Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology > Herpesviruses > Flashcards

Herpesviruses Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

What kind of infection is established by herpes viruses

A

establish life long persistent infections in host w periodic reactivations

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

Names the subfamillies of herpesviridae(family)

A

1.Alphaherpesvirinae
2.Gammaherpesvirinae
3.Betaherpesvirinae

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

Which viruses are in alphaherpesvirinae

A

HSV 1
HSV2
Varicella Zoster virus

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

Which Genus is HSV viruses in

A

simplex virus

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

Which genus is varicella zoster virus in

A

varicellovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which viruses are in gammaherpesvirinae /

A

HHV-4 (Epstein-Barr virus)
HHV-8 (kaposi-sarcoma related virus)

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

What genus is HHV-4 in

A

lymphocryptovirus

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

which genus is HHV-8 in

A

rhandinovirus

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

Which viruses are in betaherpesvirinae

A

HHV-5 (cytomegalovirus)
HHV-6 (Herpes lymphotropic virus)
HHV-7

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

which genus is HHV-5 in

A

Cytomegalovirus

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

Which genus is HHV-6 & HHV-7 in

A

Roseolovirus

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

Whats the difference between the alphaherpesvirinae & betaherpesvirinae

A

A = fast growing + cytolytic
B= slow growing

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

Which viruses in the Herpes viruses is cytolytic

A

All alphaherpesvirinae

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

Which viruses in the herpesvirinae are lymphoproliferative

A

HHV-4
HHV-6
HHV-7

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

Which viruses in Herpesvirinae are cytommegalic

A

HHV-5

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

Where do HSV-1 & HSV-2 establish latency

A

in nerve cells

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

Ho many hours does it take for HSV-1&2 take to complete replication cycle

A

8-16hrs

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

What is the target cell for the HSV-1& 2

A

Mucoepithelial cells

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

What are the portals of entry for HSV 1&2

A

Skin
mucous membranes

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

What is the pathogenesis for HSV-1&2

A

Skin - replicate in mucoepithelial cell - inaved local nerve endings - retrograde flow - to dorsal root ganglia (trigeminal/sacral) where latency established

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What causes reactivation of HSV-1 /2

A

physical stress
infection via (e.g surgery)
fever
Irradiation
menstraul cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What happens during HSV-1 & 2 reactivation

A

viruses travel via anterograde transport to the peripheral site causing replication to occur in skin & mucous membrane leading to :
-cold sores
- viral shedding
- epithelial cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the epidemiology of HSV-1& 2
-incidence?
-recurrence

A

HSV-1 = occurs early in life - young children (6-3yrs) - but stays latent for a lifetime
2 peak incidence = 0-5 & late teens
Recurrences = 45% orally infected & 60% genital herpes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is HSV-1 & HSV-2 spread?

A

HSV-1 = infected secretions ( saliva , tears , hand to mouth , kiss
HSV-2 = genital via sex : oral sex - thus can also be orally infected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are clinical presentations of HSV-1

A

1.Herpes Gingivostomatitis ( pain + bleeding gums)
2.Herpes Labialis ( cold sore ) - vesicle on lip - occur as recurrence of oral HSV
3.Ocular herpes/Keratoconjunctivitis - hand to eye
4. Herpes Whitlow = abrasion on skin & HSV enters - dentist + hospital personell - vesicle appears
5.Herpes gladiatorum - mucocutaneous infection of thorax, ear, nose , face & hands - wrestlers
6.Eczema herpeticum - infection w HSV on pple w eczema
7.(Sporadic) Encephalitis - swelling of brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Symptoms of Herpes Simplex Encephalitis

A

fever
headache
seizures
focal temporal neurologic signs
imparied consiousness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Clinical presentation of HSV-2

A
  1. Genital herpes - ulcerative lesion penis , vagina , cervix ,vulva, perinuem , sacral n roots , spinal & meninges
  2. Neonatal herpes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How is neonatal herpes acquired

A

from mother : inutero , during birth , after birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the 3 category of neonatal herpes exhibited ?

A
  1. Lesion localized to skin
    2.Encephalitis w/wo localised skin lesion
    3.Disseminated disease involving multiple organs + cns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which people with a compromised immunity are at risk on infection with Herpes simples virus

A

1.malnourished children
2.transplanted patients
3.AID patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Whats the immunity like for people with Herpes simplex virus

A

-HSV -1 antibodies appear in childhoos & HSV-2 appear adolesence
-Primary infection: IgM ; IgG & IgA persist for long period
-Cell mediated & nonspecific host factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How can HSV-1 & HSV-2 be diagnosed ?( in the lab)

A

1.PCR = specific + sensitive =PCR on CSF with large numbers of RBCs found in CSF
for genital infections – Tzank smear to show the formation of multinucleated giant cells
2. Cowdry type A intranuclear inclusions has been largely replaced by immunofluorescent staining, which can distinguish HSV-1 from HSV-2
3.Isolation & identiification of virus - identified by neutralization test/immunimmunofluorescence stain w specific antiserum
4.serology
5.cytopathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how is serology of HSV-1 & HSV2 LIMITED ?

