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MAJOR DNA Viruses Flashcards

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1
Q

Classification of medically important DNA viruses

A

DNA viruses are classified based on starnds

  • dsDNA
  • ssDNA

dsDNA

  • Enveloped
    • icosahedral (HH)
    1. Herpesviridae
    2. Hepadnaviridae
    • complex (P)
    1. Poxviridae
  • Nonenveloped (APP)
    • icosahedral
    1. Adenoviridae
    2. Papillomaviridae
    3. Polyomaviridae

ssDNA

  • Nonenveloped
    • Icosahedral (P)
    1. Parvoviridae
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2
Q

What are 4 general properties of DNA viruses?

A
  • All DNA viruses listed are icosahedral & replicate in the nucleus except for poxviruses
  • All DNA viruses listed are double stranded DNA except for the parvoviruses
  • All DNA viruses listed, except parvoviruses, encode their own DNA-dependent DNA polymerase to replicate the viral genome
  • All DNA viruses listed, except poxviruses, use cellular DNA-dependent RNA polymerases to make viral mRNA
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3
Q

What are 3 potential outcomes of infection with DNA viruses?

A
  1. Latency ==> chronic infection
  • Latently infected cells are not recognized as being infected by CD8+ T cells, thus they are not cleared
  • Virus is not actively replicating, thus there is no available target for antivirals to act upon
  1. Reactivation of productive infection
  • May or may not result in clinical disease, however, infected individual is infectious
  • Infection is endogenous & does not require re-exposure to the virus
  • May be frequent in immunocompromised hosts
  • Recurrent infections are l_ess severe, more localized & cleared more quickly_ because of immunological memory
  1. Transformation ==> oncogenesis
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4
Q

Naked/ “nonenveloped” Icosahedral dsDNA viruses (APP)

A

APP

A= Adenoviridae

P= Papillomaviridae

P= Polyomaviridae

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5
Q

Properties of PARVO-Virus (I think Turkey = Parvo in spanish)

A
  1. ssDNA virus
  2. Parvo= small ==>naked, icosahedral virus
  3. Parvovirus B19 is the only know human pathogen
  4. Erythrovirus genus
    * may be called Erythrovirus B19
  5. Recepter = erythrocyte P antigen –globoside (a type of glycosphinolipid ) on RBCs
  6. Infect RBC precursor (erythroblasts) and endothelial cells in blood vessels
  • Replicates when host cells are in the S phase of the cell cycle (mitotically active)
  • Explains why replication occurs in erythroblasts, not mature RBCs
  • Virus release requires cell lysis ==> drop in mature RBCs ==> anemia
  • Endothelial cell infection ==> rash
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6
Q

Parvovirus B19 course of infection

A

Note:

Rash and arthalgia

  • Erythema infectiosum or 5th disease
    • Most often seen in the 5-14 year age group
    • about 25% of the infections are asymptomatic
    • ~65% of adults have antibodies to B19
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7
Q

Parvovirus B19–Clinical disease

A
  1. Erythema infectiosum (5th disease)
  • Mild cold-like symptoms
  • “lacey” rash on extremities with a confluent (slapped cheek) rash on the face

2. Aplastic anemia

  • Children with chronic anemia (sickle cell anemia; thalassemia) can develop a severe anemia (aplastic crisis)

3. Arthritis

  • Immune complex-mediated
  • Small joints or hands & feet
  • More common in adult women
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8
Q

Erythema Infectiosum

A
  • Virus transmitted via respiratory route & replicates in the nasal passages
  • Phase 1
    • Mild fever; sore throat; runny nose
    • Cold-like symptoms; often unrecognized as Parvovirus B19
    • Infectious stage
  • Phase 2
    • 7-10 days later; virus has been cleared ==> no longer infectious
    • Slapped cheek rash
    • Lacey rash on trunk, arms & legs
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9
Q

Fetal infection associated with Parvovirus (clinical disease)

A

Fetal infection

  • Virus can cross the placenta
  • 1st trimester infection ==> fetal death
  • 2nd trimester infection ==> hydrops fetalis
    • Severe anemia ==> cardiac failure & fluid accumulation (subcutaneous, around lungs, heart & in abdomen) ==> fetal death
  • 3rd trimester infection ==> no apparent clinical symptoms
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10
Q

Parvovirus B19 Dx and Tx

A
  1. Diagnosis
  • Clinical appearance (slapped cheek rash)
  • Serology – can detect past exposure & immunity
  1. Treatment
  • Treat cold-like symptoms during phase 1
  • No treatment for rash; virus has been cleared
  • RBC transfusion in cases of severe anemia (including in fetus)
  1. No vaccine available
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11
Q

What are some properties of Adenoviruses?

