Virology 1 Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Viruses—A Little History

  • Virus—Latin word meaning “___”
  • Late 1800’s o Charles Chamberland in Pasteur’s lab made a filter that would hold back the ___ ___.

o Iwanowski (Russia) and Beijerinck (Holland) showed that a plant infection (___ ___ disease) could be transmitted by ____ that passed through Chamberland filter.

• Something smaller than the smallest bacteria that was known about back then

o ___ and ___ disease of cattle was also transmitted by bacteria-free filtrates.

o ____ seen with light microscope. • Largest of all the viruses

• 1928-1950’s

o Virus was grown in suspensions of minced ____ tissue.

o Virus was grown in developing __ ___.

o Discovery of antibiotics inhibited ____ of cell and tissue cultures. • So you could study viruses without contamination of bacteria

o Electron microscope developed (1939) and ___ of viruses was delineated.

• 1953—Watson and crick described the structure of DNA

A

Viruses—A Little History • Virus—Latin word meaning “poison” • Late 1800’s o Charles Chamberland in Pasteur’s lab made a filter that would hold back the smallest bacteria. o Iwanowski (Russia) and Beijerinck (Holland) showed that a plant infection (tobacco mosaic disease) could be transmitted by extracts that passed through Chamberland filter. • Something smaller than the smallest bacteria that was known about back then o Foot-and-mouth disease of cattle was also transmitted by bacteria-free filtrates. o Poxviruses seen with light microscope. • Largest of all the viruses • 1928-1950’s o Virus was grown in suspensions of minced kidney tissue. o Virus was grown in developing chick embryos. o Discovery of antibiotics inhibited contamination of cell and tissue cultures. • So you could study viruses without contamination of bacteria o Electron microscope developed (1939) and morphology of viruses was delineated. • 1953—Watson and crick described the structure of DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Properties of Viruses

  • Size: ___ nm to __ __ nm
  • ___ ____ parasites
  • Do not produce ___ or ___
  • Genome is either ___ or ____
  • Morphologic types • __ ___• ____
  • Assembled from components
A

Properties of Viruses • Size: 20 nm to several hundred nm • Obligate intracellular parasites • Do not produce energy or proteins • Genome is either DNA or RNA • Morphologic types • Naked capsid • Enveloped • Assembled from components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Viral Classification—Symmetry

  • ____ o Capsid is ___ ___ ___
  • Enveloped with helical nucleocapsid (influenza virus) o Envelope wrapped around ___ __ ____ o Contains important structures for ____ of other cells
  • ____ symmetry o ____ faces o Genome is encapsulated in there
  • Enveloped with icosahedral nucleocapsid (herpesvirus)
  • ____symmetry (poxvirus): Doesn’t match any other viral structures

Naked or Enveloped and then Helical or Icosahedral

A

Viral Classification—Symmetry • Helical o Capsid is wound around genome • Enveloped with helical nucleocapsid (influenza virus) o Envelope wrapped around host cell membrane o Contains important structures for infection of other cells • Icosahedral symmetry o Pentagon faces o Genome is encapsulated in there • Enveloped with icosahedral nucleocapsid (herpesvirus) • Complex symmetry (poxvirus): Doesn’t match any other viral structures Naked or Enveloped and then Helical or Icosahedral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Virus Classification—Type of Nucleic Acid

  • Its either DNA or RNA but its __ ___
  • Classified based on whether you ___ with DNA or RNA • No matter what you start with you need mRNA to make protein • _strand or _ strand
A

Virus Classification—Type of Nucleic Acid • Its either DNA or RNA but its not both • Classified based on whether you start with DNA or RNA • No matter what you start with you need mRNA to make protein • + strand or - strand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Virus Properties

  • naked capsid Ex) Polio
  • ___ coat • Subunits of protein coat called____
  • environmentally ___ • temperature • acid • proteases • detergents • drying
  • generally released by __ ___ • Infect cell. turn it into viral making cell. Viral prodcuts build up in cell and it bursts.
A

Virus Properties • naked capsid Ex) Polio • protein coat • Subunits of protein coat called capsomeres • environmentally stable • temperature • acid • proteases • detergents • drying • generally released by cell lysis • Infect cell. turn it into viral making cell. Viral prodcuts build up in cell and it bursts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  • enveloped
  • ___ layer
  • Derived from ___ ___ ____
  • Just like the cell membrane
  • ____ • Envelope similar to host cell membrane
  • ____ made from virus • It will insert these into its envelope
  • ____
  • Environmentally ____ • Don’t survive very long outside of a cell in which they can replicate
  • __ ___ modifications • They make modifications to the cell membrane
  • Released by ________ • Budding one at a time • Many use combo of these two approaches
A

