (Flora)
Chronic
Disease occurs slowly and stays with you for a long time, it may reoccur
Acute
Symptoms appear quick and only last for a short time
Prions
disease-causing variants of normal proteins produced in nerve cells (and a few others)
PrPc (Prion Protein cellular) normal "healthy" prions
RNA that codes for PrPc is produced in the nucleus and exits via the nuclear pore.
RNA then passes along ribosomes attached to the rough ER.
PrPc is formed in the rough ER and then progresses up through the Golgi.
At the Golgi, vesicles containing PrPc bud off and travel to the cell surface.
Vesicles fuse with the cell membrane and discharge their cargo
The cellular proteins come to sit on the exterior of the cell.
PrPsc the bad protein particle
PrPc goes bad when it encounters PrPsc prions.
(sc stands for scrapie)
Causes normal proteins change shape
PrPsc accumulates in the cell.
PrPsc vesicles may also travel to the Golgi and intercept PrPc that is being processed there.
PrPc might be switched to PrPsc at various points in and on the cell.
Prions enter the brain along the axons of neurons. Probably by a flow of prion-filled vesicles.
Another route of entry could be the blood, probably in immune cells.
Prions cause fatal neurological diseases
Produces vaculoles in the brain
Prions – Proteinaceous Infectious Particle
Symptoms
Loss of motor control
Dementia
paralysis
Wasting
Eventually death (pneumonia)
spongiform encephalopathies
Diseases caused by prions
Types of Spongiform
Mad Cow Disease (BSE, Bovine Spongiform Encephalophathy)– 1987 Great Britain
Scrapie – sheep
Sheep scrape against fences and trees until raw
CWD (chronic wasting disease) - muledeer, elk
Kuru – Human tribes in New Guinea
Cannibal ritual
Creutzfeldt-Jakob Disease (CJD) rare human disease
200 cases per year in the US
Probable genetic link or contact with tissues of infected people (tissue grafts)
Virology
the study of viruses
Viruses
Latin = Poison
General Viral Characteristics
Noncellular & Submicroscopic
10 - 100 X’s smaller than most bacteria.
Obligate intracellular parasites
Lack energy-generating systems
Lacks machinery to synthesize macromolecules
Very limited enzymatic capabilities
Do carry own genetic information!
Contains DNA or RNA, not both
May be single-stranded (ss) or double-stranded (ds)
only contains 3-100 genes
Not sensitive to normal antibiotics
“Virion”
mature, infectious, complete viral particles (NA + protein coat)
Capsid
Protein Coat
Made up of individual subunits called “capsomeres”
Capsomeres are made up of one or few kinds of protein molecules
Functions to protect genetic info.
Functions in attachment to host cells
Envelope
Lipid envelope found on some viruses
Acquired from passing through host cell membrane
Enveloped viruses lose infectivity if envelope is destroyed
Paplomeres or spikes
Found on some viruses
Often used for attachment
Helical
Cylinder w/ identical capsomeres in a spiral arrangement
nucleic acid coiled inside
Icosahedral or cubic
20-sided figure, each side equilateral D
Often appear to be spherical
Virus: Structure
Three Basic Shapes
Helical
Icosahedral or cubic
Complex or combined
They can also be pleomorphic
Viruses: Cultivation
Cannot be grown on artificial medium
Many can be grown on tissue culture
Grow host cells in a monolayer
Inoculate and look for “cytopathic” effects
On cells attached to beads in a bioreactor
Some need embryonic eggs
Some need intact animals/organisms
Example
Polio (1955 – 1961)
Viruses grown in monkey’s liver cells
Viruses killed (Salk) with formulin
Problem
Formulin doesn’t kill the SV40 simian virus
SV40 has oncogenic properties
note: Sabin vaccine = live formula
1963
Viruses: Control
Chemical Agents
Phenol - denatures capsid proteins
Formaldehyde - good for vaccine preparation
Hypochlorite – bleach
70-90% EtOH, not the best
Lipid solvents, for enveloped viruses
Physical Agents
Heating to 50-70oC for 1 hour
Freezing doesn’t work
Radiation (X-rays & UV light effective
Viruses: Classification
Based on:
Type of Nucleic acid (NA), 4 types:
Double-stranded DNA (ds-DNA)
Single-stranded DNA (ss-DNA)
Double-stranded RNA (ds-RNA)
Single-stranded RNA (ss-RNA)

Structure of capsid
Site of Replication
Host Range
Type of Transmission
Viruses: Multiplication of Bacteriophages (Lytic Cycle)
T-even Bacteriophage Lytic Cycle
ATTACHMENT (Adsorption) to Host Cell
Due to chance collisions
Virus binds to host cell receptor sites
PENETRATION
Phage tail releases lysozyme to enter bacterial cell
Sheath contracts and tail is driven through cell wall
DNA is released into the bacterial cell
BIOSYNTHESIS (Replication) of Viral Subunits.