A
  1. Naked, icosahedral, ds DNA virus
  2. Receptor = coxsackievirus adenovirus receptor (CAR)
    * Cell adhesion molecule; interacts with extracellular matrix glycoproteins
  3. Infects mucosal epithelial cells of the upper respiratory tract & GI tract
  4. Multiple serotypes cause human disease
  5. Many serotypes infect lymphoid tissue
  • Adenoids, tonsils, Peyer’s patches
  • May be persistent in adenoids and tonsils (children) or intestines (adults); typically not pathogenic
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12
Q

Clinical Dx associated with Adenovirus

A
  1. Many serotypes are transmitted via the respiratory tract & replicate in the nasal passages & airways ==> pharyngitis & conjunctivitis
  • Leading viral cause of pharyngitis
  • Pharyngoconjunctival fever
    • Often associated with outbreaks in summer camps (swimming pool conjunctivitis)
    • Not killed by chlorine treatment of swimming pools
  1. Types 4, 7 & 14 are associated with more severe lower respiratory tract infection
  • Type 14 – emerged in 2005
  • Acute respiratory distress syndrome
  • Outbreaks in military recruits
  1. Types 40 & 41 are associated with gastroenteritis; transmitted fecal/orally
  2. Types 11 & 21 are associated with hemorrhagic cystitis
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13
Q

Adenovirus Dx, management and prevention

A
  1. Diagnosis:
  • Can be isolated in culture
  • Detect viral antigen; PCR for viral sequencs
  • Serology – look for increased antibody titer
  1. Self resolves; treat symptoms
  2. Cidofovir – for severe adenovirus infections in people who are immunocompromised
    * Monophosphate cytidine analogue
  3. Live, nonattenuated oral vaccine against adenovirus types 4 & 7
    * Given to military recruits
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14
Q

What are some properties of Papillomavirus?

A
  1. Naked, icosahedral, ds DNA virus
  2. Tropism for epithelial cells of skin & mucosal membranes
  • Multiple serotypes (>100); tropism depends on serotypes
  • Causes papillomas = benign tumors of squamous cells (also called warts, condyloma or verruca)
  • Carcinoma of cervix, penis or anus
  1. Lytic infections in permissive cells
  2. Transforming infections in non permissive cells
  3. Transmission – direct contact (skin to skin); contaminated fomites; exposure during birth (birth canal); sexual transmission
  • Route of transmission depends on serotype
  • Enters through breaks in the skin; infects basal epithelial cells
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15
Q

Human Palpillomavirus (HPV) productive infection

A
  1. HPV infects basal cells
  2. Induces cell proliferation & thickening in the basal layer, stratum spinosum & stratum granulosum (forms wart)
  3. As cells differentiate, nuclear factors expressed in different layers promote transcription of different viral genes
  4. The late genes encoding structural proteins are expressed in terminially differentiated keratinocytes
  5. New viral particles are shed with dead cells of the upper layer of skin
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16
Q

HPV (Human papillomavirus) productive infection

A
  1. HPV infects basal cells
  2. Induces cell proliferation & thickening in the basal layer, stratum spinosum & stratum granulosum (forms wart)
  3. As cells differentiate, nuclear factors expressed in different layers promote transcription of different viral genes
  4. The late genes encoding structural proteins are expressed in terminially differentiated keratinocytes
  5. New viral particles are shed with dead cells of the upper layer of skin
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17
Q

HPV latent & transforming infections

A
  1. Latent infections
    * Viral DNA is not integrated
  2. Transforming infections
  • Viral DNA is usually integrated
  • Basal cells replace more differentiated epithelial cells
  • Clinical outcome = dysplasia & carcinomas
  1. Integration inactivates an HPV early gene ==> no viral DNA replication but expression of some viral genes
  2. Continued expression of HPV oncogenes E5, E6 & E7 genes
  • E5 protein activates EGF, promotes growth
  • E6 protein binds p53 and targets it for degradation
  • E7 protein binds and inactivates retinoblastoma protein
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18
Q

HPV clincal disease (Part 1 )

A

1. Cutaneous warts

  • Common warts (verruca vulgaris)
    • Often caused by types 2 & 4
    • Usually on hands & knees
  • Flat warts (verruca plana)
    • On hands, face & shins
  • Plantar warts
    • Soles of feet
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19
Q

HPV clincal disease (Part 2 )

A
  1. Genital warts – condylomata acuminata
  • Types 6 & 11
  • Vagina, vulva, cervix, penis, scrotum, around the anus
  1. Laryngeal papillomas
  • Types 6 & 11
  • Benign tumors in the airways
  • Acquired during birth from mother with genital warts
  1. Carcinoma of cervix, penis & anus
    * Types 16 & 18 – most common
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20
Q

HPV Dx

A
  1. Papillomas diagnosed clinically
  2. Infected epithelial cells have a clear halo around a shrunken nucleus & are called koilocytes
    * Papanicolaou (Pap) smears detect HPV-infected cells
  3. PCR can detect HPV sequences

image:

Papanicolaou stain of exfoliated cervicovaginal squamous epithelial cells, showing the perinuclear cytoplasmic vacuolization termed koilocytosis (vacuolated cytoplasm), which is characteristic of human papillomavirus infection (400× magnification).

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21
Q

HPV management and prevention

A

Management

  • May resolve spontaneously
  • Multiple ways to remove warts – freeze with liquid nitrogen (cryotherapy); salicylic acid; podophyllin; surgical removal; interferon (stimulate an immune response)

Recombinant vaccine

  • Nine-valent (Gardasil 9: 6, 11, 16, 18, 31, 33, 45, 52, and 58) vaccine is recommended for girls & boys starting at 11 years of age
  • Yeast cells express a capsid protein
    • L1; viral attachment protein
    • self assembles into a viral-like particle
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22
Q

What are some properties of Polyomavirus?

A
  1. Naked, icosahedral, ds DNA virus
  2. Human pathogens = JC virus & BK virus
  3. Ubiquitous viruses; infection is asymptomatic in immunocompetent individual
    * 80-90% of adults are seropositive for these 2 viruses
  4. Transmission via inhalation or fecal/oral (contact with contaminated water, stool, urine, or saliva)
  5. Infects tonsils & lymphocytes; spreads by viremia to the kidneys
  • Latent infection in the kidneys (BK virus)
  • Latent infection in the kidneys, B cells, monocyte-lineage cells (JC virus)
  • Reactivation of productive infection if individual becomes immunosuppressed
  1. Early genes = T (transformation) antigens
  • Large T & small T antigens
  • Controls viral mRNA transcription; binds to & inactivates p53 & retinoblastoma protein
  • Sends cells through the cell cycle, which facilitates productive viral replication
  • Some cells only permit expression of T antigens, not late genes (structural proteins) – may result in transformation
  1. Late genes = capsid proteins
  • VP1 – major capsid protein & viral attachment protein
  • VP2 & VP3 – minor capsid proteins
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23
Q

JC & BK viruses – course of infection

A
  1. Latent infection in immunocompetent individuals
  2. Clinical disease in immunocompromised individuals
  3. JC virus – Progressive multifocal leukoencephalopathy (PML)
  4. BK virus – hemorrhagic cystitis
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24
Q

JCV Virus and infection of the CNS

A
  1. JCV crosses the blood-brain barrier
    * Replicates in endothelial cells of capillaries
  2. Productive lytic infections of oligodendrocytes & astrocytes
    * Demyelination (destruction of myelin-producing oligodendrocytes)
  3. JCV sequences detected in brain tumors (astrocytoma, oligodendroglioma, medulloblastomas & others)
  • Causes brain tumors in animal models
  • Unclear if it is directly responsible for oncogenesis in human brain tumors
  1. Progressive multifocal leukoencephalopathy (PML) = subacute demyelinating disease
  • ~10% of people with AIDS develop PML
  • >90% fatality rate; often within 2-4 months
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25
Q

JC/BK virus Dx

A
  1. Urine cytologic tests
    * Enlarged cells with dense basophilic intranuclear inclusions consistent with JCV or BKV infection
  2. Detect gene sequences in cerebrospinal fluid, urine, or biopsy material
    * Immunofluorescence; DNA probe analysis; PCR
  3. PML diagnosis
  • Histologic examination of brain tissue (biopsy or autopsy samples) reveal areas of demyelination surrounded by oligodendrocytes with inclusions
  • PCR to detect viral DNA in cerebrospinal fluid
  • Magnetic resonance imaging or computed tomographic showing lesions
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26
Q

List the enveloped viruses

A

dsDNA, icosahedral viruses

  1. Herpesviridae
  2. Hepadnaviridae

sdDNA, complex virus

  1. Poxviridae
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27
Q

What are some properties of Herpesviruses?

A
  1. Enveloped; icosaheral
    * Tegument contains proteins that help initiate viral transcription & inhibit host protein synthesis
  2. DNA virus
  • Latency with the potential for reactivation
  • Immortalization (EBV)
  • Transformation (EBV; KSHV)
  1. (3) Subfamilies – Alpha, Beta & Gamma
  • Organization of the genome
  • Cells associated with productive & latent infection
  • Pathogenesis and disease manifestation
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28
Q

Alpha, Beta and Gamma Herpesviruses

A

See image

29
Q

Cell types infected by herpesviruses “in vivo”

A

See image

30
Q

Common clinical manifestations associated with herpesviruses

A

See image

31
Q

Describe replication of herpes simplex virus (HSV)

A

Replication of herpes simplex virus, a complex enveloped DNA virus.

  1. The virus binds to specific receptors and fuses with the plasma membrane.
  2. The nucleocapsid then delivers the DNA genome to the nucleus. Transcription and translation occur in three phases: immediate early, early, and late.
  3. Immediate early proteins promote the takeover of the cell; early proteins consist of enzymes, including the DNA-dependent DNA polymerase; and the late proteins are structural and other proteins, including the viral capsid and glycoproteins.
  4. The genome is replicated before transcription of the late genes. Capsid proteins migrate into the nucleus, assemble into icosadeltahedral capsids, and are filled with the DNA genome.
  5. The capsids filled with genomes bud through the nuclear and endoplasmic reticulum (ER) membranes into the cytoplasm, acquire tegument proteins, and then acquire their envelope as they bud through the viral glycoprotein-modified membranes of the trans-Golgi network.
  6. The virus is released by exocytosis or cell lysis. GA, Golgi apparatus.
32
Q

Replication of HSV

A
33
Q

HSV–latency and reactivation

A

1. Latency occurs in neurons

  • Virus travels up the axon to the ganglion
    • HSV-1 – trigeminal ganglion
    • HSV-2 – sacral dorsal root sensory ganglion

2. Expression of latency-associated transcripts (LATs) & no other viral gene

  • LATs do not encode a viral protein
  • encode a regulatory microRNA (miRNA) that inhibits expression of viral genes

3. Viral replication is triggered in a neuron

  • Sunlight (UV B radiation); fever; stress – emotional or physical; immunosuppression

4. New viral particle travels down the axon to the site of initial infection & productively infects epithelial cells

34
Q

Latency in *other herpesviruses:

A
  1. Latency in VZV also occurs in neurons
  • Several different transcripts & proteins can be detected in latently infected cells
  • Reactivation results in productive infection in a dermatome enervated by the neuron in which reactivation occurs
  1. Latency in EBV occurs in B cells
    * Some viral proteins are expressed; needed to establish & maintain latency
  2. Latency in CMV occurs in myeloid precursor cells, leukocytes & others
    * LATs have been identified but their role in latency has not been defined
35
Q

Alpha Herpesviruses–transmission

A
  1. HSV – contact with fluid from vesicles
  • Oral herpes – virus present in saliva
  • Genital herpes – sexual transmission
  • Contact between fingers & oral or genital secretions containing virus herpetic whitlow
    • Dentists; gynecologists
    • Thumb sucking – autoinoculation
  • Skin to skin contact (wrestlers) can spread cutaneous HSV (herpetic gladiatorum)
  1. VZV – most transmission is via respiratory route
    * Ulcerating lesions aerosolize the virus; initial replication occurs in the airways
36
Q

HSV clinical disease

A
  1. Clear vesicles on a erythematous base (HSV & VZV have similar lesions)
    * Vesicles ==> ulcers ==> crusted lesions
  2. Fluid in the lesions contain infectious virus
  3. Latency - viral genome exists as an episome in neurons
  4. HSV-1 – primary infection localized throughout the mouth
    * Latency in the trigeminal ganglion
  5. Genital herpes – remains localized at the genital mucosa
    * Latency in the sacral dorsal root ganglion
37
Q