• enveloped • outer layer • Derived from host cell membrane • Just like the cell membrane • Lipids • Envelope similar to host cell membrane • Glycoproteins made from virus • It will insert these into its envelope • proteins • Environmentally labile • Don’t survive very long outside of a cell in which they can replicate • Cell membrane modifications • They make modifications to the cell membrane • Released by budding and cell lysis • Budding one at a time • Many use combo of these two approaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Steps in Viral Replication

1-7

A

Steps in Viral Replication 1. Absorption 2. Penetration 3. Uncoding 4. Tx 5. Tlation 6. Assembly 7. Release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Virus Families

More ___ virus families than DNA virus families

Grouped based on their ___

A

Virus Families More RNA virus families than DNA virus families Grouped based on their structure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cytopathic Effects of Viruses: What do we see in viral infected cells

  • ___ ___ o Sites of virus assembly are taking place in cytoplasm o ___ viruses typically replicate in cytoplasm
  • ___ ___ o Viruses that are ___ viruses replicate in the nucleus
  • Cytoplasmic/Nuclear Inclusions
  • ___
  • ____ ____ o Form giant cells
  • ____ o Virus can cause cells to become transformed, replicate uncontrollably • Associated with cancer
A

Cytopathic Effects of Viruses: What do we see in viral infected cells • Cytoplasmic Inclusions o Sites of virus assembly are taking place in cytoplasm o RNA viruses typically replicate in cytoplasm • Nuclear Inclusions o Viruses that are DNA viruses replicate in the nucleus • Cytoplasmic/Nuclear Inclusions • Lysis • Multinucleated Syncytium o Form giant cells • Transformation o Virus can cause cells to become transformed, replicate uncontrollably • Associated with cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Effects of Viruses on Host Cells

  • Virus enters the host cell • It can go two ways depending on cell type. • Viruses have different tropisms for different cells
  • 1) ____ infection: o virus replicates in the cell and __ __→____ infection.
  • 2)____ infection: o virus gets into a cell in which it ___ ___ but it can carry out a few fcns (make some early gene products)→____ Infection.
  • ___: Small amts of virus are released overtime. • Never completely cleared by the body
  • ___: Virus sits quietly in cell and then something triggers it to replicate • Symptoms aren’t as bad subsequent times
  • ____: leads to cancer
  • ____: virus at low level with no signs or symptoms • After long period of time then the signs and symptoms will occur
A

Effects of Viruses on Host Cells • Virus enters the host cell • It can go two ways depending on cell type. • Viruses have different tropisms for different cells • 1) Permissive infection: o virus replicates in the cell and kills it→cytocidal infection. • 2) Nonpermissive infection: o virus gets into a cell in which it can’t replicate but it can carry out a few fcns (make some early gene products)→Persistant Infection. • Chronic: Small amts of virus are releasedovertime. • Never completely cleared by the body • Latent: Virus sits quietly in cell and then something triggers it to replicate • Symptoms aren’t as bad subsequent times • Oncogenic: leads to cancer • Slow: virus at low level with no signs or symptoms • After long period of time then the signs and symptoms will occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Determinants of Viral Disease

Nature of disease

  • ___ ___
  • ___ of ___
  • Virus ___ to ___ ___
  • Tissue ____ of virus
  • Cell ____ for virus ____
  • Viral ___ (___)

What determines what will happen once you are infected with a virus

A

Determinants of Viral Disease Nature of disease • Target tissue • Portal of entry • Virus access to target tissue • Tissue tropism of virus • Cell permissiveness for virus replication • Viral pathogen (strain) What determines what will happen once you are infected with a virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Severity of disease

  • ___ ability of virus • How easy to cause destruction of cells
  • ___ status • ____ • Prior ___
  • _______→Inclusion bodies
  • ___ of ___ ___
  • ___ to_____ of infection • Longer it goes on, the more severe it is
  • General ___ of person • Nutrition • Other diseases
  • __ __ of person
  • ___
A

Severity of disease • cytopathic ability of virus • How easy to cause destruction of cells • Immune status • Competence • Prior immunity • Immunopathology→Inclusion bodies • Size of virus inoculum • Time to resolution of infection • Longer it goes on, the more severe it is • General health of person • Nutrition • Other diseases • Genetic makeup of person • Age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mechanisms of Viral Cytopathogenesis

  • Inhibition of cellular ___ ___
  • Inhibition and degradation of cellular___
  • Alteration of ___ ___: ____ insertion, ____ formation, disruption of ____, _____
  • ____ bodies
  • ____ of virion components
A