A

limited by cross reactivity of HSV-1/2 (share antigens) also in the case of VZV people infected with HSV due to heterotypic anamnestic response ( this is where the immune system responds to pathogen but on a previous encounter w a different but structurally related pathogen - boost your immunity as it protects you from a pathogen that you havent even encountered yet )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

after staining the blood smear / vesicle from HSV1 & HSV2

A

presence of multinucleated giant cells = HSV-1 , HSV-2/ varicella zoster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Treatment of HSV-1 & HSV-2

A

-acyclovir
-valocyvlovir , vidarabine ( used when there is resistance to acyclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

how does acyclovir work?

A

-nucleoside analog - its monophorsphorylated by HSV thymidine kinase & then converted to triphosphate from by cellular kinases
-acyclovir triphosphate incorporated into into viral DNA by HSV polymerase which prevents chain elongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Difference between varicella & zoster ? And are they caused by the same virus?

A

varicella = primary infection + acute
Zoster = reactivation of varicella latent virus in neurons

YES caused by same virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Which cells can vzv virus be grown in

A

• can be grown in cultures of human fibrioblasts , human amnion or HeLa cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Pathogenesis of VZV

A

target cell = mucosa of upper Respiratory tract /conjunctiva
replicate in lymoh nodes
primary viremia spread virus to replicate in liver & spleen
secondary viremia - mononuclear cells infected & transport virus to skin = RASH
latency established via retrograde transport in sensory ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Where is latency established in VZV

A

sensory ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how reactivation of vzv happens

A

triggered by stimulus
travel via anterograde transport from dorsal ganglia to dermatome region innervated by the single nerve
causing severe pain in the area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the spinal cord segment + nerve that is most commonly causing pain in the area they innervate when VZV reactivated

A

T3-L3
Trigeminal nerve ( esp opthalmic branch )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

whats the epidemiology of vzv

A

varicella = children disease
• Zoster = more in adults (10-20%) , usually >50yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How is VZV spread

A

airdroplets
direct contact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are clinical presentations for varicella

A

1.chicken pox - rash + vesicles - last 5 days - infectious 48hr prior rash till vesicles crust
2.Varicella Pneumonia = common in neonates , adults & immunocompromised patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

whats the incubation period for VZV

A

10-21 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are clinical presentation of Herpes zoster

A

1.Severe pain - in area of skin/mucosa supplied by one or more groups of sensory nerves & ganglia and is unilateral - vesicles appear over skin supplied by affected nerves
2.Postherpetic pain- (seen in elderly adults) - protrcted pain that may continue for months
- MC after opthalmic zoster & around the eye
3.Zoster Opthalmicus - reactivation virus in opthalmic div of trigeminal n
- painful blisters on one side of forehead
4.Ramsay Hunt syndrome (herpes Zoster oticus)
• reactivation of latent VZV in geniculate ganglion of facial nerve
5.Varicella Zoster CNS disease (Meningitis)- can present w/wo rashes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

whats the immunity like for VZV

A

• Previous infection w varicella has lifelong immunity to varicella
• Antibodies induced by varicella vaccine persist for atleast 20years
• cell mediated immunity is most important for VZV infections
• increases in varicella antibody may occur w HSV infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Laboratory diagnosis for VZV

A

1.PCR - useful for sensitivity , specificity & rapidity
2.Isolation of VZV from vesicles in tissue culture : not sensitive
3.Serology : most frequently used are :
- FAMA(fluoroscent antibody to membrane antigen)
- ELISA
-Immuno adherant hemagglutination
Tzanck Smear – shows Cowdry type A, intranuclear inclusions; also antigen detection by PCR

50
Q

Treatment of VZV

A

• y-Globulin of high VZV antibody titer can prevent development of illness in patients exposed to varicella who are at high risk of developing severe disease
-only effective if virus has not started
• Anti-viral drugs: acyclovir, valacyclovir , famciclovir , foscarnet
• Post herpetic neuralgia & acute neuritis
- analgesics,gabapentin , amitryptyline , lidocaine patch , glucocorticoid
• varicella - zoster immunoglobulin -for post exposure prophylaxis of high risk patients who lack serologic evidence of immunity

