Showing posts with label Virology. Show all posts
Showing posts with label Virology. Show all posts

11 August 2014

Ebola Virus Ppts and 200 latest publications



Viral Hemorrhagic Fevers
Philip W. Smith, MD
http://webmedia.unmc.edu

Filoviruses
http://www.unco.edu

HIV-1 and Ebola virus
Juan Martin-Serrano, Trinity Zang & Paul D. Bieniasz
http://www.csus.edu

Ebola Virus Outbreak
Erin Goode
http://facstaff.bloomu.edu

Concerns that Ebola may be transmitted through air
Gil Rivera
http://alpha.lasalle.edu/

 Viral Hemorrhagic Fevers - Filoviridae
http://www.uky.edu

Ebola
Karan Chopra, Mohan Bolisetty
http://www.rci.rutgers.edu

Scientific Name: Ebola Virus
http://www.pleasval.k12.ia.us/highschool

Ebola - The Deadly African Virus
Claudia Hacker
http://www2.yk.psu.edu

Ebola Virus - Hemorrhagic Fever
http://homepage.smc.edu

Viral Hemorrhagic Fever
http://www.cfsph.iastate.edu

Ebola Hemorrhagic Fever
Anderson Coates, Michael Mastropole
http://courses.bio.unc.edu

Hemorrhagic Fevers
http://www.columbia.edu Marburg.ppt

Case Study- Ebola Virus
Shahrzad Morim, Monica Delgado, Janine Gilkes
http://instructional1.calstatela.edu/

Latest 200 Published articles on Ebola Virus

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03 May 2012

Respiratory Viruses ppt and 171 free scholarly articles



Respiratory Viruses
David J. Miller, M.D., Ph.D.
Respiratory-viruses.ppt

What are Viral Pathogens?
Brian Tsao and Mirella Urbina
What are Viral Pathogens?.ppt

Models of infection: Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)
Dr. Amelia Woolums
PRRSV.ppt

RNA Viruses
RNA Viruses.ppt

Viral Pneumonia - Fellows conference
Cheryl Pirozzi, MD
Viral_Pneumonia_cpirozzi.ppt

Nipah Virus
Nipah.ppt

Diseases of the Respiratory System
Respiratory.ppt

Introduction to viruses
Viruses.ppt
171 Published scholarly articles free access

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27 April 2012

Respiratory syncytial virus - RSV 200 full text articles free



Respiratory Syncytial Virus
Nancy Bernal, Shan Kuang, Sahar Yaftaly
Respiratory Syncytial Virus.ppt

What is RSV?
Sarah Carrante, Veronica Cavera, Marlena Piehler, Kirsten Tandberg
What is RSV?.ppt

Virus-Induced Immunopathology
Immunopathology.ppt

Respiratory Syncytial Virus
Respiratory Syncytial Virus.ppt

Viral Diseases of the Respiratory System
Louise S. Thai, M.D.
Viral Diseases of the Respiratory System.ppt

Viral Pneumonia
Viral_Pneumonia_cpirozzi.ppt

Introduction to RNA interference
Toumazos Theodorou
RNAi.ppt

Respiratory Syncytial Virus
Sonia Leng, Heather Leonard
RSV.ppt

Respiratory Syncytial Virus
Rachael McClurg, Ridhi Mehta, Eun Hye Kim
RSvirus.ppt

RSV Bronchiolitis
Mark A. Brown, M.D.
RSV Bronchiolitis.ppt

Immunoprophylaxis for Prevention of Severe RSV Bronchiolitis
Ma. Teresa C. Ambat, MD
RSV Bronchiolitis .ppt

Respiratory Syncytial Virus
Rsv.ppt

Respiratory Syncytial Virus Bronchiolitis in Infants
Amanda Snodgrass, Dr. Bill Grimes
Respiratory Syncytial Virus Bronchiolitis in Infants.ppt

Respiratory Syncytial Virus: Beyond fluids and oxygen
Joseph Y. Allen, MD
Respiratory_Syncytial_Virus_Talk.ppt
200 free full text articles

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01 March 2012

Subacute Sclerosing Panencephalitis Ppt



Subacute sclerosing panencephalitis (SSPE) is a rare chronic, progressive encephalitis that affects primarily children and young adults, caused by a persistent infection of immune resistant measles virus (which can be a result of a mutation of the virus itself). No cure for SSPE exists, but the condition can be managed by medication if treatment is started at an early stage.

Viruses,  Viroids, and Prions
Lectures  prepared by Christine L. Case
Viruses,  Viroids, and Prions.ppt

Subacute-sclerosing  panencephalitis (SSPE)
Virology/NegStrandRNA2005B.ppt

Paramyxoviruses Measles, mumps,  parainfluenza virus, respiratory syncytial virus,  human metapneumovirus
AM_Paramyxo.ppt

Global  Health Update: Travel  & Tropical Medicine Seminar
Tropical Medicine Seminar.ppt

Latest 50 Published articles:

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12 March 2010

Concentration and detection of hepatitis A virus and rotavirus



Concentration and detection of hepatitis A virus and rotavirus in spring water samples by reverse transcription-PCR
By: Journal of Virological Methods 123 (2005) 163-169
Julie Brassard, Karine Seyer, Alain Houde, Carol Simard, Yvon-Louis Trottier
Presentation by Kristen M. Castro

What is Rotavirus?

* belong to the Reoviridae family.
* Seven major groups, groups A, B,C infect humans,
* group A most common and widespread
* cause vomiting and diarrhea 4-8 days, low grade fever
* common cause of severe diarrhea in children,
* kills around 600,000 children per year
* vaccines have been shown to be safe and effective in 2006
* genome consists of 11dsRNA segments surrounded by there-layered icosahedral protein capsid
* cause acute gastroenteritis AKA "Infantile diarrhea", "winter diarrhea", "stomach flu", "acute nonbacterial infectious gastroenteritis", and "acute viral gastroenteritis"
* infective dose is presumed to be 10-100 infectious viral particles
* infection can be acquired through contaminated hands, objects, or utensils
* Asymptomatic rotavirus is documented and may play a role in endemic disease.
* incubation period from 1-3 days
* Temporary lactose intolerance may occur
* people recover but severe diarrhea without fluid and electrolyte replacement could result in death
* Childhood death from rotavirus is low in the U.S.
* 100 cases/year, and reaches over 500,000 cases/year worldwide
* Association with other enteric pathogens may play a role in the severity
* viruses are transmitted via fecal-oral route
* usually through contaminates drinking water or food like raw shellfish, fresh fruit, vegetables, and ready to eat food

Rotavirus Why Do This Experiment?
* Rotavirus are stable under extreme conditions like pH, temperature and moisture
* resistant to disinfectants or wastewater treatments
* contribute to their existence in the environment
* contamination of wastewater, recreational water, drinking water, irrigation water, ground or subsurface water, is reportedly the primary source for gastro-enteritis or hepatitis outbreaks
* microbiological quality of water is based on quantitative methods for fecal bacterial like E. coli
* these indicators cant be used to predict contamination or presence of enteric viruses in the water
* water treatment systems are more or less adequate in detection and elimination of resistant enteric viruses
* must develop a method to detect enteric viruses and detect them at a low concentration

Materials and Methods Cell culture and virus
* Grown FRhK-4 and MA-104 cells in Eagles minimum essential medium
* Incubate cells w/o CO2 and grown to confluence
* human rotavirus strain Wa put into MA-104 cells, HAV strain HM-175 put into FRhK-4 cells
* cells were frozen and thawed 3 times and clarified using low speed centrifugation then divided into aliquots and stored at -70ºC

Materials and Methods Viral titration
* Tissue culture infectious dose (TCID) 50% method used to determine the titer of stock suspension and viral dilutions
* 96 well cell culture plates seeded with 2.0x10ˆ4 FRhK (HAV) per well and incubated for 24hrs at 37°C with 5% CO2
* cell infection performed by serial dilutions of HAV strain HM-175 were made in EMEM w/ supplements and 2% foetal bovine serum
* well plates washed with phosphate buffer saline (PBS)
* 50 uL viral dilution placed in 4 wells of a microplate w/ 175uL of maintenance medium
* plates incubated at 37°C w/ 5% CO2 and observed after 3-8 days

Materials and Methods Concentration and elution
* Spring water samples were inoculated with 1.0x10ˆ3 to 1.0x10ˆ-3 TCID50% of HAV and rotaviruses (conc. and elution step Fig 1)
* 100mL of viral dilution filtered through a positively charged Zeta Plus 60S filter to absorb virus
* to elute the virus from filter, 5mL of different eluents were used
* to the 5mL of eluate w/ viral particles, pH adjusted to 7.0-7.4, w/ 1N HCL
* re-concentration to 150 uL with Microsep 100
* retained concentrate was used for RNA extraction

Flow Chart of Concentration and Elution

Materials and Methods Extraction of viral RNA from water concentrates

* Virus concentrate incubated at 37°C w/ 1%SDS and 100ug of proteinase K for 1 hour
* 450uL of RLT buffer added to the concentrate and reheated at 56°C for 2 min, then 5 min room temp incubation
* 500uL of absolute ethyl alcohol added to the concentrate and vortexed for 15 mins
* suspension transferred to spin column in 700uL aliquots until lysate was loaded
* before elution step, column was washed 2 times
* RNA eluted 2 times w/ 30 and 20 uL of sterile RNAse free water
* viral RNA concentrated with SpeedVac
* viral RNA resuspended in a final volume of 5uL and kept at -70°C until use