Mechanisms of Viral Cytopathogenesis • Inhibition of cellular protein synthesis • Inhibition and degradation of cellular DNA • Alteration of cell membrane: Glycoprotein insertion, Syncitia formation, disruption of cytoskeleton, permeability • Inclusion bodies • Toxicity of virion components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Viral Pathogenesis—Initiation of Infection

  • ___ ___ must be able to initiate infection.
  • Cells at the site of infection must be ____, ___ and ____ for the virus.
  • Local host ____-___l defense systems must be __ or ___ ____. • Ex) sIgA
  • Viruses can get into any opening in the human body. They can also shed from those sites.
A

Viral Pathogenesis—Initiation of Infection • Sufficient virus must be able to initiate infection. • Cells at the site of infection must be accessible, susceptible, and permissive for the virus. • Local host anti-viral defense systems must be absent or initially ineffective. • Ex) sIgA • Viruses can get into any opening in the human body. They can also shed from those sites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diagnosis of Viral Disease

  • ___ and ____ provide first clues; often allow ___ of bacterial and fungal infections
  • laboratory studies are done to:
  • ___ the clinical diagnosis by ____ the virus • Maybe you can trt it depending on the virus • define the disease process
  • allow ____ ____. Many viruses have to be reported to the centers for disease control
  • methods
  • ___/___
  • ___ ___
  • ___ ___
  • _____/____ /____ • Using Antibodies to identify infection
  • detection of viral ___ ___→PCR
  • ____ • Look in serum for Ab to the virus
A

Diagnosis of Viral Disease • history and symptoms provide first clues; often allow exclusion of bacterial and fungal infections • laboratory studies are done to: • confirm the clinical diagnosis by identifying the virus • Maybe you can trt it depending on the virus • define the disease process • allow epidemiologic monitoring • Many viruses have to be reported to the centers for disease control • methods • cytology/histology • electron microscopy • cell culture • immunohistochemistry/immunofluorescence/immunoassays • Using Antibodies to identify infection • detection of viral nucleic acids→PCR • serology • Look in serum for Ab to the virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

cytology/histology • ___ • Many nuclei in one cell • ___ ___ • ______s→ HPV infection

electron microscopy • ___ ___ stain of specimen • immunoelectron microscopy

growth in cell culture • Inoculation of ____cells

detection of viral proteins • ____ & immunohistochemistry • Fluorescent or enzyme labeled ___

detection of viral nucleic acids • ___• Gel Electrophoresis to detect amplified DNA • Real time PCR

Immunoassays Like a pregnancy test

serology • Detection in patient serum

A

cytology/histology • Syncytia • Many nuclei in one cell • inclusion bodies • koilocytosis→ HPV infection electron microscopy • direct negative stain of specimen • immunoelectron microscopy growth in cell culture • Inoculation of susceptible cells detection of viral proteins • immunofluorescence & immunohistochemistry • Fluorescent or enzyme labeled Ab detection of viral nucleic acids • PCR • Gel Electrophoresis to detect amplified DNA • Real time PCR Immunoassays Like a pregnancy test serology • Detection in patient serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Interferon–Induction of the Anti-Viral State

• Functions

o inhibition of ___ ___

o inhibition of ___ ___

o ______

• Types (Have different sources)

o α-interferon—___ interferon

o β-interferon—___ interferon

o γ-interferon—activated ___ cells and __ cells

  • IFN is important for fighting viral infections
  • Virus gets in the cell and induces production of ___
  • ___ ____ NA are better at inducing IFN
  • Cell dies from viral infection and IFN is ____
  • IFN will signal

o uninfected cells to destroy the ___ and reduce __ ___ • So virus can produce protein in the cell

o ____ of infected cells

o Activation of ____ cells

• Alpha and Beta produced in response to ___ infection and then Gamma comes in to ____

A

Interferon–Induction of the Anti-Viral State • Functions o inhibition of viral multiplication o inhibition of cell division o immunomodulation • Types (Have different sources) o α-interferon—leukocyte interferon o β-interferon—fibroblast interferon o γ-interferon—activated T cells and NK cells • IFN is important for fighting viral infections • Virus gets in the cell and induces production of IFN • Ds NA are better at inducing IFN • Cell dies from viral infection and IFN is released • IFN will signal o uninfected cells to destroy the RNA and reduce protein syn • So virus can produce protein in the cell o Apoptosis of infected cells o Activation of immune cells • Alpha and Beta produced in response to viral infection and then Gamma comes in to fight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

New Test for Viral Infections

  • ___ ___ ____ ___
  • Use ___ ___ to express proteins of wide variety of viral proteins
  • See persons ____ to wide variety of viruses
A