51
Q

True or false? EBV is the most harmful herpesvirus

A

true

52
Q

What are some properties of EBV
- genome
- no genes encoded
- strains of EBV

A

genome = 172kbp
• has G+C content of 59%
• Encodes 100 genes
2 major strains of EBV : type A & type B

53
Q

What is the target cell of VZV

A

mucoepithelial cells of upper respiratory tract

54
Q

Which receptor does EBV bind to & on which cell type

A

CD21 on b cell - and acts as Bcell mitogen

55
Q

Explain pathogenesis of EBV

A
  • Target : mucosal epithelium + B cells
  • virus replicate in epithelium
  • spread to waldeyers ring
  • EBV bind to CD21 receptor ( also receptort for C3d component of complement system)
  • Causes Bcell immortilization w retention of Bcell activity ( production of antibodies )
  • Latent infection established in B cell - viral DNA incorporated into host DNA but remain inactive
  • limited set of genes are exposed : some invariable some variable
56
Q

Which genes are expressed by the EBV during latency

A

EBNA ,
EBER (Rna’s)
LMP ( latent membrane proteins )

57
Q

Which viral gene of EBV is invariable and why ?

A

EBNA-1 - mainatins viral DNA in form of episomes ensuring virus genetic material remains stable in host

58
Q

Which are the variable viral genes of EBV

A

EBNA-2,
EBNA 3
EBNA 3B
EBNA 3C
LP

59
Q

How does EBV evade Immune system

A
  • EBV- Bcell can still produce antibodies
  • Downregulatio of MHC 1 on surface of infected cells thus avoid cytotoxic T cells
  • EBNA-1
60
Q

How can EBV affect memory b cell

A
  • infects preexisting memory Bcells in memory Bcell resevoir
  • Or infected EBV -bcells = differentiate to form infected memory B cells
61
Q

Whats the immune response of EBV infection to Bcells

A

production of atypical reactive CD8+T cells (Downey cells - look like wine spill)
Downey cells may constitute up to 70% of WBC count
heterophile antibodies are produced to B cell mitogenesis

62
Q

Reactivation of EBV

A
  • Triggers such as : weakened immune system , stress , infections , hormonal changes
  • activation of early genes (BZLF1 & BRLF1)
    expressiion of lytics genes
  • viral replication
  • the new virus particles are assembles & released from infected cell causing host cell to burst releasing virus particles into surrounding
  • virus particles go on to infect other cells(like uninfected naive Bcells ) - spreading infection
63
Q

Whats incubation period of EBV

A

4-6weeks

64
Q

What are the 3 CLASSES of viral antigens of EBV

A
  1. Latent phase antigens - EBNA & LMP : EBNA1 is the only one invariably expressed : LMP1 mimics an acitvated growth factor receptor
    - reveals EBV genome is present
    2.early antigens = non structural proteins whose synthesis is not dependent on viral DNA replication
    - production of these indicates onset of viral replication
    3.Late antigens are the structural proteins ( capsid , envelope)
    - are produced in cells undergoing productive viral infection
65
Q

Epidemiology of VZV

A

• EBV occurs in all parts of world
• 90% of adults are seropositive
• Infection occurs early in life (>90% children are infected by 6 years ) = asymptomatic
• Primary infection in adults & adolescents tend to develop infectious mononucleosis

66
Q

Clinical findings of EBV

A
  1. Infectious mononucleosis
    2.Cancer
67
Q

Types of cancer caused by EBV

A
  • Burkitt lymphoma- jaw
  • gastric carcinoma - stomach
  • nasopharyngeal carcinoma - epithelial cells
    -hodgkin & non-hodgkin lymphoma
68
Q

What are major symptoms of infectious mononucelosis + duration of disease

A

SORE THROAT
ENLARGED LYMPH NODE ( posterior auricular cervical lymphadenopathy)
splenomegaly
FATIGUE
fever
malaise
headache

Self limited disease = lasts 2-3 weeks

69
Q

Burkitt lymphoma
- type tumor?
- epidemiology?

