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ID unit 1 > herpes viruses > Flashcards

herpes viruses Flashcards

1
Q

Define the shared properties of all herpesviruses

A

same morphology, large linear dsDNA genomes, lytic and latent phases of replication, labile and easy to kill in environment, viral genome is delivered to host nucleus where it forms an episome.

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2
Q

Structure of herpes viruses

A

spherical, enveloped dsDNA viruses with icosahedral capsid surrounded by tegument

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3
Q

define tegument

A

viral proteins with some RNAs and cellular proteins used to reprogram newly infected host cell

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4
Q

morphology of lytic phase

A

Nuclear and cytoplasmic inclusions. Cytomegalic cells and syncytia formation. Lytic phase kills cells and release infectious particles.

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5
Q

Genes of lytic infection

A

immediate early (IE) genes-set up environment conducive for viral replication and needed for expression of E and L genes.Early (E) genes-encode replication enzymes and nonstructural viral proteins. Late (L) genes- encode viral structural proteins needed for packaging a new virion and egress from infected cell

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6
Q

How do herpes viruses replicate

A

Herpesvirus DNA replication occurs in the nucleus using viral-encoded DNA polymerase and accessory viral proteins. Encapsidation of genome occurs in the nucleus. Thus, intranuclear inclusions (accumulated viral capsid proteins) are often diagnostic on histopathology for herpesvirus infection.

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7
Q

List the alpha herpes viruses, growth rate and location of latency

A

HSV1, HSV2 and VZV. Grow rapidly and lyse infected cells (12-24hrs). Establish latent infection in neurons of peripheral nervous system, primarily sensory nerve ganglia

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8
Q

List the beta herpes viruses, growth rate and location of latency

A

cytomegalovirus, human herpes virus-6, HHV-7. Grow slowly (80-120hrs) and infect wide variety of cells. Establish latent infections in cells of myeloid lineage (neutrophils, basophils, eosinophils,) and endothelial cells. Replication in glandular epithelial cells allows for viral secretion in saliva, urine, breast milk.

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9
Q

List the gamma herpes viruses, growth rate and location of latency

A

EBV, kaposis sarcoma associated herpesvirus. Grow slowly (80-120hrs) and infect wide variety of cells. Replicate in lymphoid cells and undergo lytic replication in epithelial cells, endothelial cells and fibroblasts. Latency in B cells, and endothelial cells. Capable of transforming these cells

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10
Q

HSV-1 and HSV-2 mechanisms of spread

A

Localized oral and genital epithelial lesions and spread only into sensory neurons that innervate the site of epithelial replication. Both are transmitted via mucosal shedding of virus in oral cavity or genital secretions.

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11
Q

VZV mechanism of spread

A

Initially infects upper respiratory epithelium and spreads to lymph noes and reticuloendothelial system (Liver/spleen). Dendritic cells and Tcells are largely the vehicles for dissemination that causes vesicular rash (chickenpox) and spread from local skin sites up sensory neuron axons to the dorsal root ganglia. Primary VZV is transmitted by respiratory droplets.

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12
Q

CMV mechanism of spread

A

Infects various mucosal epithelial cell surfaces (oral or genital). Local replication results in dissemination by peripheral blood monocytes & dendritic cells. Spread via all body fluids and can be transmitted placentally.

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13
Q

EBV mechanism of spread

A

Infects oral mucosal epithelial Cells and adjacent Bcells. Rapidly establishes latency in resting memory Bcells. Transmitted to new host in saliva.

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14
Q

3)list the steps of the general lytic replication cycle of herpesviruses

A

Attachment and entry > uncoating > gene expression > genome replication > virion assembly/ maturation

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15
Q

Function of viral glycoproteins

A

Bind virion to cellular receptor, resulting in conformation change of viral glycoprotein and fusion of viral envelope with cell membrane. Mediate cellular tropism (which cells can be infected) and act as targets of adaptive immune response

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16
Q

Transmission of herpes viruses

A

respiratory secretions: VZV only. Blood transfusions, BMT or SOT: CMV, HHV6, HHV7, EBV and KSHV. Oral/genital mucosa, abraded skin, saliva, cervical/vaginal secretions, semen, breast milk, urine: HSV-1, HSV-2, CMV, HHV6, HHV7, EBV, KSHV

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17
Q

steps of viral gene expression and replication

A

Viral/cellular transactivators stimulate IE gene expression > IE viral proteins activate viral E gene expression > viral gene replication via viral DNA polymerase

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18
Q

steps of virion assembly and egress

A

L protein synthesis of structural viral proteins including capsid result in packaging and egress through ER (tegument is acquired) and gogli, then out of the cell. Expression of capsid proteins in nucleus cause viral inclusions

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19
Q

MOA of antiviral therapy for herpes

A

Nucleoside analogues terminate viral DNA synthesis by integrating into growing viral DNA and preventing chain elongation. They are prodrugs which must be activated by viral kinases (thymidine kinase from HSV and VZV, or UL97 protein kinase from CMV)

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20
Q

List the common antivirals used for HSV, VZV and CMV

A

HSV and VZV: acyclovir. CMV: ganciclovir

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21
Q

Describe innate responses to herpes infection

A

TLRs recognize virus and trigger interferon signaling and initiation of non specific NK and dendritic cells to control lytic infection

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22
Q

describe adaptive responses to herpes infection

A

Primary mechanism of control for primary infection and reactivations is cellular response. T-cell CD8 responses eliminate infected cells. Neutralizing antibodies are generated to herpesvirus glycoproteins

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23
Q

describe herpesvirus countermeasures to the innate immune response

A

block induction of type I interferons and
production of other cytokines. block dendritic cell maturation. prevent complement activation. alter NK cell functionsblock induction of type I interferons and
production of other cytokines. block dendritic cell maturation. prevent complement activation. alter NK cell functionsblock induction of type I interferons and
production of other cytokines. block dendritic cell maturation. prevent complement activation. alter NK cell functionsblock induction of type I interferons and
production of other cytokines. block dendritic cell maturation. prevent complement activation. alter NK cell functionsblock induction of type I interferons and
production of other cytokines. block dendritic cell maturation. prevent complement activation. alter NK cell functions

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24
Q

describe herpes virus countermeasures to adaptive immune response

A

Cytokine and chemokine mimetics and
decoy receptors. Fc receptor binding proteins. Interfere with antigen presentation to T-cellsCytokine and chemokine mimetics and
decoy receptors. Fc receptor binding proteins. Interfere with antigen presentation to T-cellsCytokine and chemokine mimetics and
decoy receptors. Fc receptor binding proteins. Interfere with antigen presentation to T-cellsCytokine and chemokine mimetics and
decoy receptors. Fc receptor binding proteins. Interfere with antigen presentation to T-cellsCytokine and chemokine mimetics and
decoy receptors. Fc receptor binding proteins. Interfere with antigen presentation to T-cells

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25
Q

define latency

A

Maintenance of viral genomes in a cellular reservoir in the absence of the production of infectious viral particles

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26
Q

compare location of HSV1 vs HSV2 latency

A

HSV1- trigeminal ganglion. HSV2- lumbar sacral ganglion

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27
Q

HSV pathogenesis

A

HSV invades through breaks in integument. Cells at and above basal layer are infected and lyse to cause an inflammatory response (papule). Lysis of many cells with resultant cytokines and inflammation leads to fluid production and a

vesicle. Subsequent leukocyte response transforms this into a pustule, which dries to a scab. HSV ascends in the local sensory nerve to reach the dorsal root ganglia and remains there in a latent form for lifeHSV invades through breaks in integument. Cells at and above basal layer are infected and lyse to cause an inflammatory response (papule). Lysis of many cells with resultant cytokines and inflammation leads to fluid production and a
vesicle. Subsequent leukocyte response transforms this into a pustule, which dries to a scab. HSV ascends in the local sensory nerve to reach the dorsal root ganglia and remains there in a latent form for lifeHSV invades through breaks in integument. Cells at and above basal layer are infected and lyse to cause an inflammatory response (papule). Lysis of many cells with resultant cytokines and inflammation leads to fluid production and a
vesicle. Subsequent leukocyte response transforms this into a pustule, which dries to a scab. HSV ascends in the local sensory nerve to reach the dorsal root ganglia and remains there in a latent form for lifeHSV invades through breaks in integument. Cells at and above basal layer are infected and lyse to cause an inflammatory response (papule). Lysis of many cells with resultant cytokines and inflammation leads to fluid production and a
vesicle. Subsequent leukocyte response transforms this into a pustule, which dries to a scab. HSV ascends in the local sensory nerve to reach the dorsal root ganglia and remains there in a latent form for lifeHSV invades through breaks in integument. Cells at and above basal layer are infected and lyse to cause an inflammatory response (papule). Lysis of many cells with resultant cytokines and inflammation leads to fluid production and a
vesicle. Subsequent leukocyte response transforms this into a pustule, which dries to a scab. HSV ascends in the local sensory nerve to reach the dorsal root ganglia and remains there in a latent form for life

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28
Q

HSV1 vs HSV2 location of infection

A

HSV1: above the belt. HSV2: below the belt

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29
Q

describe oral HSV

A

usually HSV1 but can be HSV if oral-genital contact. Most have minor illness. 20% have systemic sx. Herpetic gingivostomatitis can occur, but responds to antivirals. Severe pharyngitis in older pts can b caused by HSV2.

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30
Q

HSV shedding

A

Shedding of infectious virus can occur without any symptoms

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31
Q

describe HSV reactivation and triggers

A

Prodrome of sensory symptoms (hours) followed by tender papule, vesicle then crusting. shortened course compared to first episode. Rarely systemic symptoms. Fever and sun exposure are recognized triggers. Antiviral therapy is not standard of care

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32
Q

complications of HSV-1 in normal host and treatment

A
  1. herpetic keratitis: infection of eye. 2.HSV encephalitis: latent virus in trigeminal ganglion can proceed towards meninges of middle and anterior fossa of skull and middle cerebral artery causing fever, headache, focal CNS findings (seizures). CSF shows mononuclear cells and HSV DNA by PCR. High dose acyclovir IV 8 hrs
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33
Q

clinical course of genital HSV, treatment

A

HSV2 > HSV1. most patients have a minor illness- fever, headache, lesions, 20% have significant symptoms. Illness peaks in 7-10 days; heals in next 1- 2 weeks. Ameliorated by early antiviral therapy.

34
Q

complications of genital HSV

A

urethritis, meningitis, yeast superinfection, perianal/perirectal dz.

35
Q

recurrence of genital HSV

A

Shortened version of first episode infection. Prodrome phase, lasts 4-5 days Mean recurrence frequency is 3-4 recurrences/ year; declines over time. Psychosocial significance. Antiviral therapy decreases morbidity minimally, but is effective as prophylaxis

36
Q

Who is more susceptible to HSV infections

A

People with defective T-cell immunity (including newborns and immunosuppressed). High suspicion if chronic ulcer, chronic crusted lesion, chronic mouth sores

37
Q

Diagnosis of HSV

A

PCR is best (takes 1-2 days) and is the only method for detecting HSV in late lesions such as crusts and drying ulcers.. Immunocytology only takes 2-3 hrs but has low sensitivity

38
Q

VZV latency

A

paraspinal sensory nerve ganglia - dorsal and cranial

39
Q

VZV pathogenesis

A

doplet nuclei in the air or direct contact with fluid or fomites from lesions. Initially infects lymphoid tissue in pharynx where T cells are infected and enter blood to seed multiple organs and the skin.

40
Q

Varicella time course and incubation period

A

Incubation period: 10-21 days. Minor malaise > low grade fever > papules > vesicles > pustules > scabs. Fever ends in 4-5 days and new lesions stop appearing at this time. Lesions are mainly on face and trunk

41
Q

Chickenpox complications

A

Bacterial superinfection of skin lesions. Rare neurological complications (cerebellitis, encephalitis). Pneumonitis (adults). In immunocompromised can cause pneumonitis, hepatitis and encephalitis.