New Test for Viral Infections • Systemic viral epitope scanning • Use bact viruses to express proteins of wide variety of viral proteins • See persons immunity to wide variety of viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Antivirals

  • most viral diseases, except HIV disease, are ___ ___ and do not require treatment
  • current antivirals target ____viruses, ____ viruses (B and C), ____ viruses, ____syncytial virus and ___
  • field is rapidly evolving as viruses become ___ to ___ ___
A

Antivirals • most viral diseases, except HIV disease, are self-limited and do not require treatment • current antivirals target herpesviruses, hepatitis viruses (B and C), influenza viruses, respiratory syncytial virus and HIV • field is rapidly evolving as viruses become resistant to older drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Human Herpesviruses

• ___ and ___

____

____

_____

____

____
____

A

Human Herpesviruses • herpes simplex virus (HSV-1 and HSV-2) • varicella-zoster virus (VZV) • cytomegalovirus (CMV) • Epstein-Barr virus (EBV) • human herpesvirus 6 (HHV-6) • human herpesvirus 7 (HHV-7) • human herpesvirus 8 (HHV-8)

21
Q

• ____

NA: , ___ ___

  • encode___ ___e and___ ___ • Distinct form those in mammals • Good targets for drugs
  • ___, ___, ___, ____ infections
  • ___ infections and/or associated with orofacial tissues and saliva
A

• enveloped, ds DNA • encode thymidine kinase and DNA polymerase • Distinct form those in mammals • Good targets for drugs • lytic, persistent, latent, and immortalizing infections • oral infections and/or associated with orofacial tissues and saliva

22
Q

Pathogenesis of HSV Infection

• Initial Infection

o Often Occurs in ____

____ infection

o Oral mucosa becomes infected

o May have___ signs and symptoms or may have a ___ infection

o Virus transported to __ ___ ___ at the site of primary infection

  • HSV1: ____ ganglia • HSV2: ___ ganglia, sexually transmitted
  • Latency

o Sits in those ganglia and makes latency associated proteins but its ___ ____ o Can be maintained here for a long time

• Reactivation

o Can be triggered by variety of things: Hormone fluxes, exposure to sun, immunosuppression, stress

o Virus travels ___ ___ the nerve to __ ___ where it will replicate and you will see ___ caused by virus

• Transmission

o___ ____:Both 1 and 2

o This can lead to transmission→sexually, thru infected birth canal, exchange of oral fluids

A

Pathogenesis of HSV Infection • Initial Infection o Often Occurs in childhood o Oralfacial infection o Oral mucosa becomes infected o May have severe signs and symptoms or may have a subclinical infection o Virus transported to sensory nerve ganglia at the site of primary infection • HSV1: trigeminal ganglia • HSV2: Sacral ganglia, sexually transmitted • Latency o Sits in those ganglia and makes latency associated proteins but its not replicating. o Can be maintained here for a long time • Reactivation o Can be triggered by variety of things: Hormone fluxes, exposure to sun, immunosuppression, stress o Virus travels back up the nerve to mucosal surface where it will replicate and you will see lesions caused by virus • Transmission o Mucosal shedding:Both 1 and 2 o This can lead to transmission→sexually, thru infected birth canal, exchange of oral fluids

23
Q

HSV Disease Syndromes

Normally 1 infects ___ the waist and 2 is ___ the waist but can cross over

A

HSV Disease Syndromes Normally 1 infects above the waist and 2 is below the waist but can cross over

24
Q

Clinical Course of HSV Infection

Primary Infection

  1. Incubation peiod: ____ days
  2. ___ symptoms: ___ or ___
  3. Systemic symptoms: __ ___ symptoms

4___ appear. New lesions for ___days Fluid in lesions is ___ with virus

  1. Viral ____: ____ days
  2. Vesicles __ ___
  3. Healing in ___-___ days
A

Clinical Course of HSV Infection Primary Infection 1. Incubation peiod: 3-14 days 2. Prodromal symptoms: Tingling or itching 3. Systemic symptoms: Flu like symptoms 4. Vesicles appear New lesions for 5-6 days Fluid in lesions is full with virus 5. Viral Shedding: 10-15 days 6. Vesicles Crust over 7. Healing in 18-21 days

25
Q

Recurrent Infection

  1. Reactivated virus travels to ___ or ____ surface
  2. Prodromal symptoms
  3. ____ systemic symptoms
  4. __ __ of vesicles New lesions for ___ days
  5. Viral Shedding:___ days
  6. Vesicles Crust over
  7. Healing in___ days
A

Recurrent Infection 1. Reactivated virus travels to epidermal or mucosal surface 2. Prodromal symptoms 3. Minimal systemic symptoms 4. Small group of vesicles New lesions for 1-2 days 5. Viral Shedding: 3-5 days 6. Vesicles Crust over 7. Healing in 9-10 days