A
  • tumor of maxilla & mandible (abdomen in sporadic form)
  • African children + young adult
  • Malaria cofactor = foster enlargement of pool of EBV infected cells
70
Q

Nasopharyngeal carcinoma

A

tumor of epithelial cells
predominately in asia ( chinese men )

71
Q

What clinical presentations are associated with AID patients infected w EBV

A
  • EBV associated lymphoma
  • Oral hairy leukoplakia - epithelial focus of EBV replication
72
Q

how is Hodgkin B Cell Lymphoma of Mixed Cellularity caused by EBV diagnosed

A

diagnosed with Reed-Sternberg cells that look like owl eyes

73
Q

Laboratory diagnosis of EBV

A
  1. PCR assay
  2. nucleic acid hybridization
  3. Heterophile-antibody positive (IgM antibodies that recognize the Paul-Bunnell antigen on sheep and bovine RBCs)
  4. Mono-spot test for rapid diagnosis
  5. Serology
    IgM to viral capsid antigen = indicates current infection
    IgG to viral capsid antigen = Indicates past infection + immunity
74
Q

What is the paul bunnel test

A

Bcell infected with EBV undergo polyclonal explainsion. The antibodies include IgM heterophile antibody
Agglutination of horse or sheep RBC by serum absorbed to exclude natural antibody is basis of this test

75
Q

True or false is CMV the most common cause of congenital infection

A

TRUE

76
Q

How is EBV spread

A

salivary secretions
blood transfusions
semen via sexual contact
organ transplantation

77
Q

Where do EBV establish latency

A

Bcells

78
Q

What is the target cell of EBV

A

mucoepithelial cells
Bcells

79
Q

Properties of CMV

A
  • largest genetic content ( 240kbp)
  • replicates slowly in culture
  • produces cytopathic effect and multinucleated cells can be seen
80
Q

Treatment for EBV

A
  • For uncomplicated Mono, treatment is symptomatic; if mistakenly given amoxicillin or ampicillin, can develop maculopapular rash
  • avoid contact sports due to risk of splenic rupture
    -ACyclovir = reduce EBV shedding from oropharynx
81
Q

Pathogenesis of CMV

A
  • enters through gential tract / upper respiratory tracts
  • CMV infects the salivary glands epithelial cells
  • virus spreads throuhg bloodstream to various organs & tissues
  • establishes a persistent infection in fibroblasts, epithelial cells, and macrophages;
  • latency is established in mononuclear leukocytes like B
    and T cells and macrophages , myeloid progenitor cells
82
Q

Where is latency established by CMV

A

monocytes & myeloid progenitor cells

83
Q

How can reactivation of CMV occur

A

stress
immunodeficieny
immunosuppressive medication

cause viral genetic material to be trasncribed & translated leading to production of new virus particles

84
Q

Whats the incubation period of CMV

A

4-8 weeks

85
Q

How CMV affects normal host , immunosuppressed hosts , congenital & perinatal

A

normal host
• Virus causes systemic infection : lung , liver , oesophagus , colon , kidneys , monocytes , T & B lymphocytes
• cell mediated immunity is depressed w primary infection & may take several months for cellular responses to recover

Immunosuppressed host
- primary infection more severe
-Viral excretion is increased & prolonged

Congenital & perinatal infections
- its severe
• Babies have developmental defect & mental retardation
• Virus can be transmitted inutero(40%) w both primary & reactivated maternal infections
- acquired through delivery / breast milk

86
Q

How is CMV spread

A

• How transmission happens: through close person - person contact
- urine , saliva , semen , breast milk , cervical secretions , blood transfusions

87
Q

Disease caused by CMV in normal hosts

A
  1. infectious mononucleosis syndrome
    - CMV causes 20-50% of heterophil - negative (non-EBV) mononucleosis
    2.Subclinical hepatitis
    3.Hepatosplenomegaly = in children younger than 7 years
88
Q

Disease caused by CMV in immunosuppressed patients

A

1.pneumonia , colitis , retinitis / hepatitis /disseminated infection
2.Virus associated leukopenia = common in solid organ transplant
3. Obliterative bronchiolitis = seen in lung transplant
4.AIDS patients = CMV causes disseminated disease in untreated patients (CD4+ <50-100/ul)
- colitis & chorioretinitis (may cause blindness)

89
Q

Disease caused by CMV in infants

A
  • Cytomegalic inclusion disease
  • isolated pneumonia & hepatitis
90
Q

What two systems does cytomegalic inclusion disease involve

A

1.CNS
2. Reticuloendothelial system

91
Q

Clinical features of cytomegalic inclusion disease

A

*jaundice
*hepatosplenomegaly
*thrombocutis purpura (blueberry muffin baby)
CNS disease
microcephaly
Intrauterine growth retardation
thrombocytopenia(low platelet levels )

Survivors : sensorineural hearing loss in children

92
Q

Immunity to CMV

A

• antibodies to CMV in human sera increases with age (40% in teens to 80% in those more than 60yrs)
• Reactivation of latent infection occurs in presence of humoral immunity
• Presence of antibody in breast milk does not prevent transmission of infection to breastfeeding infants - they protect more againt devt serious disease rather than virus transmission