Materials and Methods
RT-PCR

* Viral RNA extracted from inoculated water samples and heated at 98°C for 5 mins then chilling on ice
* 2 RT-PCR systems for the detection of the virus and 1 multiples RT-PCR were used for analyses
* Table 1 for sequences and localization's of oligonucleotides
* RT_PCR for each amplification system performed in 20uL reaction mixture with 2uL of extracted RNA using the Quiagen One Step RT-PCR
* amplification conditions used for the 226bp HAV fragment using prot. 1 and prot. 2 primers: 30 mins @ 50°C for reverse transcription step, 95°C for 15 mins for initial denaturation, 35 cycles for 45sec @ 94°C for denaturation, 45sec @ 47°C for annealing, 1 min @ 72°C for extension and final extension
* transcription and amplification conditions for RT-PCR were the same for rotavirus and multiplex HAV-rotavirus same as above, annealing temperatures (43°C) and final extension (5 mins) were different
* rotavirus, Rota-1 and End-9 primers were used for amplification of 268bp fragment
* UV light was used for amplified products after electrophoresis on a 2% agarose gel w/ EtBr


Primers and Probes Used
Materials and Methods Southern Blot
* RT-PCR products confirmed by Southern blot hybridization using internal oligoneucleotide probes (table 1)
* PCR products denatured and transferred from agarose gel to positively charged nylon membrane
* amplified DNA was crosslinked to membrane by 3 min exposure to UV light
* membrane was pre hybridized for 30 mins @ 55°C in hybridization solution w. 5x SSC0.1% N-laurylsarcosine, 0.02% sodium dodecyl sulfate (SDS), and 1% protein blocking reagent
* membrane was hybridized overnight in 50 pmol of labeled oligoneucleotide probe per milliliter
* membrane washed twice @ room temp for 5 mins in 2x SSC w/ 0.1% SDS and 2 times for 15 mins @ 55°C in 0.5x SSC w/ 0.1% SDS
* membrane incubated in blocking sln
* anti-DIG-peroxidase concentration of 75U/ml added to blocking sln
* membrane incubated 30 mins and washed 5 times in PBS
* positive result characterized by blue precipitate when peroxidase substrate was added to membrane

Results
Titration of HAV and rotavirus

* Before inoculation, water samples viral titer of HAV HM-175 and rotavirus Wa stock suspensions determined by TCID 50% method
* viral titers of HAV and rotavirus were 4.0x10ˆ7 TCID50%/ml and 1.25x10ˆ6 TCID50%/ml respectively
* titers of viral dilutions to inoculate spring water samples were determined and corresponded to estimated values
* titrations were performed in triplicate
Viral concentration and RNA extraction
* Adsorption of viral particles to the membrane due to electrostatic interactions between the viral capsid and the membrane
* larger filtration is possible and eliminate potential inhibitors of RT-PCR reaction increasing the detection of lower levels of viral particles in the water sample
* to increase yield of purified RNA of rotavirus the viral load was incubated prior to extraction step with 1% SDS and 100ug/ml of proteinase K
* due to a double capsid RNA rotavirus extraction is more difficult than others
* low yields of rotavirus were observed
* there was no beneficial effects or detriments on the RNA yield for HAV

Results
Detection limit of RT-PCR from experiments with artificially inoculated spring water samples
* 2 RT-PCR methods were used for detection of HAV and rotavirus
* “multiplex” RT-PCR used to detect HAV and rotavirus simultaneously
* analytical sensitivity was evaluated by using known titers of HAV and rotavirus in artificially inoculated samples of bottled water
* compared to the “multiplex” RT-PCR, the analytical sensitivity of the RT-PCR performed in the single mode was found to be at least 100 fold more sensitive for rotavirus (10ˆ-3 TCID50%/ml) and at least 10 fold more sensitive for HAV (10ˆ-1 TCID50%/ml)
* “multiplex” RT-PCR offers a detection of both viruses from a single amplification step with analytical sensitivities of at least 1 TCID50%/ml for HAV and at least 0.1 TCID50%/ml for rotaviruses

M=Molecular Ladder
N=Negative Control
P=Positive Control
M=Molecular Ladder
N=Negative Control
P=Positive Control (HAV and Rotavirus)
R=Positive Rotavirus Control

Results
Confirmation of RT-PCR results by Southern blot hybridization

* RT-PCR amplified fragments confirmed by Southern blot hybridization using specific primers (table 1)
* hybridization of the digoxigenin-labeled probes matched location of RT-PCR amplicons on the agarose gel

Discussion

* Due to viral outbreaks of HAV and rotavirus the confidence in the safety of the drinking water is disrupted
* bottle water per capita in the United States increased 9.4% in 1998 and grew by more than 50% since 1991 (source: Beverage Marketing Report)
* increase is due to the false conception that bottled water (spring or treated) is pure and does not contain any micro-organisms
* pilot study in Quebec City area said 56% of consumers drink bottled water on a regular basis
* spring or mineral water is defined by the Health Canadas Food and Drug Administration “bottled water derived from an approved underground water source and not from a public community water supply”
* spring water and mineral water even though treated for the removal of unwanted chemical and microbiological components can not be labeled as “natural”
* due to the packaging and distribution of bottled water that has not been treated for pathogenic microorganisms, there is a possibility of risk due to exposure from the presence of these microorganisms
* European study shows in 3 brands of bottled drinking water, detection of 53 noroviruses out of 159 samples tested (33 percent)
* RNA signals were detected after 1 year of storage
* it is beneficial, for the public, to make available a new test to detect enteric viruses in water
* quality controls are based on routine monitoring of fecal contamination with bacterial indicators like fecal coliforms, coliforms, and E. coli
* there is no correlation that can be established between the presence of bacterial indicators and the presence of enteric viruses
* due to low quantities of viral presence, methodologies must be designed to detect the viruses at low levels
* use of positively charged membranes have been integrated in efficient virus concentration systems such as noroviruses, rotaviruses, hepatitis A, poliovirus, and coxsackievirus
* the method in this study allows for detection of a viral particle (concentrate the total viral load) present in the water sample and obtain a detection limit of 0.001 TCID50%/ml for rotavirus and 0.1 TCID50%/ml for HAV
* In contrast to immunocapture technology, a charged membrane enables the concentration of all viral particle types present in the sample
* RT-PCR in the study for detection of HAV and rotavirus gives a better analytical sensivity than the multiplex
* multiplex system has the advantage of detecting both viruses simultaneously at levels of 1 TCID50%/ml for HAV and 0.1 TCID50%/ml for rotavirus
* multiplex approach is less expensive for detection of enteric viruses in large amounts of bottled water
* single RT-PCR approach is the method of choice for detection of single virus types in lower concentrations
* water samples can be processed in 8 hours from concentration step up to detection of targets on agarose gel
* the system could be expanded to include other waterborne enteric viruses
* can be used to concentrate any vial particle from a water sample and eliminate time of interference in the molecular amplification process
* extracted RNAs can be used in different molecular detection systems like RT-PCR, PCR (DNA viruses), nucleic acid sequence based amplification (NASBA) and Quantitative Real-Time PCR

* Routinely monitoring of enteric viruses that contaminate spring or mineral bottled water, underground or subsurface water, should be considered by manufactures as an important monitor of bacterial indicators for protecting the consumer and the general population for protection against pathogens associated with the viruses

Concentration and detection of hepatitis A virus and rotavirus.ppt

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06 February 2010

Drugs for Viral Infections



Drugs for Viral Infections

Virus vs. Bacteria

* Compare and contrast structural components of bacteria and viruses
* Describe a viron.
* Identify indications for viral infection pharmacotherapy.

Challenges of Anti-Viral Therapy
* Rapid mutation
* Intracellular nature of virus
* Drugs have narrow spectrum of activity

HIV vs. AIDS
* Discuss the difference between a virus and a retrovirus.
* Differentiate between HIV infection and AIDS.
* Describe the replication of HIV.

Pharmacotherpy for HIV-AIDS
* Identify the therapeutic goals of therapy.
* Classifications:
o Nucleoside reverse transcriptase inhibitors (NRTI)
o Nonnucleoside reverse transcriptase inhibitors (NNRTI)
o Protease Inhibitors
o Neucleotide reverse transcriptase inhibitor (NtRTI)
o Fusion (entry) inhibitor

HIV-AIDS Pharmacotherapy
* Compare and contrast the mechanism of action of:
o Reverse transcriptase inhibitors
o Protease inhibitors
o Fusion inhibitors
* Identify reasons treatment failures occur.

Antiretrovirals: NCs
* Drug is not a cure
* Prior to RX: assess for sx of HIV, opportunistic infection, use of herbals
* Monitor viral load
* Verify ordered combination drugs
* Common side effects:
o Fatigue, headache, GI disturbances
* Other side effects dependent upon specific drug

Antiretrovirals: NCs

* Most contraindicated: pregnancy, lactation
* Side effects can influence ADLs
* NRTIs: cautiously: pancreatitis, PVD, neuropathy, kidney or liver disorders, cardiac disease, alcohol abuse
* NNRTIs: judiciously use in liver impairment, CNS disease
* PIs: potential risks if sensitive to sulfonamides, liver disorders, renal insufficiency

Antiretrovirals: NCs

* Variations in administration instructions:
o NRTIs: empty stomach, water only, no fruit juice
o Nevirapine (Viramune) and saquinavir (Invirase) – take with food to decrease GI upset
o Contact HCP before taking any OTC med or supplement

Antiretrovirals: Client Teaching

* NRTIs: report fever, skin rash, abd pain, n/v, numbness or burning of hands/feet
* NNRTIs: report fever, chills, rash, blistering or reddening of the skin, muscle or joint pain
* PIs: report rash, abd pain, headache, insomnia, fever, constipation, cough, fainting, visual changes

Antiretrovirals: Client Teaching

* Wash hands frequently; avoid crowds
* Increase fluid intake; empty bladder frequently
* Abstinence or barrier contraception
* Do not share needles
* Take medications as ordered
* Sufficient rest and sleep; healthy diet
* Keep all scheduled appts and lab visits

Perinatal HIV Transmission
Discuss pharmacotherapy for the prevention of perinatal transmission.

Occupation Exposure
* Identify risk factors for occupational exposure to HIV.
* Describe post HIV exposure prophylaxis.

Herpesvirus Infections
* HSV-1
* HSV-2
* CMV
* VZV
* EBV
* Herpesvirus 6
o Children: roseola
o Immunocompromised: hepatitis or encephalitis

Herpesvirus Infections
* Triggering events:
o Immunosuppression
o Physical challenges
o Emotional stress

* Pharmacologic goals:
o Relieve acute symptoms
o Prevent recurrences

Antivirals: NCs
* Baseline: VS, wt, CBC, viral cultures, LFTs, RFTs
* Cautiously: pre-exisiting renal or liver dysfunction
* Judiciously: pregnancy
* Routes: IV, oral, topical, inhalation
o instruct re: proper technique
o Emphasize compliance

Antivirals: NCs
* Generally well tolerated:
o Take with food if GI upset
* Severe adverse reactions:
o Renal Failure, Thrombocytopenia
* More frequently side effects:
o Headache
o Fatigue
o Dizziness

Antivirals: Client Teaching

* Meds do not prevent transmission
o avoid activities that may transmit
* Immediately report: hematuria, bruising, jaundice, fever, chills, confusion, nervousness, dizziness, nausea, vomiting
* Complete full course of treatment
* Keep scheduled appts and lab visits

Antivirals: Client Teaching

* Caution while performing hazardous activities
* No other prescription, OTC, herbals or supplements without HCP approval
* Apply topicals with applicator or glove
* No other creams, ointments, or lotions to infected sites

Influenza

* Describe the characteristics of influenza.
* Differentiate between primary and secondary pharmacotherapy for influenza infections.
* Differentiate between antiviral and neuroaminidase inhibitor therapy.

Viral Hepatitis
* Caused by several different viruses with unique clinical features
* All cause inflammation and necrosis of liver cells
* Acute
o Fever, chills, fatigue, anorexia, nausea, vomiting
* Chronic
o Prolonged fatigue, jaundice, liver cirrhosis, hepatic failure

Viral Hepatitis

* Differentiate between Hepatitis A, Hepatitis B, and Hepatitis C.
* Compare and contrast pharmacotherapy for Hepatitis A, Hepatitis B, and Hepatitis C.

Viral Hepatitis Exposure
Compare and contrast post-exposure prophylaxis for Hepatitis A, Hepatitis B, and Hepatitis C.

Drugs for Viral Infections.ppt

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Board review - Viral infections



Rubeola (nine-day or red measles)

* Prodromal symptoms - fever, malaise, dry (occasional croupy) cough, coryza, conjunctivitis c clear d/c, marked photophobia
* 1-2 days p prodromal symptoms - Koplik spots on the buccal mucosa
* Koplik spots - tiny, bluish-white dots surrounded by red halos

rubeola (nine-day or red measles)

* Day 3 or 4 - blotchy, erythematous, blanching, maculopapular exanthem appears
* Rash begins at the hairline and spreads cephalocaudally and involves palms and soles
* Rash typically lasts 5 - 6 days
* Can see desquimation in severe cases

rubeola (nine-day or red measles)

* Patients can be systemically ill
* Incubation period 9-10 days
* Patients contagious from 4 days prior to the rash until 4 days after the resolution of the rash
* Highly contagious - 90% for susceptible people

rubeola (nine-day or red measles)

* High morbidity and mortality common in children in underdeveloped countries
* Peak season is late winter to early spring
* Potential complications - OM, PNA, obstructive laryngotracheitis, acute encephalitis
* Vaccination is highly effective in preventing disease

rubeola (nine-day or red measles)

Rubella (german measles)

* Little or no prodrome in children
* In adolescents - 1-5 days of low-grade fever, malaise, headache, adenopathy, sore throat, coryza
* Exanthem - discrete, pinkish red, fine maculopapular eruption - begins on the face and spreads cephalocaudally
* Rash becomes generalized in 24 hours and clears by 72 hours

rubella (german measles)

* Forchheimer spots - small reddish spots on the soft palate - can sometimes be seen on day 1 of the rash
* Arthritis and arthralgias - frequent in adolescents and young women - beginning on day 2 or 3 lasting 5-10 days
* Up to 25% of patients are asymptomatic - serology testing may be necessary to establish the diagnosis

rubella (german Measles)

* Important in establishing the diagnosis if the patient is pregnant or has been in contact c a pregnant woman
* Peaks in late winter to early spring
* Contagious from a few days before the rash to a few days after the rash
* Incubation period 14-21 days
* Complications - rare in childhood - arthritis, purpura c or s thrombocytopenia, mild encephalitis

rubella (german Measles)

Varicella (chickenpox)

* Caused by varicella-zoster virus
* Highly contagious
* Brief prodrome of low-grade fever, URI symptoms, and mild malaise may occur
* Rapid appearance of puritic exanthem

varicella (chickenpox)

* Lesions appear in crops - typically have 3 crops
* Crops begin in trunk and scalp, then spread peripherally
* Lesions begin as tiny erythematous papules, then become vesicles surrounded by red halos
* Lesions began to dry - umbilicated appearance, then surrounding erythema fades and a scab forms

varicella (chickenpox)

* Hallmark - lesions in all stages of evolution
* All scabs slough off 10-14 days
* Scarring not typical unless superinfected
* Cluster in areas of previous skin irritation
* Puritic lesions on the skin
* Painful lesions along the oral, rectal, and vaginal mucosa, external auditory canal, tympanic membrane

varicella (chickenpox)

* Occurs year-round, peaks in late autumn and late winter through early spring
* Incubation period ranges from 10-20 days
* Contagious 1-2 days prior to rash until all lesions are crusted over
* Complications - secondary bacterial skin infections (GAS), pneumonia, hepatitis, encephalitis, Reye syndrome

varicella (chickenpox)

* Severe in the immunocompromised host - can be fatal
* Can have severe CNS, pulmonary, generalized visceral involvement (often hemorrhagic)
* Need to get varicella-zoster immunogloblin 96 hours post-exposure to possible varicella

varicella (chickenpox)

Adenovirus

* 30 distinct types
* Variety of infections including conjunctivitis, URIs, pharyngitis, croup, bronchitis, bronchiolitis, pneumonia (occ fulminant), gastroenteritis, myocarditis, cystitis, encephalitis
* Can be accompanied by a rash - variable in nature
* Typically can see - conjunctivitis, rhinitis, pharyngitis c or s exudate, discrete, blanching, maculopapular rash

adenovirus

* Can see anterior cervical and preauricular LAD, low-grade fever, malaise
* Peak season is late winter through early summer
* Contagious during first few days
* Incubation period 6-9 days

Coxsackie hand-foot-and-mouth disease

* Brief prodome - low-grade fever, malaise, sore mouth, anorexia
* 1-2 days later, rash appears
o Oral lesions - shallow, yellow ulcers surrounded by red halos
o Cutaneous lesions - begin as erythematous macules then evolve to small, thick-walled, grey vesicles on an erythematous base

Coxsackie hand-foot-and-mouth disease

* Highly contagious
* Incubation period 2-6 days
* Lasts 2-7 days
* Peak season summer through early fall
* If no cutaneous lesions - herpangina
o less painful and less intense than herpes gingivostomatitis

erythema infectiosum (fifth disease)

* Caused by Parvovirus B19
* Affects preschool and young school aged children
* Peak incidence in late winter and early spring, but it is seen year round
* Characterized by rash - large, bright red, erythematous patches over both cheeks - warm, but non-tender

erythema infectiosum (fifth disease)

* Facial rash fades, then see a symmetrical, macular, lacy, erythematous rash on the extremities
* Resolution occurs within 3-7 days of onset
* Transmitted by respiratory secretions, replicates in the RBC precursors in the bone marrow
* Can cause aplastic crisis in patients with sickle cell disease, other hemogloblinopathies, and other forms in hemolytic anemia

erythema infectiosum (fifth disease)

roseola infantum (exanthem subitum)

* Febrile illness affecting children 6-36 months
* Human herpesvirus 6 is causative agent
* Symptoms include:
o fever, usually >39
o anorexia
o irritability
o these symptoms subside in 72 hours

roseola infantum (exanthem subitum)

* As fever defervenscences, usually an erythematous, maculopapular rash that appear on the trunk and then spread to the extremities, face, scalp, and neck
* Occurs year-round
* More common in late fall and early spring
* Incubation period thought to be 10-15 days

roseola infantum (exanthem subitum)

Infectious mononucleosis

* Acute self-limiting illness of children and young adults
* Caused by EBV
* Transmission by oral contact, sharing eating utensils, transfusion, or transplantation
* Incubation period 30-50 days (shorter, 14-20 days, in transfusion-acquired infection)
* Don’t usually see “classic mono” in young children

Infectious mononucleosis

* Prodrome - fatigue, malaise, anorexia, HA, sweats, chills lasting 3-5 days
* Symptoms
o fever - can have wide daily fluctuations
o pharyngitis c tonsillar and adenoidal enlargement c or s exudate, halitosis, palatal petechiae
o LAD - anterior cervical and posterior cervical - in classic cases, generalized LAD toward end of wk 1

Infectious mononucleosis

* Symptoms cont:
o splenomegaly - develops in 50% of patients in 2nd-3rd wk
o hepatomegaly in 10% of patients
o exanthem - erythematous, maculopapular, rubelliform rash in 5-10% of patients

Infectious mononucleosis

* Complications:
o pneumonia
o hemolytic anemia and thrombocytopenia
o icteric hepatitis
o acute cerebellar ataxia, encephalitis, aseptic meningitis, myletis, Guillain-Barre
o rarely myocarditis and pericarditis

Infectious mononucleosis

* Complications cont:
o upper airway obstruction from tonsillar and adenoidal enlargement
# seen more often in younger patients
# children < 5 yrs of age c obstruction are more likely to have secondary OM, recurrent bouts of OM, tonsillitis, and sinusitis
o splenic rupture

Infectious mononucleosis

* Diagnosis:
o classic finding - lymphocytosis (50% or more) c 10% atypical lymphocytes
o 80% or more of patients c elevated liver enzymes
o Monospot - detects heterophil antibodies - specific, not as sensitive - 85% of adolescents + and fewer younger patients
o specific EBV antibody titers and PCR

Infectious mononucleosis

* DDx
o If fever and exudative tonsillitis predominate
# GAS, diphtheria, viral pharyngitis
o If LAD and splenomegaly predominate
# CMV, toxo, malignancy, drug-induced mono
o If severe hepatic involvement
# viral hepatitis, leptospirosis

herpes simplex infections

* Primarily involve the skin and mucous surfaces
* Can be disseminated in neonates and immunocompromised hosts
* Produces primary infection - enters a latent or dormant stage, residing in the sensory ganglia - can be reactivated at any time

herpes simplex infections

* HSV-1
+ >90% of primary infections caused by HSV-1 are subclinical
+ more common
* HSV-2
+ usually the genital pathogen
+ usual pathogen of neonatal herpes

herpes simplex infection

* Diagnosis
o usually made clinically
o can scrap base of vesicle and a special stain - Giemsa-stained (Tzanck)
# ballooned epithelial cells c intranuclear inclusions and multinucleated giant
o viral cultures take 24-72 hours

Primary herpes simplex infections

* Herpetic gingivostomatitis
o high fever, irritability, anorexia, mouth pain, drooling in infants and toddlers
o gingivae becomes intensely erythematous, edematous, friable and tends to bleed
o small yellow ulcerations c red halos seen on buccal and labial mucosa, tongue, gingivae, palate, tonsils

primary herpes simplex infections

* Herpetic gingivostomatitis
o yellowish white debris builds on the mucosal surfaces causing halitosis
o vesiculopustular lesions on perioral surfaces
o anterior cervical and tonsillar LAD
o symptoms last 5-14 days, but virus can be shed for weeks following resolution

primary herpes simplex infections

* Skin infections
o fever, malaise, localized lesions, regional LAD
o direct inoculation (usually cold sores)
o lesions are deep, thick-walled, painful vesicles on an erythematous base - usually grouped, but may be single
o lesions evolve over several days - pustular, coalesce, ulcerate, then crust over

primary herpes simplex infections

* Skin infections
o most common sites are lips and fingers or thumbs (herpes whitlow)
o eyelids and periorbital tissue infection can lead to keratoconjunctivitis - dx by dendritic ulcerations on slit lamp exam
# can lead to visual impairment - consult ophtho

Eczema herpeticum (kaposi varicelliform eruption)

* Onset of high fever, irritability, and discomfort
* Lesions appear in crops in areas of currently or recently affected skin (for those with atopic eczema or chronic dermatitis)
* Lesions begin as pustules, then rupture and crust over the course of a couple of days
* Lesions can become hemorrhagic

Eczema herpeticum (kaposi varicelliform eruption)

* Multiple crops can appear over 7-10 days (like varicella)
* Can be mild or fulminant, depending (in part) on the underlying dermatitis
* If area of involvement is large, can be lots of fluid loss and potentially fatal
* Treat promptly c acyclovir
* Risk of secondary bacterial infections

Eczema herpeticum (kaposi varicelliform eruption)

Recurrent herpes simplex infection

* Triggers include fever, sunlight, local trauma, menses, emotional stress
* Seen most commonly as cold sores
* Prodrome of localized burning, itching or stinging before eruption of grouped vesicles

recurrent herpes simplex infection

* Vesicles contain yellow, serous fluid and are often smaller and less thick-walled than the primary lesions
* Vesicular fluid becomes cloudy after 2-3 days, then crusts over
* Regional, tender LAD

herpes zoster (shingles)

* Caused by varicella-zoster virus
* After primary infection, virus lies dormant in genome of sensory nerve root cell
* Postulated triggers include mechanical and thermal trauma, infection, debilitation as well as immunosuppression
* Lesions are grouped, thin-walled vesicles on an erythematous base distributed along the course of a spinal or cranial nerve root (dermatome)

herpes zoster (shingles)

* Lesions evolve from macule to papule to vesicle then crusted over a few days
* May have associated nerve root pain - not common in pediatrics - usually short-lived unless it involves a cranial nerve root dermatome
* +/- fever or constitutional symptoms
* Regional LAD common

herpes zoster (shingles)

* Thoracic, cervical, trigeminal, lumbar, facial nerve dermatomes (order of frequency)
* If cranial nerve involvement - prodrome of severe HA, facial pain, or auricular pain prior to the eruption
* Affected patients can transmit varicella, but less of a problem b/c lesions are often covered by clothing and the o/p is not involved in most cases

herpes zoster (shingles)

gianotti-crosti syndrome

* Papular acrodermatitis
* Associated c amicteric hepatitis B, EBV, echovirus, coxasckievirus, parainfluenza virus, CMV, and RSV
* Most patients between 1-6 years old (range 3 months to 15 years)
* Prodrome of low-grade fever and malaise
* May be associated c generalized LAD, hepatomegaly, URI symptoms, and diarrhea

gianotti-crosti syndrome

* Lesions appear within a few days - discrete, firm, lichenois papules c flat tops ranging from 1-10 mm (larger in infants and smaller in older children)
* Papules can be flesh colored, pink, red, dusky, coppery, or purpuric
* Distributed symmetrically over extremities (including palms and soles), buttocks, and face - relative sparing of the trunk and scalp
* No mucosal involvement and non-purtitic

gianotti-crosti syndrome

* Usually clears in 2-3 weeks, but can last for 8 weeks or more
* Lab studies are generally non-specific, but liver enzymes should be obtained and if abnormal - hepatitis B or EBV serology should be done
* Treatment is supportive
* Steroid creams contraindicated b/c they can make the rash worse

gianotti-crosti syndrome

Board review - Viral infections.ppt

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05 October 2009

HUMAN PAPILLOMA VIRUS (HPV)



HUMAN PAPILLOMA VIRUS (HPV)
By: Nathalia Cruz

What is a Virus?
* Exceptionally simple living microbes.
* Contain a single type of nucleic acid (DNA or RNA) and a protein coat.
* Obligatory intracellular parasites.
* Range from 20 to 14.000 nm in length.
* It’s classification is based on type of nucleic acid, strategy for replication, and morphology

HUMAN PAPILLOMA VIRUS
* HPV is the virus that causes warts.
* More than 100 different kinds, 30-some of this cause genital HPV.
* Spread by sexual contact or from mother to baby.
* Genital warts appear 6 weeks to 8 months after contact with an HPV infected person.
* The most common sexually transmitted disease worldwide.
* Certain types of HPV are linked with cervical cancer.
* Divided into 2 subcategories: Genital Warts and Cervical Dysplasia.
* Most people do not know they have it.
* There are high risk and low risk types of it.

HISTORY
* The papillomaviruses are part of the PAPOVAVIRIDAE family of DNA tumor viruses.
* First discovered in the early 40’s.
* Gained notoriety in the early 80’s when it was discovered that some types of HPV caused cervical cancer.

MORPHOLOGY
* Papilloma virus genome is circular covalently closed double stranded DNA of about 8 kbp.
* All PV genes are coded in one of the 2 DNA strands utilizing the alternative splicing for the individual expression of each gene.
* Papillomavirus expression is characterized by a large array of mRNAs cells coding for different genes.
* 55 nm in diameter.

MECHANISM OF INFECTION
* All PV exhibit extreme specificity for infection on epithelial cells.
* The papillomavirus epitheliotrophy resides in the interaction of specific transmission factors with the viral regulatory region LCR.
* The infection normally results in hyperproliferation of the host cell and may lead to transformation and immortalization.

GENITAL WARTS
* Sometimes called condylomata acuminata.
* Are soft, moist or flesh colored, and appear in the genital area within weeks or months after infection.
* Sometimes appear in clusters and are either raised or flat, small or large.
* Women: appear in the vulva, cervix, vagina and anus.
* Men: Can appear on the scrotum or penis.

LIFE CYCLE (HPV-16)
* Starts with the infection of the host cell.
* The virus DNA is released within the nucleus
* Numerous cellular transcription factors interact with the non-coding viral regulatory region (LCR), starting transcription of the two hpv-16 transforming early genes (E6 and E7).
* The transforming proteins interact with the cellular antioncogenic regulator p53 disrupting the cell cycle.

HPV TYPES
* Numbered in order of discovery.
* 30 HPV types primarily infect the squamous epithelium of the lower anogenital tracts of both males and females.
* HPV types 6, 11, 42, 43, or 44 present as papillary condylomas, may also present as flat lesions that may or may not be visible to the unaided eye are part of the “low-risk” HPV types.
* Types 16, 18, 31, 33, 35, 45, 51, 52, and 56 are considered “high-risk” types because they have been found in cervical and other lower genital tract cancers.

HPV GENOMIC ORGANIZATION
* Three main regions (early, late and the long control region)
* (E) resides the transformation and immortalization potential.
* (L) Two capsid genes.
* (LCR) contains all the cis-regulatory elements.

HOW HPV CAUSES CANCER
* HPV DNA integrates into the host genome.
* The proteins E6 and E7 are produced from the resultant DNA.
* E6 binds and degrades p53 (a tumor suppressor gene).
* If the DNA is altered, the cell keeps replicating. The mutation rate of the cell increases.
* E7 binds and degrades retinoblastoma (another tumor suppressor gene).
* Retinoblastoma normally keeps the cell from growing too fast or responding to growth stimulators. This inhibitory factor is now lost.
* without these two mechanisms to slow down cell growth and prevent mutation. . .
* Malignant Transformation Occurs.

HPV TREATMENT
* Genital warts can be treated by a doctor and by different methods.
* Podofilox gel: A patient-applied treatment for external genital warts.
* Imiquimod cream: A patient-applied treatment.
* Chemical treatments (including trichloracetic acid and podophyllin), which must be applied by a trained health care provider to destroy warts.
* Cryotherapy: Uses liquid nitrogen to freeze off the warts.
* Laser therapy: Uses a laser beam or intense lights to destroy the warts.
* Electrosurgery: Uses and electric current to burn off the warts.
* Surgery: Can cut away the wart in one office visit .
* Interferon: an antiviral drug, which can be injected directly into warts.

CURE
* There is currently no cure for human papillomavirus.
* Once an individual is infected, he or she carries the virus for life even if genital warts are removed.
* The development of a vaccine against HPV is under way, but is still not available.
* If left untreated, some genital warts may regress on their own.

HUMAN PAPILLOMA VIRUS.ppt

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25 September 2009

PicornaVirus- Characteristics



PicornaVirus- Characteristics
* pico = small, rna =RNA Viruses
+ icosahedral 30 nm
o naked nucleocapsid = Nonenveloped
o plus strand(+) RNA m-RNA
+ single stranded and capped for infectivity and packaging
+ this genome is infectious(should it be introduced into a cell)
o vertices of capsid creates canyon-like depressions which contain the VAP’s, VAP -1, VAP -2, VAP -3
+ most VAP bind to intracellular adhesion molecule -1(ICAM-1) expressed on epithelial cells, fibroblasts, and endothelial cells

PicornaViruses - Pathogens
* Four genera in this Family cause most Human disease
o Enterovirus enteroviruses
# stable at pH 3(acidic conditions), in detergents, sewage, etc
# replicate at temperature> 33 C
o Rhinovirus rhinoviruses
# sensitive and unstable at pH 3 (acidic conditions)
# replicates best at temperatures =33 C
* thus, confining them to the upper respiratory tract
o Hepatovirus
o Aphthovirus

PicornaViruses – Virus Cycle
* Adsorption the susceptible cells
+ appropriate receptors determine host range
+ ICAM - 1 or similar cellular receptors bind VAP’s
* Penetration
+ internalized by endocytosis
+ sometimes by viropexis thru small channels in the cytoplasmic membrane which removes the capsid
* Uncoating
+ genome released by acidic conditions in the endosome
+ capsid removed by passage thru channels in the membrane

PicornaVirus – Replication
* Viruses replicate in the cytoplasm
+ genome binds directly to ribosomes where in functions as m-RNA
+ viral polyprotein is synthesized in 10 -15 minutes
# polyprotein in cleaved into viral products
* cleavage proteases
* viral RNA dependent RNA polymerase
* misc proteins which inhibit cellular functions
+ negative strand(+) template produced by viral RNA polymerase
# these templates then generate new plus stranded RNA
PicornaVirus – Virus Cycle
* Maturation/Assembly
+ structural proteins VP0, VP1, VP3 ect are cleaved from the polyprotein by the viral induced protease
+ structural protein component assembly, then genome is inserted to complete maturation
* Release
+ virions are released by cell lysis

PicornaVirus - Pathogenesis
* Enteroviruses
o most enteroviruses are cytolytic
o they cause direct damage to the cell by preventing cellular m-RNA from binding to the ribosomes
o also viral m-RNA competes with cellular m-RNA for ribosomal binding sites
o symptoms vary with the tissue trophism of the enterovirus
o most enteroviruses cause viremia
* Rhinoviruses
o bind to ICAM-1 receptors on respiratory epithelial cells
o produce a slow cytolytic effect; not via cellular m-RNA mechanism
o temperature and pH restrict viruses to the upper respiratory tract
o no viremia occurs in Rhinovirus infections
o most Rhinovirus replication occurs in the nose
o infected cells secrete bradykinin and histamine which cause “runny nose”
# these cytokines also enhance the expression of ICAM-1receptors and may cause the virus to spread to adjacent cells

Picornaviridae - Enteroviruses
* Polio Viruses
* Coxackie Viruses
* Echo Viruses
* Entero Viruses

Rhinovirus – Clinical Disease
* Acute Rhinitis = Common Cold
+ nasal obstruction accompanied by sneezing, rhinorrhea (runny nose), mild pharyngitis, headache, and malaise
+ without secondary bacterial infection, rhinovirus infections seldom are accompanied by fever
+ symptoms peak in 3-7 days, but may last up to 3 weeks
# 500 - 1000 infectious virions per milliters of nasal secretion
+ virally infected cells secrete interferon which limits the progression of infection , but also contributes somewhat to symptoms
+ nasal secretory IgA, and serum IgG also contribute to recovery, but produce minimal long term protection due to serotype variation(type specific immunity)
+ cell-mediated immunity plays very little role in controlling rhinoviruses

Enterovirus – Clinical Disease
* Poliomyelitis polio
o symptoms range from asymptomatic (in the oropharynx and gut) to mild febrile illness(fever, headache, sore throat, malaise, to aseptic meningitis (headache, and pain in neck and back), to paralysis( destruction of anterior horn cells and motor cortex cells), to death(destruction of medullary center and cranial nerves)
o Paralytic polio is generally to result of lower motor neuron damage and leading to a flaccid paralysis of the lower extremity
o Bulbar polio – causes damage to the respiratory centers in the medulla

Poliomyelitis - Pathogenesis
* initial virus replication is in lymphoid tissues of tonsils and pharynx
o virus is swallowed (resists acid and bile) and replicates in the lymphoid cells of the Peyers patches
# primary viremia takes the viruses to CNS, anterior horn cells and brain motor cortex - producing paralysis of the extremities
* virus may cross the blood brain barrier into CNS
* or virus may move via peripheral nerves to the CNS
o if virus spreads to other areas of the CNS, like medulla and cranial nerve, then bulbar paralysis of respiration, pharynx, vocal cords, etc
# if virus is shed back to the blood from the CNS, this is secondary viremia
+ pathogenically polio viruses are neurotrphic (narrow trophism)
+ humoral antibody is required for recovery and prevention

PicornaViruses – Other Clinical Diseases
* Herpangia = fever, sore throat with painful swallowing, anorexia and vomiting
o vesicular ulcerated lesion on the soft palate and uvula
o etiological agent is Coxsackie virus A, an enterovirus
o virus is shed from the lesions, respiratory droplets and in the feces(fecal-oral)
* Hand-Foot-Mouth Disease vesicular exanthem
o vesicular lesions on the hands, feet, mouth, tongue accompanied by mild fever
+ Coxsackie virus A16
+ etiological agent is virus is shed/transmitted from lesions and is also shed in the feces(fecal-oral)
* Pleurodynia acute onset of fever and unilateral lowthoracic, pleuritic chest pain which may be excruciating = “devils grip”
o somtimes abdominal pain and vomiting; muscles very tender on affected side
+ etiological agent is Coxsackie virus B
* Myocarditis/Pericarditis acute febrile illness with sudden onset of heart faliure giving symptoms of myocardial infarction
o etiological agent is Coxsackie virus B
o occurs at all ages, but most like threatening in neonates
* Aseptic Meningitis acute febrile illness accompanied by headache, pain in neck and back including nuchal rigidity(signs of meningeal irritation)
+ etiological agent is Coxsackie viruses A, B and Echoviruses
+ may also lead to polio-like paralysis
* Respiratory Tract Diseae common cold (rhinitis)
+ Coxsackie viruses A21/A24; Echoviruses 11/20
* Acute Hemorrhagic Conjunctivitis
+ Enterovirus 70 and CoxsackieVirus A24
* Diabetes insulin-dependent
+ Coxsackie B virus destruction of the Islets of Langerhans
* Hepatitis A Infectious Hepatitis
o Hepatovirus

PicornaVirus - Diagnosis
* Enteroviruses
o Laboratory
+ Clinical Chemistry
# cerebrospinal fluid from CNS disease reveals
* lymphocytic pleocytosis (25 - 500 cell/ml)
# CSF glucose and protein
* glucose normal or slightly depressed
* protein normal or slightly elevated
+ Serology
# detection of specific viral antibody in IgM fraction
# four fold increase in IgG from acute to convelescence
o Culture performed only for epidemiological confirmation
# polioviruses from pharynx or feces
# coxsackie or echoviruses from throat or feces
* monkey kidney tissue culture
* human embryo kidney tissue culture
# culture virus is specifically identified with antibody assays

PicornaViruses - Diagnosis
* Rhinoviruses
o mostly based upon symptoms
o laboratory identification of Rhinoviruses uses
+ serology no antigen in common with all Rhinoviruses
# must find antibody to specific serotype
+ culture human diploid fibroblasts at 33 C

Picornavirus - Epidemiology
Enteroviruses
o enteroviruses are exclusively human pathogens = human reservoir
o modes of transmission
+ Polioviruses
# p-p, indirect, fecal-oral
+ coxsackie and echoviruses
# p-p, aerosol droplets, and fecal-oral
* Rhinoviruses
o account for more than one-half of all upper respiratory tract infections defined and the “common cold”
o transmitted by respiratory droplets (aerosol), contact, and fomites
# hands are a major vector; 40 - 90 % people with colds
o Non-enveloped viruses are stable and survive on hands and fomites for hours

Enterovirus - Polio Control
* control of polio has centered around stimulation artificial active immunity via vaccines
o to shift the ratio of susceptible/immunes.
* Two Polio Vaccines
o Salk Vaccine - three strains of inactive polio viruses(IPV)
o Sabin Vaccine -three strain of active attenuated viruses(TVOPV)
# attenuated viruses are supposed to grow only in the oropharynx or intestinal tract, but not in nerve cells. In absence of reversion, this is the case and system responds immunologically
* Polio will be the next communicable disease to be eradicated
o Changes in Polio immunization guidelines – 1998
+ Use only inactive (Salk) vaccine
+ To reduce reversion of attenuated strains

ParamyxoViruses - Characteisteristics
* single-stranded, negative sense RNA viruses
o helical(spherical) nucleocapsid surround by envelope (150 - 300nm)
+ envelope glycoproteins
# F(fusion) protein - promotes fusion of virus with host cell
* all viruses in this group caused cell-cell fusion of infected cells forming synctytia and giant cells
# VAP - Hemagglutinin-Neuraminidase Paramyxovirus/Mumps
* Hemagglutinin Morbillivirus
* G protein RSV
o various enzymes/proteins carried in virion
+ L protein is the RNA dependent RNA polymerase
+ P protein facilitates RNA synthesis

Paramyxovirinae – Human Pathogens
* Respirovirus = Parainfluenza
* Rubulavirus = Mumps
* Morbilliviruse = Measles
* Pneumovirus = Respiratory Syncytial Disease

ParamyxoVirus- Viral Cycle
* Adsorption
+ VAP’s(HN, H, or G) bind virion envelope to cell surface receptors(sialic acid)
* Penetration
+ F protein promotes fusion of the virion envelope with host cell membrane
# this same protein is expressed on virally infected cells and causes them the fuse forming syncytia(multinucleated giant cells)
* Replication occurs in the cytoplasm of host cells
+ a positive sense(+) template is madefrom the negative-sense(-) RNA
# catalyzed by the virion based RNA dependent RNA polymerase
+ the positive sense(+) RNA serves as the m-RNA for a protein synthesis and as the template for replication of the new negative-sense(-) RNA
* Maturation/Assembly
+ new negative-sense genomes interact with the other viral proteins both structural and non-structural(L, NP, P,) to forms nucleocapsids
+ virions then associate with host cell membrane via virus encoded matrix(M) protein
* Release
+ Nucleocapsids bud from host cell membrane and acquire their envelope with its glycoproteins ( F/HN)

ParamyxoViruses – Clinical Disease
* Measles also called Rubeola
o serious febrile disease with symptoms of high fever and cough, coryza, conjunctivitis(three C’s) and photophobia
+ incubation period = 7 - 13 days
+ within 2 days of prodromal fever lesion known as “Kopliks” appear on the mucous membranes especially the buccal mucosa. = diagnosis
* within 12 - 24 hrs after Kopliks appear the exanthem appears
o maculopapular rash starting below the ears and spreading over the entire body - lesions often run together = confluence
+ patient is sickest and fever is highest the day rash appears
o classic childhood exanthem caused by Morbillivirus
o pathogenesis
+ virus spreads from initial site of infection in lymphocytes and blood (viremia)
+ in the tissues, the virus shows a major propensity to causedcell fusion resulting the giant cell formation
+ virus can pass from cell to cell and escapes detection by antibody
+ infection usually results in cell lysis
+ rash is due to T-cells attacking the virus infected endothelial cells lining the small blood vessels

ParamyxoViruses – Clinical Disease
* Mumps
o febrile illness characterized by parotitis( acute benign swelling of the salivary glands
+ incubation period = 7 - 14 days
+ glands become infected during incubation period when virus multiplies in respiratory epithelial cells and spreads via Stenson duct or by viremia (or both) to the salivary glands
+ the viremia carries the virus to tissues throughout the body( testes,ovary,pancreass, thyroid, etc.) and especially the the CNS
+ CNS involvement occurs in approx 50% of patients and forms the basis for aseptic meningitis
o etiological agent is Rubulavirus

ParamyxoViruses - Diagnosis
* Measles
o symptoms - the clinical symptoms are so distinct that laboratory comfirmation is seldom necessary
o laboratory virus may be found in respiratory secretion, urine, blood, and sometimes in brain tissue
+ antigen detection =immunofluorence of pharyngeal cells
+ antibody response = IgM when rash appear; four fold increase in IgG
+ cytopathology multinucleated giant cells with cytoplasmic inclusion bodies seen in respiratory cells and urine sediment
+ culture virus grows in human or monkey primary cell cultures
* Mumps
o symptoms although often asymptomatic
o laboratory virus found in salvia, urine, pharynx, Stensens duct, and cerebrospinal fluid
# serological detection of mumps specific IgM
# or fourfold increase in mumps specific IgG
o cytopathology multinucleated giant cells in monkey kidney cell cultures
+ also infected cells “hemadsorb” guinea pig erythroctyes

Paramyxoviruses – Disease Complications
Measles Complications

o pneumonia accounts for 60% of deaths from measles
o Subacutesclerosing panencephalitis virus becomes a “slow virus” in the brain and appears as an extremely severe neurological sequalae
* Mumps
o Aseptic meningitis
o Ochitis
o Pancreatitis

ParamyxoViruses - Epidemiology
* Measles
o human reservoir virus is spread in respiratory secretion before symptoms(incubation carrier) and several days after symptoms appear(3 - 4 days after the apppearenc of the rash)
o measles is highly contagious via p - p, direct, respiratory droplets
# 85 % of susceptibles in an exposed group (household) become infected by one single symptomatic individual
* Mumps
o human reservoir both symptomatic and asymptomatic
o highly communicable before immunization 90% of U.S. population was exposed before age 15
o p-p, direct, respiratory droplet transmission; some direct contact
# incubations carriers are infectious 7 days before symptoms

ParamyxoViruses – Clinical Disease
* Parainfluenza
o mild cold-like infection of the upper respiratory tract with symptoms of fever, coryza, pharyngitis, and mild bronchitis = common cold
o may progress to a more severe bronchiolitis and pneumonia
+ generally more serious in children in whom in progresses to laryngotracheobronchitis ( also known a “Croup”)
# Croup is due to subglottal swelling which closes the airway
# Croup ranks second only to RSV as the most severe lower respiratory tract infection in infants and children
o two serotypes of Respirovirus Viruses ( types 1&3)
o viruses remain localized in the respiratory tract; there is no viremia
o Cell-mediated immunity is responsible for cellular damage as well as recovery
o Antibody, esp IgA is protective and prevents additional infection for a short time; but re-infections are common throughout life

ParamyxoViruses – Clinical Disease
* Respiratory Syncytial Disease
o respiratory tract infections ranging from the common cold to pneumonia
+ rhinorrhea is a prominent symptom in older children and adults
+ bronchiolitis is a more severe manifestation in infants
# cell-mediated immunity causes necrosis of the bronchi and bronchioles with the formation of “plug” of mucus, fibrin. This obstructs the narrow airways in young infants leading to suffocation
# this traps air and decreases ventilation
# very fatal in premature infants
o caused by the Pneumovirus (also called RSV) single serotype

ParamyxoViruses - Diagnosis
* Parainfluenza Croup in children in very diagnostic; otherwise symptoms cannot be distinguished from the “common cold”
+ virus and virally infected cells are present in nasal washings and respiratory secretions; and can be detected by cytopathology or immunofluorence antigen detection methods
+ specific antibody (IgM) can be found using hemadsorption or hemmagglutination test
* Respiratory Syncytial Disease
+ cannot be grown in cell culture
+ most labaratory diagnosis is done on nasal washings and respiratory secretions using immunofluorescenc or enzyme immunoassay
+ serological finding of fourfold increases in IgG provides confirmation

ParamyxoViruses - Epidemiology
* Parainfluenza
+ human reservoir -viruses are ubiquitous and infection is very common
+ p-p, direct, respiratory droplets transmission; some direct contact
+ reinfection throughout life is common since immunity is short lived
+ some serotypes are seasonal
# parainfluenza 1, 2 (major agent of croup) in the autumn
# parainfluenza 3 occurs throughout the year
* Respiratory Syncytial Diseae
+ human reservoir very common in young children
# 65 - 98% of children in day-care setting are infected by age 3
# infects everyone by age 4
# 25 - 33% of cases in children involve the lower respiratory tract
+ RSV infections almost always occur in the winter and epidemic occur every year; unlike influenza which sometimes skips a year
+ highly contagious with an incubation period of 4 -5 days
+ most common cause of fatal acute respiratory tract disease in children under the age of 2

ParamyxoViruses - Immunity
Measles

o T-cells contribute to symptoms, but also are thebasis of resolution and recovery ; antibody (B-cells) forms the basis of prevention and protection
+ antibody does not contribute to complete recovery because the virus moves from cell to cell(direct extension
o antibody based immunity is “ lifetime”; does not often reoccur in same person
+ only one serotype of Morbilli(measles) virus
* Mumps
o same as with measles
o only one serotype of Mumps virus
o antibody based immunity is “lifetime”; does not often reoccur
* Parainfluenza
o Protective immunity following infection is short lived
+ Only IgM antibody response which has not memory
o Therefore, reinfections throughout life are common
* Respiratory Syncytial Disease
o same as with Parainfluenza; no natural passive immunity

ParamyxoViruses - Control
* Measles
+ active attenuated measles virus; one antigen in the polyvalent MMR
+ inactive vaccine did not provide protection and complicated natural disease
* Mumps
+ active attenuated mumps virus; one antigen in the polyvalent MMR
* Parainfluenza
+ no vaccine available
+ immune system support is only treatment and protection
* RSV
+ no vaccine available
+ passive immunization is sometimes used in premature infants
+ treated with Ribavirin