Host DNA is degraded
Viral DNA in the cytoplasm is transcribed and translated
Phage initially uses hosts nucleotides, ribosomes, enzymes and amino acids
Host cell makes:
new enzymes (if needed) to replicate viral NA
new viral NA
new viral structural proteins
MATURATION- Reassembly of viruses
Put together from pools of subunits made by host cell
RELEASE OF VIRUSES
Viruses lyse out of host cell
NA is incorporated (recombined) into the host DNA
Viruses: Replication in animal cells
ATTACHMENT (Adsorption) to host cell
Most have very narrow host range
Virus binds to host cell receptor sites
*this stage determines what cells can be infected.
Virus receptors located on
Spikes
Envelope of enveloped viruses
Capsid
PENETRATION
Different mechanisms
Many are engulfed by an endocytosis process
Many enveloped viruses fuse their envelope with host cell cytoplasmic membrane
UNCOATING - removal of protein coat & release of NA
Usually involves degradation by proteolytic enzymes provided by host cells
BIOSYNTHESIS (Replication) of Viral Subunits.
Method depends on type of NA
Some types require special enzymes (see notes on bacteriophages)
Reassembly of viruses
Put together from pools of subunits made by host cell
Not very efficient - many empty capsids released
RELEASE OF VIRUSES
Some by lysis of host cell
Enveloped viruses usually “bud” out
Effects of Viruses on Host:
“Cytopathic Effects (CPE)” = visible changes due to viral infection
Formation of “Inclusion Bodies”
Aggregates of viral components or cell debris
May be useful diagnosis tool
Formation of “Giant Cells” = large multi-nucleated host cells
“Plaque Formation” in tissue cultures
Viruses: Infection outcomes
Cell destruction
cell death & lysis
large # viruses released
usually causes acute-type disease
Persistence of Virus in Host Cell
host cell usually not killed
both viral & cell macromolecules make
viruses may be released gradually
may cause chronic infection i.e. Hepatitis
may cause latent (hidden) infection i.e. Herpes simplex
may cause autoimmune disorders
Host Cell Transformation
Integration of viral NA into host cell DNA
Causes a nonproductive infection - new viruses not made
Integrated NA may carry or turn on a existing tumor-causing genes or “oncogenes” in a normal cell.
This cell changes and is called “transformed!”
Viral Oncogenes and CANCER
Interferon Production
Excreted by infected cells
Interacts with membranes on adjacent cells
Shuts down viral protein synthesis
“Nonspecific” - protects against all viruses
May be artificially induced
Potential role in antitumor therapy
More later
Biotechnology
“any alteration of organisms, cells or biological molecules to achieve specific practical goals”
Selective breeding
Genetic engineering
Genetic engineering
Watson and Crick 1953, explained the DNA molecule. Since that time, efforts have been make to manipulate genes.
Genetic Recombination
taking a gene from one DNA molecule and tagging it on to another. Genetic info. is mixed

DNA can be added to the genome of another organisms