93
Q

Laboratory diagnosis of CMv

A
  1. PCR
    2.Monoclonal antibodies against viral antigens
    3.Human fibroblast - used for virus isolation & cultured
    -has small foci of swollen translucent cells w large intranuclear inclusions
    owl eye inclusions seen on biopsy
    4.resistance testing - sequence viral kinase & DNA polymerase
    • UL97 Mutations = confer resistance to ganciclovir
    • UL54 mutations = confer resistance to ganciclovir , cidofovir & foscarnet
94
Q

Drugs that can be used for CMV infections

A

Ganciclovir ( nucleoside related to acyclovir)
Cidofovir (nucleoside polymerase inhibitor)
Foscarnet ( analog of inorganic pyrophosphate)
Acyclovir
Valacyclovir
Prophylatic ganciclovir

95
Q

How/who does Ganciclovir work against CMV

A
  • for immunosuppressed patients
    -reduces severity of CMV retinits , esophagitis & colitis , disseminated CMV disease
  • controls progressive hearing loss in neonattes w congenital infect
96
Q

How does Cidofovir & forscarnet work against CMV

A
  • treat CMV retinitis & ganciclovir resitant CMV strains
97
Q

Which patients is acyclovir & valacyclovir used for in CMV Infections

A

bone marroe & renal transplant patients

98
Q

How does prophyaltic gangciclovir work against CMV infections

A

-for solid organ transplant ptnt - prevent devt of CMV disease - must be weighed againt the possibility for ganciclovir to cause leukopenia

99
Q

how to control CMV infections

A

• isolation of newborn w cytomegalic inclusion disease from other newborns
• Screen transplant donor & recipients for CMV antibody to prevent transmissions

100
Q

Where was the first HHV-6 isolated from

A

Blood of patients with AIDS grown in T cell cultures

101
Q

How is HHV-6 spread

A

oral secretions: saliva

102
Q

True or false ? HHV-6 has two variant A&B

A

TRUE

103
Q

Properties of HHV-6

A

Viral DNA = 160-170kbp
has cross reactivity with HHV-7

104
Q

Where does HHV-6 establish latency

A

CD4 T lymphocytes

105
Q

Which receptor does HHV-6 bind to

A

CD46

106
Q

What is the disease caused by both HHV-6 & HHV-7

A

Exanthem Subitum (ROSEOLA INFANTUM /SIXTH DISEASE)

107
Q

Clinical presentation of Sixth disease

A

high temp fever for 3-5 days
can cause febrile seizure
after fever subsides
lacy body rash appears that SPARES FACE

108
Q

Who is most likely affected by sixth disease

A

children (6months - 2yrs)

109
Q

laboratory diagnosis of HHV-7

A

•PCR assay for viral DNA in saliva /blood test
• Seroepidemiologic studies using immunofluorescence tests for serum antibodies

110
Q

True or false ? Are both HHV-6 & HHV-7 T-lymphotropic

A

TRUE

111
Q

Where was the first HHV-7 isoated from ?

A

activated T cells recovered from peripheral blood lymphocyes of a healthy individual

112
Q

Where do HHV-7 infections establish

A

salivary glands

113
Q

Properties of HHV-8

A

Lymphotropic
genome= 156kbp
closely related to EBV & Herpes virus saimiri

114
Q

Diseases caused by HHV-8

A

karposi sarcoma
vascular tumor
multicentric castleman disease
primary effusion lymphoma

115
Q

How is HHV-8 spread

A

oral secretions , vertically ( blood /organ transplants),sexually

116
Q

Clinical features of kaposi sarcoma

A
  • erythematous(skin redness)
  • violaceous lesions on nose , mucus membranes (of GI tract) but not common on hard palate
  • lesions may be present as plaque, patch , macuole/nodule they arise from primitive vascular forming mescenchymal cells
117
Q

What is primary effusion lymphoma caused by HHV-8

A

HHV-8 Infects Bcells as well which can cause B cell lymphoma

118
Q

Epidemiology of HHV-8

A

common in africans
acquires early in life

119
Q

Drugs that can be used to treat HHV-8

A

• Foscarnet , famciclovir , gangciclovir & cidofovir = work against KSHV replication

120
Q

Laboratory diagnosis for HHV-8

A

• PCR assay
• Serologic assays - measure persisent antibody to KSHV by indirect immunofluorescence , western blot , enzyme linked immunosorbent assay format

Microbiology (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions