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

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

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

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:

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

Read more...

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

Read more...

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)

Read more...

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.

Read more...

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

Read more...

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

Read more...

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?

Read more...

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

Read more...

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.

Read more...
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