OrthomyxoViruses - Characteristics
* pleomorphic, enveloped, negative -sense RNA having a segmented genome
+ 7 - 8 individual strands of RNA
# nucleoprotein(NP) and transcriptase associated with each strand
+ envelope has two glycopreteins
# hemaggluttinin(HA) - projects as spikes and promotes adsorption
* genetic mutation (instability) producing antigenic variation
# neuraminidase(NA) - projects as spikes and promotes adsorption and release
+ matrix proteins line the virion and compose the capsid
o transcription and replication of influenza viruses occurs in the nucleus
o assembly occurs in the cytoplasm; close association with membrane
o release is by budding through the cytoplasmic membrane
o viruses are prone to genetic variation via mutation(recombination)
# antigenic drift
# antigenic shift
OrthomyxoViruses – Viral Cycle
* Adsorption
+ Hemagglutin (HA) is the viral attachment protein
# Binds the virion to the sialic acid component of epithelial cell receptors
# The viral component that causes hemagglutination of chicken and guinea pig red blood cells
# Is antigenic: antibody against it is protective(neutralizing)
* mutations in the virus genome cause changes in the HA and are responsible for antigenic shift and drift in type A viruses
+ Neuraminidase(NA) facilitates adsorption by hydrolyzing the sialic acid (neuramic acid) in respiratory mucous and thus exposing the sialic acid receptors to which the HA binds
o Penetration
+ Virion is taken into host cell by endocytosis
# The virus is released from the endosome when the fusion-promoting portion of the HA fuses the viral envelope with the endosomal membane
# Acidification of the Matrix and NP also uncoat the virus during release from the endosome; genome is this taken into cell nucleus

OrthomyxoViruses – Viral Cycle
* Replication
+ virions carry three variants of RNA dependent RNA polymerase
# during transcription of the viral RNA segments the polymerases used the cellular m-RNA in the nucleus as a primer; this removes the methylated cap form the cellular m-RNA so that it cannot bind to the ribosomes; resulting in cessation of cellular protein synthesis(translation)
+ positive sense(+) templates are produced for each RNA segment
# these templates are then used to polymerize new negative sense RNA
+ m-RNA formed in the nucleus is translated in to a spectrum of viral proteins by the ribosomes in the cytoplasm
# among the proteins synthesized are the HA and NA glycoproteins which are processes by the endoplasmic reticulum and the golgi and then incorporated into the host cell membrane

OrthomyxoViruses – Viral Cycle
* Maturation/Assembly
+ the negative sense replicas are transported to the cytoplasm where they associate with new polymerase and NP molecules
+ these segment are held together by matrix protein(M2) which then bind it to the cell membrane via matrix protein(M1)
+ since the mature virion must have 8 different RNA segments, only a few virions mature; the others are defective but antigenic
o Release
+ The complete and defective virions bud from the host cell membrane
+ The envelope with its HA and NA glycoproteins is acquired during this process
+ The cycle take about 8 hours
OrthomyxoViruses – Clinical Disease
* Influenza
+ a prodrome of malaise and headache(lasting a few hours) leads to abrupt onset of fever, servere myalgia, and usually a nonproductive cough
# the viruses infect the cells of the upper respiratory tract
* the infection first affects the mucous-secreting cells, and ciliated epithelial cells plus other cells the respiratory epithelium
+ these changes in the upper respiratory barrier, allow the virus to move into the lower respiratory tract and infect the bronchial and alveolar epithelium
+ virally infected cells binds opportunistic bacteria; setting the stage for secondary bacterial pneumonia
+ ultimately the mucosal surfaces throughout the respiratory tree become inflamed; causing submucosal edema, hyaline membrane disease, and necrosis of alveolar walls
+ incubation period of 1 - 4 days; acute illness last approx 3 days; but the cough may last more than a week
+ influenza is more severe in young children and the elderly
+ complications are bacterial pneumonia and Reye’s syndrome
# Reyes syndrome is an acute encephalitis that affects children who have acute febrile illness; and is promoted by salicylates

OrthomyxoViruses - Diagnosis
* symptoms especially when community epidemics occur laboratory distinguishes influenza from other respiratory viruses
+ respiratory secretion
# cultured non-specific cytopathology; hemadsorption; hemagglutionation
+ serology
# hemagglutinatin-inhibition
+ Antigen detection
# Detection of Types A and B envelope glycoproteins
OrthomyxoViruses - Epidemiology
* Reservoir Human and Animal Strains
o Source In the U.S. infected human
# In Asia/Orient both infected humans and infected animals
o Antigenic Changes
+ Antigenic Drift Influenza types A and B exhibit slights changes in the HA and NA antigens due to mutution; perhaps some reassortment
# has only minor affect on the susceptibility of a population
# occurs every two to three years
+ Antigenic Shift Only occurs in Influenza Type A viruses; mostly due to reassortement of genes between human and animal strains
# results in complete changes in HA and NA antigens
# affects the susceptibility status of a population significantly
# occurs every 8 - 10 years Fig 56-5
o Mode of Transmission
+ person-to-person, direct, respiratory droplets acute phase
# incubation carriers

OrthomyxoViruses - Epidemiology
* Pandemic resulting from Antigenic Shift
+ 1918 HswH1 orignal swine flu
+ 1947 A/FM/47/H1N1
+ 1957 A/Singapore/57/H2N2
+ 1968 A/HongKong/68/H3N2
+ 1977 A/USSR/77/H1N1
+ 1979 A/Bangkok/79/H3N2
+ 1989 A/Beijing/89/H3N2
+ 1991 A/Texas/91/H1N1

OrthomyxoViruses - Control
* Interrupt transmission this is almost possible to accomplish
* Immunization
+ Inactivated(formalized) vaccine is produced each year and contains the three or four most recent antigenic strains which have affected the world
# intact virus
# splitt virus
PicornaVirus.ppt

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Human CytomegaloVirus



Human CytomegaloVirus - Characteristics
* ubiquitous among HerpesViruses
* lymphotrophic
* largest genome of all Herpes Viruses
* replicates only in human cells
+ permissive cells include fibroblasts, epithelial cells, and macrophages
+ semipermissive cells include mononuclear lymphocytes, the stromal cells of the bone marrow, and others = basis of latency
+ Infected cells become significantly enlarged = cytomegaly
* Highly species-specific
+ Only infected humans
+ There are cytomegaloviruses specific for other animals

CytomegaloVirus - Pathogenesis

* Replicative Cycle is the same as other herpeviruses
+ replication occurs in epithelial cells and virus is shed into most body fluids
+ virus then infects cells like lymphocytes and macrophages
# virus is highly cell-associated and is transmitted by these cells
# Envelope glycoprotein protects virus from host antibody
* Binds Fc portion of immunoglobulins
* Virus establishes latent infection in monouclear cells and in organs such as kidney, liver, heart; fibroblasts and mononuclear cells in these organs
+ reactivation due to various factors including imunosuppression
+ reactivation sheds virus into body fluid including semen, breast milk, and urine
+ also reactivation often follows blood transfusion and organ transplants

Human CytomegaloVirus – Clinical Diseases

* asymptomtic infection
+ in most healthy individuals infection may occur without symptoms
+ however, virus is shed; these people are healthy carriers
+ if symptoms develops they appear as mononucleosis or hepatitis
* Mononucleosis-like syndrome
+ much like EBV with atypical lymphocytosis
+ mild pharyngitis and variable lymphadenopathy
+ heterophile antibody negative
* Hepatitis = liver dysfunction similar to hepatitis, but no evidence of classical hepatitis viruses
* Cytomegalic Inclusion Disease
+ Congenital
+ Perinatal

CMV– Cytomegalic Inclusion Disease
Human CytomegaloVirus – Risk Factors
CytomegaloVirus - Epidemiology

* Cytology
+ hallmark of CMV infection is the “cytomegalic cell” ; an enlarged cell in which the nucleus contains a dense, central, basophilic intranuclear inclusion body; often looks like an “owls eye”
+ infected cells may be found in any tissue and in urine
+ Papaicolaou or hematoxylin-eosin stains
* Antigen Detection Rapid and Sensitive Tests
+ Antigen detection using enzyme or fluorescent labeled monoclonal antibody
+ Nucleic acid detection using similarly labeled DNA probes
* Serology
+ Seroconversion,(antibody response) in an excellent marker for primary infection(IgM) or recurrent infection(IgG)
* Culture
+ CMV grows in diploid-fibroblast cell cultures
+ characteristic CPE observed in 4 - 6 weeks
+ not routinely used for diagnosis; much used epidemiologically

Human Herpes Virus, Type 6
Human Herpes Virus, type 6 – Roseola
Human Herpes Virus, type 6 - Epidemiology
ParvoViruses - Characteristics
ParvoViruses- Virus Cycle
ParvoViruses - Pathogenesis
Human Parvovirus, B19 – Erythrema infectiousm
Erythrema infectiosum; Fifth’s Disease
ParvoViruses – Other Clinical Diseases
ParvoVirus, B19 - Diagnosis
ParvoVirus, B19 - Epidemiology
ParvoVirus- Control
PoxViruses - Characteristics
PoxViruses – Clinical Diseases
Molluscum contagiosum – Clinical Disease
Small Poxvirus - Epidemiology
* Human Reservoir
o Respiratory droplets
o Scabs from lesions
* Most common mode of transmission
o Person-to-Person, direct, respiratory droplet

Smallpox - Control
* Active Attenuated Vaccine – chemically stabilized
o Vaccinia Virus– naturally attenuated zoonotic strain
+ Obtained from vesicular lesion of calves
+ Later virus were grown in chicken embryos
o From early experiment conducted by Edward Jenner -1796
* First microbial disease to be eradicated via herd immunity from a vaccine
o Routine vaccination in the U.S ceased in 1971
o Routine vaccination in the World ceased in 1978
* Epidemiology/Control
o The importance of smallpox today is that it is and example of the disease which was eradicated by producing “herd immunity” through the process of vaccination( use of active vaccinia virus)


Human CytomegaloVirus.ppt

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07 May 2009

Sore Throat



Sore Throat
Presentation by:Richard Usatine, MD

What are causes of sore throats?

* Infectious - viral, bacterial, mycoplasma, chlamydiae, candida
* Allergic - allergic rhinitis
* Acid Reflux - GERD
* Trauma – e.g., swallowing a chicken bone
* Chemical irritants or burns
* Epiglottitis
* Thyroiditis
* Retropharyngeal abscess


Infectious Causes of Pharyngitis
Cause
Strep throat versus viral pharyngitis
Why do we want to diagnose and treat GABHS?
Downside of using antibiotics

Case 1
What is the differential diagnosis in order of likelihood?

* Strep
* Viral
Sensitivity and Specificity
True negative
False negative

False positive
True positive
Positive Predictive Value (PPV)

* Changes based on the prevalence in the population
* True positives/all positives
* Higher prevalence increases the PPV
How well does PE predict strep throat?
Injected Pharynx
Tonsillar Swelling
Tonsillar Exudate
Anterior Cervical adenopathy
Positive Predictive Value
Specificity
Sensitivity
How well does history predict strep throat?
History and Physical
Clinical Prediction Rule for Strep Throat
Fever over 38 C
Absence of cough
Tender ant. cervical adenopathy
Tonsillar swelling or exudate
McIsaac modification of the Centor Criteria
Probability of Strep throat based on points (pretest probability)
How many points does our patient have?
Tender ant. cervical adenopathy
Tonsillar swelling or exudate
What are the tests?
* Rapid strep test
o Done in minutes in the office
* Throat culture
o Gold standard – how can you get false negatives or positives?
* ASO titer – not useful for practicing medicine
How to swab for rapid strep test or culture.
Rapid Strep Test Done
Antibiotic treatment
What symptomatic treatment could you offer the patient?
* Acetaminophen
* gargling with warm salt water
* throat lozenges
* fluids, warm or cold, can be soothing

Case 2
Case 3
Case 4
Case 5
Peritonsillar Abscess
Case 6
Case 7
Strep Throat
Candida in a man with AIDS
Viral
Herpangina
Coxsackie A16 Virus

Summary

* Use of clinical prediction rule to diagnose sore throat (useful in other diseases)
* Clinical prediction rule helps to establish pretest probability and put patient in one of three categories
o No test, no treat
o Test and treat based on result
o No test, just treat
* Use antibiotics for sore throat when probability of strep throat is above your treatment threshold

Sore Throat.ppt

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Enteroviruses



Enteroviruses
Presentation by: Dr. J. David Gangemi

OBJECTIVE: Review of enterovirus biology, pathogenesis, and immune response to infection
KEY WORDS: Polioviruses, echoviruses, coxsackie A & B viruses, enteroviruses, aseptic meningitis, paralytic disease, Salk vs Sabin vaccines,herpangina, pleurodynia, myocardiopathy

Outline of Major Teaching Points

I. BACKGROUND
II. CLASSIFICATION
III. BIOLOGICAL PROPERTIES
IV. VIRAL PATHOGENESIS
V. IMMUNITY
VI. DISEASE


Picornaviridae Rhinoviruses Enteroviruses Heparavirus
1) Echoviruses
2) Coxsackie viruses
3) Polioviruses

Cardiovirus Apthovirus
Enterovirus Prototype: “Poliovirus”
Diseases Associated with Enterovirus Infections

1. Non-specific Febrile Illness
2. Perinatal Infection
3. Febrile Disease With Rash
4. Meningitis
5. Myocarditis
6. Hepatitis
7. Pleurodynia
8. Poliomyelitis

I. BACKGROUND

The enteroviruses have been among the most intensively studied of all human pathogens. The war on poliomyelitis produced many breakthroughs in the science of virology (Salk/Sabin/Enders and Weller).


II. CLASSIFICATION
General Features Used For Taxonomy
III. Biological Properties
IV. VIRAL PATHOGENESIS

* Virus enters the body through the mucosa of the oropharynx and upper respiratory tract, then begin to multiply in the tissues around the oropharynx.
* Because the Enteroviruses are stable in acid they are able to pass through the stomach into the intestines, where they undergo further rounds of replication.
* Roughly at the same time as it reaches the intestine, the virus begins to spill into the systemic circulation. This early (primary) viremic phase is usually asymptomatic and involves fairly low titers of virus in the blood.
* During the primary viremia, tissues are seeded according to the tropism of the virus as determined by Vp1
* In the case of the polioviruses, the tissues infected include neurons, especially the anterior horn cells of the spinal cord

V. IMMUNITY

* Antibodies can be detected in the circulation by the seventh to tenth day after exposure, roughly the same time as the symptomatic disease and secondary viremia occur.
* With the exception of the gastrointestinal tract, viral replication in tissues soon slows to a halt. In contrast, gastrointestinal tract viral multiplication and fecal shedding can continue for weeks after the development of high neutralizing antibody titers.

VI. Disease
The Enteroviruses:

o Cause a variety of clinical syndromes, with a great deal of overlap among the different serotypes
o Viral tropism, as determined by the Vp1 capsid protein, ultimately determines tissue involvement and the clinical syndrome which each serotype can cause

Aseptic Meningitis

Symptoms- headache, neckache, rigidity of neck and back, malaise

Cause- while several viruses can cause aseptic meningitis (enteroviruses, mumps, lymphocytic choriomeningitis, herpes, etc.), there are other causes of nonpurulent meningitis (chlamydia, leptospira). Certain other bacteria and fungi may also cause nonpurulent spinal fluids but with altered chemistry compared to viral meningitis.

Poliomyelitis
* Poliovirus was once thought to be the main cause of paralysis before the advent of polio vaccines
* Poliovirus did account for a large portion of paralytic cases but many cases were caused by other agents or were due to unknown causes

Poliomyelitis: Disease Characteristics
Poliomyelitis: Prevention Diseases Associated with Coxsackie Viruses

Enteroviruses.ppt

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05 May 2009

Human papilloma Viruse(HPV)



Human papilloma Viruse(HPV)
Presentation By:Nathalia Cruz

What is a Virus?
* Exceptionally simple living microbes.
* Contain a single type of nucleic acid (DNA or RNA) and a protein coat.
* Obligatory intracellular parasites.
* Range from 20 to 14.000 nm in length.
* It’s classification is based on type of nucleic acid, strategy for replication, and morphology

HUMAN PAPILLOMA VIRUS

* HPV is the virus that causes warts.
* More than 100 different kinds, 30-some of this cause genital HPV.
* Spread by sexual contact or from mother to baby.
* Genital warts appear 6 weeks to 8 months after contact with an HPV infected person.
* The most common sexually transmitted disease worldwide.
* Certain types of HPV are linked with cervical cancer.
* Divided into 2 subcategories: Genital Warts and Cervical Dysplasia.
* Most people do not know they have it.
* There are high risk and low risk types of it.

HISTORY

* The papillomaviruses are part of the PAPOVAVIRIDAE family of DNA tumor viruses.
* First discovered in the early 40’s.
* Gained notoriety in the early 80’s when it was discovered that some types of HPV caused cervical cancer.

MORPHOLOGY

* Papilloma virus genome is circular covalently closed double stranded DNA of about 8 kbp.
* All PV genes are coded in one of the 2 DNA strands utilizing the alternative splicing for the individual expression of each gene.
* Papillomavirus expression is characterized by a large array of mRNAs cells coding for different genes.
* 55 nm in diameter.

APPEARANCE
MECHANISM OF INFECTION
* All PV exhibit extreme specificity for infection on epithelial cells.
* The papillomavirus epitheliotrophy resides in the interaction of specific transmission factors with the viral regulatory region LCR.
* The infection normally results in hyperproliferation of the host cell and may lead to transformation and immortalization.

GENITAL WARTS

* Sometimes called condylomata acuminata.
* Are soft, moist or flesh colored, and appear in the genital area within weeks or months after infection.
* Sometimes appear in clusters and are either raised or flat, small or large.
* Women: appear in the vulva, cervix, vagina and anus.
* Men: Can appear on the scrotum or penis.

LIFE CYCLE (HPV-16)

* Starts with the infection of the host cell.
* The virus DNA is released within the nucleus
* Numerous cellular transcription factors interact with the non-coding viral regulatory region (LCR), starting transcription of the two hpv-16 transforming early genes (E6 and E7).
* The transforming proteins interact with the cellular antioncogenic regulator p53 disrupting the cell cycle.

LIFE CYCLE
HPV TYPES
HPV GENOMIC ORGANIZATION
HOW HPV CAUSES CANCER
* HPV DNA integrates into the host genome.
* The proteins E6 and E7 are produced from the resultant DNA.
* E6 binds and degrades p53 (a tumor suppressor gene).
* If the DNA is altered, the cell keeps replicating. The mutation rate of the cell increases.
* E7 binds and degrades retinoblastoma (another tumor suppressor gene).
* Retinoblastoma normally keeps the cell from growing too fast or responding to growth stimulators. This inhibitory factor is now lost.
* without these two mechanisms to slow down cell growth and prevent mutation. . .
* Malignant Transformation Occurs.


HPV TREATMENT

* Genital warts can be treated by a doctor and by different methods.
* Podofilox gel: A patient-applied treatment for external genital warts.
* Imiquimod cream: A patient-applied treatment.
* Chemical treatments (including trichloracetic acid and podophyllin), which must be applied by a trained health care provider to destroy warts.
* Cryotherapy: Uses liquid nitrogen to freeze off the warts.
* Laser therapy: Uses a laser beam or intense lights to destroy the warts.
* Electrosurgery: Uses and electric current to burn off the warts.
* Surgery: Can cut away the wart in one office visit .
* Interferon: an antiviral drug, which can be injected directly into warts.

CURE

* There is currently no cure for human papillomavirus.
* Once an individual is infected, he or she carries the virus for life even if genital warts are removed.
* The development of a vaccine against HPV is under way, but is still not available.
* If left untreated, some genital warts may regress on their own.


SOURCES

* http://cinvestav.mx/genetica/MyFiles/Papillomavirus/PAPepi.html
* http://www.life.umd.edu/classroom/bsci424/BSCI223WebSiteFiles/LectureList.htm#LectureList
* WWW.STDSERVICES.ON.NET/STD/WARTS
* http://www.ashastd.org/stdfaqs/hpv.html
* http://www.niaid.nih.gov/factsheets/stdhpv.htm

Human papilloma Viruse.ppt

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