26
Q

HSV Infections

  • ____: Oral
  • ____: lesions on cornea, can go blind, autoinoculation from touching lesion on lip and then rubbing the eye
  • ____: Can get lesions in nail bed, can autoinoculate yourself
  • Herpes ____
  • ____: usually only in immunosupressed
  • ____s: Get into brain
  • ___ Herpes: Infected birth canal, can be fatal
A

HSV Infections • Gngivostomatitis: Oral • Keratitis: lesions on cornea, can go blind, autoinoculation from touching lesion on lip and then rubbing the eye • Whitlow: Can get lesions in nail bed, can autoinoculate yourself • Herpes Gladiatorum • Esophagitis: usually only in immunosupressed • Enccephalitis: Get into brain • Neonatal Herpes: Infected birth canal, can be fatal

27
Q

HSV Infections—Epidemiology

  • ___ infection
  • ____ disease is source of ___
  • ___ ____ (HSV-__ > HSV-__) o Have virus in absence of any lesions
  • seroprevalence • 55% infected with HSV-1 • 17% infected with HSV-2 • rates increase with ___
  • transmission • most often from an __ ___ • ___, ___ secretions, lesion___ on mucosa
  • about one in six persons between ages of 14 and 49 years have genital HSV-2 infection in the U.S.
  • transmission from an infected ___ to a ___ partner is more likely than from an infected female to her male partner
A

HSV Infections—Epidemiology • lifelong infection • recurrent disease is source of contagion • asymptomatic shedding (HSV-2 > HSV-1) o Have virus in absence of any lesions • seroprevalence • 55% infected with HSV-1 • 17% infected with HSV-2 • rates increase with age • transmission • most often from an active lesion • saliva, vaginal secretions, lesion fluids on mucosa • about one in six persons between ages of 14 and 49 years have genital HSV-2 infection in the U.S. • transmission from an infected male to a female partner is more likely than from an infected female to her male partner

28
Q

Genital Infections–HSV-1 vs. HSV-2

____ features of initial infection:

____ genital lesion:

days to ___ ___

avg ____s/yr

viral____

A

Genital Infections–HSV-1 vs. HSV-2

Clical features of initial infection: indisting

duration genital lesion: 1<2

days to first recurrence1<2

avg reccurences/yr 1<2

viral shedding 1<2

29
Q

HSV Infections—Treatment

  • ___ or ___ the course of primary or recurrent disease
  • does not eliminate___
  • ____
  • most prescribed anti-HSV drug
  • Works on viral ___ ___
  • Takes the acyclovir and converts it to a ___ that is incorporated into ___ ___ and prevents its synthesis
  • highly ____; activation requires the __ __ ___
  • valacyclovir (Valtrex); penciclovir (Denavir); famcyclovir (Famvir)
A

HSV Infections—Treatment • prevents or shortens the course of primary or recurrent disease • does not eliminate latency • Acylcovir • most prescribed anti-HSV drug • Works on viral thymidine kinase • Takes the acyclovir and converts it to a NA that is incorporated into viral DNA and prevents its synthesis • highly selective; activation requires the viral thymidine kinase • valacyclovir (Valtrex); penciclovir (Denavir); famcyclovir (Famvir)

30
Q

Pathogenesis of VZV—Chickenpox

  • Spread by ___ ___→Then it gets into the ____s→ ___, ___ → start to get a ____ (flu like symptoms)→ go to ___ ___ or ___→ all the____ pop up→ latency in ____
  • complications

o __ ___ of skin lesions

o___

o ____l varicella syndrome

o ____

A

Pathogenesis of VZV—Chickenpox • Spread by resp tract→Then it gets into the lymphatics→ Liver, spleen → start to get a viremia (flu like symptoms)→ go to mucous membrane or skin→ all the lesions pop up→ latency in neuron • complications o bacterial infection of skin lesions o pneumonia o congenital varicella syndrome o encephalitis

31
Q

Pathogenesis of VZV—Shingles (Recurrent disease of chicken pox)

• complications

o ___ ___ ____Pain syndrome, nerve pain

o ____

o ____

o ___ ___s
o _____

• Lesions only occur on__ ___ of the body→doesn’t cross the midline

A

Pathogenesis of VZV—Shingles (Recurrent disease of chicken pox) • complications o post-herpetic neuralgia Pain syndrome, nerve pain o vasculopathy o myelopathy o retinal necrosis o encephalitis • Lesions only occur on one side of the body→doesn’t cross the midline