42
Q

VZV and pregnancy

A

VZV can cause fetal damage when it occurs during the first 16-20 weeks of pregnancy

43
Q

Diagnosis of VZV

A

Usually clinical. Can culture from skin lesions, stan early lesions or use PCR in older lesions/scabs. If dz is severe, PCR is commonly used

44
Q

Varicella prevention

A

live attenuated vaccine- two doses administered in childhood

45
Q

Zoster clinical syndrome

A

vesicular rash in a single dermatome (area of skin innervated by a single sensory nerve). Thus the rash does not cross the midline. Usually a painful prodrome in the affected area precedes the
rash by 3-5 days. Systemic symptoms are uncommon. vesicular rash in a single dermatome (area of skin innervated by a single sensory nerve). Thus the rash does not cross the midline. Usually a painful prodrome in the affected area precedes the
rash by 3-5 days. Systemic symptoms are uncommon. vesicular rash in a single dermatome (area of skin innervated by a single sensory nerve). Thus the rash does not cross the midline. Usually a painful prodrome in the affected area precedes the
rash by 3-5 days. Systemic symptoms are uncommon. vesicular rash in a single dermatome (area of skin innervated by a single sensory nerve). Thus the rash does not cross the midline. Usually a painful prodrome in the affected area precedes the
rash by 3-5 days. Systemic symptoms are uncommon.

46
Q

Zoster complications

A

local pain, bacterial superinfection, eye involvement when frist division of trigeminal nerve is affected, muscular weakness, post-herpetic neuralgia (prolonged pain in area of healed skin lesions that may persist for months)

47
Q

Zoster treatment

A

acyclovir- but post herpetic neuralgia remains common in older pts

48
Q

Zoster pathogenesis

A

Latent VZV in neurons reactivates throughout life, but T cell immunity prevents a breakout. As immunity declines with age or immune suppression, VZV propagation down a ganglion may occur. Prodromal pain occurs as the virus travels down the nerve. This boost in immune response usually insures that second cases are not common

49
Q

Zoster prevention

A

VZV vaccine after age 50 to boost immunity

50
Q

CMV latency

A

monocytes, endothelial cells, bone marrow progenitors (CD34+),

51
Q

CMV transmission and Sx - perinatal

A

Sero-positive pregnant women frequently shed CMV into the birth canal. The frequency of shedding increases toward term, and is a major source of initial CMV infection for children. Mothers also shed CMV into their milk. Children
infected from the mother are generally asymptomatic or have a minor “viral” syndrome, which is rarely appreciated. Probably the newborn is partially protected by maternal antibody.Sero-positive pregnant women frequently shed CMV into the birth canal. The frequency of shedding increases toward term, and is a major source of initial CMV infection for children. Mothers also shed CMV into their milk. Children
infected from the mother are generally asymptomatic or have a minor “viral” syndrome, which is rarely appreciated. Probably the newborn is partially protected by maternal antibody.Sero-positive pregnant women frequently shed CMV into the birth canal. The frequency of shedding increases toward term, and is a major source of initial CMV infection for children. Mothers also shed CMV into their milk. Children
infected from the mother are generally asymptomatic or have a minor “viral” syndrome, which is rarely appreciated. Probably the newborn is partially protected by maternal antibody.

52
Q

CMV in early childhood- Sx. Transmission

A

Young children are generally infected by their playmates; infected young children have prolonged CMV shedding. Most children are asymptomatic or have a minor illness. Occasionally a sicker child will be investigated for
prolonged fever or adenopathy. If this occurs hepatitis or pneumonitis may be appreciated.Young children are generally infected by their playmates; infected young children have prolonged CMV shedding. Most children are asymptomatic or have a minor illness. Occasionally a sicker child will be investigated for
prolonged fever or adenopathy. If this occurs hepatitis or pneumonitis may be appreciated.Young children are generally infected by their playmates; infected young children have prolonged CMV shedding. Most children are asymptomatic or have a minor illness. Occasionally a sicker child will be investigated for
prolonged fever or adenopathy. If this occurs hepatitis or pneumonitis may be appreciated.

53
Q

CMV in adolescence- Sx, transmission

A

CMV is sexually transmitted. Periodic shedding throughout life occurs in saliva and genital secretions of previously infected individuals. Infection rates vary with the extent and type of sexual activity

54
Q

Describe CMV mononucleosis- incubation period, Sx, labs

A

Primary CMV infection after puberty. 2-4 week incubation period. Fever, malaise, adenopathy, mild hepatitis, sore throat. Atypical lymphocytes in blood.

55
Q

contrast EBV vs CMV mono

A

In CMV mononucleosis, in contrast to EBV mononucleosis, there are no heterophil antibodies produced. Detecting these antibodies is a common diagnostic test for EBV mononucleosis.

56
Q

CMV diagnosis

A

Culture virus va spin-amplifactin method. Also can detect IgM antibody against CMV (recent infection vs IgG which indicates prior infection). PCR is also used

57
Q

Post transfusion syndrome

A

CMV is found in some circulating lymphocytes in
previously infected people, thus can be present in donated blood. Thus, blood transfusions may lead to a febrile illness that sometimes resembles mononucleosisCMV is found in some circulating lymphocytes in
previously infected people, thus can be present in donated blood. Thus, blood transfusions may lead to a febrile illness that sometimes resembles mononucleosisCMV is found in some circulating lymphocytes in
previously infected people, thus can be present in donated blood. Thus, blood transfusions may lead to a febrile illness that sometimes resembles mononucleosis

58
Q

Who is more susceptible to severe CMV infections?

A

Pts with deficient T cell immunity- pts on steroids, chemo, radiation, post-transplant, HIV. Risk factors include prior infection with CMV (risk of reactivation) or CMV in donor blood. Severity is worse if CMV positive blood given to CMV seronegative recipient, older pts or severe immunosuppression

59
Q

CMV infection in immunocompromised patient- Sx

A

Interstitial pneumonia- severe, often fatal (50%). Can also infect the liver, colon, esophagus, bone marrow and retina

60
Q

CMV treatment

A

Ganciclovir. Acyclovir will not work because CMV does not have the enzyme needed to activate acyclovir. Foscarnet and cidofovir are antivirals with a different mechanism of action, and do not require the activation step, that can be used as an alternative therapy

61
Q

CMV prevention

A

Screen blood products/organs. Prophylactic ganciclovir and/or CMV hyperimmune globulin to inhibit clinical sx. Pre-emptive therapy- monitor CMV in blood regularly and when small amounts of CMV are detected start ganciclovir

62
Q

CMV Primary vs reactivation intrauterine infection and severity of Sx in neonate

A

When the mother is having her first CMV infection the baby is more likely (10%) to be symptomatic at birth and to have a serious illness (10-20% mortality). When the mother has reactivation
disease the baby is rarely symptomatic, but is subject to non-fatal sequellae (hearing
loss) later in childhood. This is due to maternal immunity When the mother is having her first CMV infection the baby is more likely (10%) to be symptomatic at birth and to have a serious illness (10-20% mortality). When the mother has reactivation
disease the baby is rarely symptomatic, but is subject to non-fatal sequellae (hearing
loss) later in childhood. This is due to maternal immunity When the mother is having her first CMV infection the baby is more likely (10%) to be symptomatic at birth and to have a serious illness (10-20% mortality). When the mother has reactivation
disease the baby is rarely symptomatic, but is subject to non-fatal sequellae (hearing
loss) later in childhood. This is due to maternal immunity

63
Q

Describe symptomatic newborn CMV infection

A

hepatitis, bone marrow suppression in the newborn. CMV that occurs early in pregnancy will interfere with development of brain, eyes and ears. Head is small, seizures common.

64
Q

Describe asymptomatic newborn CMV infection

A

normal at birth but has a chance of hearing loss.

65
Q

HHV 6 and HHV7 transmission

A

present in saliva of adults and children of all ages. HHV6 is in the genital tract of women at term and may be transmitted in utero or by breast feeding. Maternal antibody protects against infection early in infancy. HHV6 causes infection in most young children. HHV7 rises slowly through 4 years and peaks from teens to age 30

66
Q

HHV6 and 7 pathogenesis

A

These viruses infect tissues, probably epithelial cells, in the back of throat (?peritonsillar), where circulating B and T cells then become infected and
spread virus throughout the body to cause the characteristic illnessThese viruses infect tissues, probably epithelial cells, in the back of throat (?peritonsillar), where circulating B and T cells then become infected and
spread virus throughout the body to cause the characteristic illness

67
Q

HHV6 and 7 latency

A

B and T cells and their precursors

68
Q

HHV6 and 7 clinical presentation

A

Exanthema subitum (aka roseola infantum): children less than 2, high fever mild lethargy, irritability, injected pharynx, tonsils and tympanic membranes. Diarrhea/ vomiting may occur. Adenopathy of head and neck. Anterior fontanelle bulging in HHV6. Rash begins on trunk and spreads to face, neck, extremities as fever subsides. Rash has rose-pink macules or maculopapules, nonpruritic, coalescing and dissappear in 1-2 days without pigmentation or desquamation. Adults may have mono syndrome

69
Q

HHV6 and 7 in immune compromised

A

If T-cell mediated immunity is defective, multiorgan disease (pneumonia, colitis, hepatitis, bone marrow suppression, encephalitis) may occur

70
Q

HHV 6 and 7 diagnosis and treatment

A

Clinical assessment mainly, but can use PCR in immune compromised. Treatment: none if immune function is adequate. If immune compromised, treat like CMV

71
Q

EBV latency

A

EBNA1 (EB Nuclear antigen 1) links the viral genome to the cellular chromosome so that the virus genome is replicated and partitioned into dividing cells. EBNA2 is a transcription factor that controls EBV-driven transcription and growth,
activating other viral latent genes and a range of cellular-activation genes including the oncogene c-myc.EBNA1 (EB Nuclear antigen 1) links the viral genome to the cellular chromosome so that the virus genome is replicated and partitioned into dividing cells. EBNA2 is a transcription factor that controls EBV-driven transcription and growth,
activating other viral latent genes and a range of cellular-activation genes including the oncogene c-myc.

72
Q

Cancers associated with EBV

A

Burkitt Lymphoma, B cell lymphoma, leiomyosarcoma, nasopharyngeal carcinoma, gastric adenocarcinoma

73
Q

EBV epidemiology

A

> 90% of adults have EBV.

74
Q

EBV pathogenesis

A

EBV from secretions infects epithelial cells in pharynx. B cells in lymphoid tissue (peritonsillar and around pharynx) are infected and viremia seeds lymphoid and reticulo-endothelial structures. T cell immunity develops and destroys EBV infected B cells, causing inflammation and tissue damage recognized as signs/sx of EBV infection. EBV becomes latent in memory B cells leading to salivary shedding

75
Q

EBV clinical manifestations

A

Young children have mild illness- irritability, sore throat, lymphadenopathy. Older pts have infectious mononucleosis- after 4-6 week incubation fever and malaise (released cytokines), exudative pharyngitis, lymphadenopathy, splenomegaly, hepatomegaly/heptatitis, rash (in pts treated with antibiotics), soft palate petechiae and eyelid edema

76
Q

EBV diagnosis

A
  1. heterophil antibodies- aka monospot test. Pt makes antibodies that cross react with animal tissues such as sheep or horse RBCs. 2. EBV-specific antibodies- used if monospot is negative. IgG against EBV capsid indicates prior infection +/- acute. IgM against EBV capsid indicates current infection. IgG to EBV nuclear antigen indicates pas infection..
77
Q

EBV histology

A

Atypical lymphocytes (reactive T cells) seen on blood smear. Not specific for EBV

78
Q

EBV complications

A

Usually cleared within 14 days but may have prolonged fatigue. Pharyngeal swelling may obstruct airway. Neurological syndromes

79
Q

what is kaposis sarcoms

A

angioproliferative inflammatory lesion that is facilitated by suppressed immune function, and also probably by HIV proteins, and cytokines/ growth factors induced by HHV 8

80
Q

HHV8 transmission and latency

A

latency in B cells and is periodically shed asymptomatically in saliva- spread among families. Also sexually transmitted

81
Q

HHV8 clinical manifestations

A

kaposi’s sarcoma, primary effusion lymphoma (B cell malignancy of serosal surfaces in HIV+), and multicentric castlemans disease (lymphoid tumor in both HIV + and -)

82
Q

HHV8 treatment

A

reduce immune suppression and cancer chemo

ID unit 1 (12 decks)

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