32
Q

VZV Infections—Epidemiology

  • ____ infection (Latent in ___)
  • recurrent disease is ____ of infection

o people with shingles can give someone chicken pox o People with chicken pox can’t give someone shingles, need to have had chicken pox to get shingles

  • primary disease more severe in ____
  • 500,000 to 1,000,000 shingles episodes occur annually in the U.S.
  • lifetime risk of shingles estimated to be ____%
  • 50% of persons living until age 85 will develop shingles (long term effectiveness of ____ unknown)
A

VZV Infections—Epidemiology • lifelong infection (Latent in ganglia) • recurrent disease is source of infection o people with shingles can give someone chicken pox o People with chicken pox can’t give someone shingles, need to have had chicken pox to get shingles • primary disease more severe in adults • 500,000 to 1,000,000 shingles episodes occur annually in the U.S. • lifetime risk of shingles estimated to be 32% • 50% of persons living until age 85 will develop shingles (long term effectiveness of vaccine unknown)

33
Q

VZV—Treatment and Prevention

  • ____ and derivatives in ____ cases
  • ____® (Merck) first released in 1995;___ _____ vaccine; can be used for ___ ____ ____ (Enough time bw initial infection and appearance of lesions that you can develop immunity to it)
  • Live virus that can’t cause disease
  • administered at about ___ year of age; booster recommended at age ___
  • some vaccinated children eventually get ____→ Immunity goes away after awhile
  • also available as ProQuad® (Merck); ___ and ____
  • Zostavax® (Merck) approved by FDA in May 2006 for reduction of shingles in people 60 yrs of age and older
  • vaccination reduces occurrence of shingles by about 50% in those 60 years or older • reduces post-herpetic neuralgia in those that develop the disease
  • long-term effectiveness____

___ ____ of attenuated virus than Varivax®

A

VZV—Treatment and Prevention • acyclovir and derivatives in severe cases • Varivax® (Merck) first released in 1995; live, attenuated vaccine; can be used for post-exposure prophylaxis (Enough time bw initial infection and appearance of lesions that you can develop immunity to it) • Live virus that can’t cause disease • administered at about 1 year of age; booster recommended at age 4 • some vaccinated children eventually get chickenpox→ Immunity goes away after awhile • also available as ProQuad® (Merck); MMR and varicella • Zostavax® (Merck) approved by FDA in May 2006 for reduction of shingles in people 60 yrs of age and older • vaccination reduces occurrence of shingles by about 50% in those 60 years or older • reduces post-herpetic neuralgia in those that develop the disease • long-term effectiveness unknown • larger dose of attenuated virus than Varivax®

34
Q

Pathogenesis of EBV

  • Initial infection occurs thru ____
  • Causes____ ____: Kissing Disease
  • Virus gets into throat and can cause severe___ ___ initially and it infects ____ epithelium initially
  • There it begins to be ___• This infection is associated with ____ ____
  • Throat is infected in that person
  • Start to shed virus and causes it to spread
  • Target cells infected: ___ ____ ____ ____ ____
  • It targets the ___ ___. It causes them to be activated in ____ way
  • Symptoms that occur are due to __ ___being activated and trying to __ ___all of the nonspecifically activated B cells. Get ____ lymphocytes. \
  • Often that works and disease resolves
  • When B cells are replicating the make an ___.

Basis of tests to diagnosis is presence of ___ ___ that are know to cross react with certain ___ on surface of ___ _____

• If B cells aren’t controlled by T cells you can develop ___ ___

A

Pathogenesis of EBV • Initial infection occurs thru saliva • Causes infectious mononucleosis: Kissing Disease • Virus gets into throat and can cause severe sore throat initially and it infects pharyngeal epithelium initially • There it begins to be shed • This infection is associated with Nasopharyngeal carcinoma • Throat is infected in that person • Start to shed virus and causes it to spread • Target cells infected: Brain, lymph nodes, skin, Liver, spleen • It targets the B cell. It causes them to be activated in polyclonal way • Symptoms that occur are due to T cells being activated and trying to kill off all of the nonspecifically activated B cells. Get atypical lymphocytes. • Often that works and disease resolves • When B cells are replicating the make an Ig. Basis of tests to diagnosis is presence of polyclonal Ab that are know to cross react with certain Ag on surface of animal red blood celss • If B cells aren’t controlled by T cells you can develop Burkits Lymphoma

35
Q

EBV—Infectious Mononucleosis

Ig are ____ Ab

Atyipical lymphocytes are called __ ___

Oral signs: Get hemorrhages or ____on the____

A

EBV—Infectious Mononucleosis Ig are Heterophile Ab Atyipical lymphocytes are called Downey cells Oral signs: Get hemorrhages or petechiae on the palate

36
Q

EBV Infection—Epidemiology

  • ____infection
  • 95% of adults are seropositive in developed world

Most have ___ to EBV but didn’t have mono. We had _____infection

  • Infection occurs by age 2 in developing world (people live closer)
  • Transmission via ___ ____ in saliva • ____ FDA-approved drugs or vaccines
A

EBV Infection—Epidemiology • lifelong infection • 95% of adults are seropositive in developed world Most have Ab to EBV but didn’t have mono. We had subclinical infection • Infection occurs by age 2 in developing world (people live closer) • Transmission via asymptomatic shedding in saliva • no FDA-approved drugs or vaccines

37
Q

EBV—Other Syndromes

  • ___lymphoma
  • ____ lymphoma
  • ___ ____ lymphoma in ____ patients
  • ___ ____
  • post-transplant_____e disease
  • ___ ___ in ___patients
A

EBV—Other Syndromes • Burkitt’s lymphoma • Hodgkin’s lymphoma • non-Hodgkin’s lymphoma in HIV+ patients • nasopharyngeal carcinoma • post-transplant lymphoproliferative disease • hairy leukoplakia in HIV+ patients

38
Q

EBV’s Role in Carcinogenesis

Latent infection of ___ cells→ ___ ___ ___

Latent infection in ___ ___ (rare) →____predisposition and ___ ___s → ____

A

EBV’s Role in Carcinogenesis Latent infection of B cells→ PTLD, BL, and HL Latent infection in pharyngeal epithelium (rare) →genetic predisposition and dietary carcinogens → NPC

39
Q

Endemic Burkitt’s Lymphoma

  • ___ ___ ___ ___in equatorial Africa
  • most often occurs in the ____
  • 95% of children in endemic areas infected with EBV by age 3
  • EBV ___ and __ __found in most cases
A

Endemic Burkitt’s Lymphoma • most common childhood cancer in equatorial Africa • most often occurs in the jaw • 95% of children in endemic areas infected with EBV by age 3 • EBV DNA and gene products found in most cases

40
Q

Nasopharyngeal Carcinoma

  • occurs most often in people of ____or Asian ancestry
  • promoting events may be exposure to ____ in foods and carcinogens from s____g
  • higher risk associated with specific____ ___ ____genotypes
  • EBV DNA and gene products found in most cases; reduced responses to _____ signals
A

Nasopharyngeal Carcinoma • occurs most often in people of Chinese or Asian ancestry • promoting events may be exposure to nitrosamines in foods and carcinogens from smoking • higher risk associated with specific HLA class I genotypes • EBV DNA and gene products found in most cases; reduced responses to differentiation signals

41
Q

EBV-Induced Oral Lesion in HIV+ Patients

  • hairy leukoplakia
  • one of the most common, ___-____ ____ diseases in patients with HIV infection
  • generally on ___ ___ of the ____
  • prevalence is about 25% • more common in __ • more common in ___ ___
  • not well-correlated with ___count or onset of ___
  • anti-___and anti-____l therapy reduces prevalence
  • occurs in other i_____ patients (like transplant patients)
  • not ___t or ____
  • often a____c, or mild __, strange sensation, and ___ ___
  • often ___
A

EBV-Induced Oral Lesion in HIV+ Patients • hairy leukoplakia • one of the most common, virally-induced, oral diseases in patients with HIV infection • generally on lateral border of the tongue • prevalence is about 25% • more common in men • more common in cigarette smokers • not well-correlated with CD4 count or onset of AIDS • anti-retroviral and anti-herpesviral therapy reduces prevalence • occurs in other immunosuppressed patients (like transplant patients) • not premalignant or malignant • often asymptomatic, or mild pain, strange sensation, and taste changes • often recurs

42
Q

Pathogenesis of CMV

  • In a normal person you become an ___ ___ or get mild case of _____ (different than EBV because don’t get Heterophile Ab)
  • In baby of seronegative infection • If mother gets infection during pregnancy you can get ____ ____ disease • Virus can cross placenta
  • In people with AIDS or immunosuppressed→ ___ ____ disease
  • productive infection of ____ and other cells
  • latent infection: we don’t know ___ or what ____ it
  • diseases
  • subclinical infection
  • ___ ___
  • oral ____
  • most ___ ___ ____ in ____t patients
  • ____ ____disease—most prevalent ___ ___ disease
A

Pathogenesis of CMV • In a normal person you become an asymptomatic carrier or get mild case of mononucleosis (different than EBV because don’t get Heterophile Ab) • In baby of seronegative infection • If mother gets infection during pregnancy you can get cytomegalic inclusion disease • Virus can cross placenta • In people with AIDS or immunosuppressed→ multisite symptomatic disease • productive infection of epithelial and other cells • latent infection: we don’t know where or what reactivates it • diseases • subclinical infection • infectious mononucleosis • oral ulcerations • most frequent viral pathogen in transplant patients • cytomegalic inclusion disease—most prevalent viral congenital disease

43
Q

CMV Infection—Epidemiology

  • ____ infection
  • recurrent disease ____of contagion
  • ___ shedding
  • transmission
  • ___, ___ ___, all ____
  • ___ and ___ routes
  • in___ and at ___
  • severe cases treated with ____• ____ toxic than acyclovir
  • often reactivated in ____t patients during intense ____
A

CMV Infection—Epidemiology • lifelong infection • recurrent disease source of contagion • asymptomatic shedding • transmission • blood, organ transplants, all secretions • oral and sexual routes • in utero and at birth • severe cases treated with ganciclovir • More toxic than acyclovir • often reactivated in transplant patients during intense immunosuppression

44
Q

CMV in Immunocompomised Patients

  • Opportunistic pathogen
  • ___ primary disease •____t disease

Disease sites • ___, ____, _____/____, ____, ____

A

CMV in Immunocompomised Patients • Opportunistic pathogen • symptomatic primary disease • recurrent disease • Disease sites • lung • retina • colon/esophagus • brain • mouth

45
Q

• HHV-6 • two types—__ and __

___ most prevalent

  • infection ___ in life
  • nearly ___% of adults are seropositive worldwide
  • present in ___ and spread by ___ ___
  • replicates in ___ ___
  • latent infection of ___ and ____
  • controlled by ___ ___ immunity
  • causes high ___ and ___—exanthem subitum (____)
  • problem in ___ individuals
  • can co-infect ____ cells and lead to increased HIV replication
A

• HHV-6 • two types—A and B; B most prevalent • infection early in life • nearly 100% of adults are seropositive worldwide • present in saliva and spread by oral secretions • replicates in salivary glands • latent infection of lymphocytes and macrophages • controlled by cell-mediated immunity • causes high fever and rash—exanthem subitum (roseola) • problem in immunocompromised individuals • can co-infect HIV+ cells and lead to increased HIV replication

46
Q

• HHV-7 • nearly ___% of adults are seropositive • fever___ or ___ rash; similar to ____ • transmitted through ___ and ___ ___

A

• HHV-7 • nearly 100% of adults are seropositive • fever with or without rash; similar to roseola • transmitted through saliva and breast milk

47
Q

• HHV 8

discovered by ___in biopsy specimens of ___ ___ (KS), ___ ___ ___, ____ disease

  • Infects ___ cells, ___ cells, and some ____ cells
  • Encodes several ____ homologues to cellular proteins that promote ___ and prevent ___ of infected cells
  • ___ homologue inhibits ____signaling and tumor cells become dependent on ___ for ____ (viral IL6)

____ homologue (____ protein)

• ___ and chemokine ____s

____ factors • Allow tumors to grow blood vessels

• presence of HHV-8 in blood portends the development of ____

A

• discovered by PCR in biopsy specimens of Kaposi’s sarcoma (KS), primary effusion lymphoma, Castleman’s disease • Infects B cells, spindle cells, and some epithelial cells • Encodes several protein homologues to cellular proteins that promote growth and prevent apoptosis of infected cells • IL-6 homologue inhibits interferon signaling and tumor cells become dependent on vIL-6 for proliferation (viral IL6) • Bcl-2 homologue (Antiapoptic protein) • Chemokines and chemokine receptors • Angiogenic factors • Allow tumors to grow blood vessels • presence of HHV-8 in blood portends the development of KS

48
Q

HHV-8—Epidemiology

  • seroprevalence ____ widely 1-3 % in blood donors in North America • 70% in endemic regions of Africa
  • higher among family members of seropositive persons (probably transmitted via ___)
  • high in injecting ___ ___ and women with ____ sex partners
  • no definitive ___ ___ for infection identified although sexual transmission is suggested in men who have sex with ___
A

HHV-8—Epidemiology • seroprevalence varies widely 1-3 % in blood donors in North America • 70% in endemic regions of Africa • higher among family members of seropositive persons (probably transmitted via saliva) • high in injecting drug users and women with multiple sex partners • no definitive risk factors for infection identified although sexual transmission is suggested in men who have sex with men

49
Q

Kaposi’s Sarcoma

____ lesion Skin, eye, mouth In early days, dentists were first to suspect person was HIV positive

A

Kaposi’s Sarcoma Purplish lesion Skin, eye, mouth In early days, dentists were first to suspect person was HIV positive