HSV clinical disease part 2

A
  • HSV-1 – important cause of viral encephalitis
  • HSV-2 – can cause meningitis; encephalitis associated with neonatal HSV
  • Both HSV-1 & HSV-2 can cause genital herpes but HSV-2 is a more common cause of genital infection
  • Neonatal herpes is acquired as the baby passes through the birth canal of a mother shedding virus, thus is usually caused by HSV-2
38
Q

VZV—clinical infection

A

Dermatome: area of skin in which sensory nerves derive from a single spinal nerve root

  • Following exposure, VZV infects mucosal dendritic cells of the nasal pharyngeal region, along with Langerhans and plasmacytoid dendritic cells in the respiratory mucosa.
  • VZV-infected dendritic cells migrate to draining lymph nodes where resident T cells become infected and express cutaneous lymphocyte-associated antigen along with chemokine receptor type 4 .
  • The infected CD4+ T cells expressing skin homing factors transit to dermal endothelial cells, where the virus infects dermal fibroblasts and keratinocytes .
  • As the infection proceeds, cytokine-induced inflammation results in the formation of the characteristic varicella rash
39
Q

Reactivation: HSV vs. VZV

A

See image

40
Q

HSV and VZV–DX

A
  1. Tzanck smear – scraping from the base of the lesion
    * syncytia (multinucleated cells) & Cowdry type A intranuclear inclusion bodies
  2. Viral culture (vesicle fluid; not crusted lesions)
  3. Detect viral antigen or DNA in tissue sample or vesicle fluid
    * PCR of CSF used to diagnose herpes encephalitis
  4. Serology
  • with HSV, a significant increase in titer may not occur with reactivation
  • VZV antibody titers do increase in patients with zoster
41
Q

HSV and VZV– management and prevention

A
  1. HSV & VZV can be treated with the antiviral acyclovir
  2. C-section for mothers shedding virus at the time of birth protects the baby from neonatal herpes
    * The risk of neonatal herpes is increased if the mother is having a primary infection as opposed to reactivation of genital herpes
  3. VZV vaccine – protects against both varicella & zoster
    * Attenuated live vaccine
  4. A child who is immunocompromised & develops varicella can be given anti-VZV immunoglobulin
42
Q

Beta Herpesviruses–Transmission and primary infection

A

cytomegalovirus

HHV 6 & HHV 7

43
Q

Beta herpesviruses–clinical diseases

A

HHV 6 & HHV 7

  1. Exanthem subitum (roseola, sixth disease) in infants
  2. HHV-6 more frequently than HHV-7
44
Q

CMV –clinical diseases

A
  1. Mononucleosis-like syndrome
  • Heterophile antibody negative mononucleosis
  • Responsible for 5-10% of cases of infectious mononucleosis
  • Less severe than EBV mononucleosis but similar symptoms
  • Fever, fatigue, lymphadenopathy, malaise, myalgias, headache, splenomegaly
  • Exudative pharyngitis is rare (unlike EBV mononucleosis)
  1. Immunocompromised individuals – at risk for disseminated disease
  • Pneumonia & encephalitis
  • Retinitis & colitis or esophagitis are common manifestations in AIDS patients
  • Responsible for the failure of many kidney transplants
  • Can complicate heart, lung, liver & bone marrow transplants
  1. Cytomegalic inclusion disease
  • Most common viral cause of congenital disease
  • 0.5-2.5% of newborns in the US are infected in utero
  • ~5-10% of infected fetuses – clinical symptoms
  • Symptomatic disease in a newborn is usually associated with a primary infection during pregnancy
    • Hearing loss, visual impairment & mental retardation
  • Reactivation during pregnancy
    • Maternal antibody is protective
    • Healthy newborn but prolonged shedding of virus
45
Q

Gamma Herpesviruses–EBV (Epstein-Barr Virus)

A
  1. EBV receptor = CR2 / CD21 (receptor for C3d component of complement)
  2. Expressed on B cells & epithelial cells of the oropharynx & nasopharynx
  • B cells – productive, immortalizing or latent infection; transformation
  • epithelial cells – productive infection; transformation
  1. MHC class II molecules are used as co-receptor
  2. Proteins associated with productive infection
  • Viral capsid antigen (VCA)
  • Early antigen (EA)
  • Membrane antigen (MA)
  • Zebra – transcription activator; activates immediate early genes
46
Q

Non-productive infection of B cells

A
  1. Latency, immortalization or transformation
  2. Some immediate early genes are expressed
  • Epstein-Barr nuclear antigens (EBNAs 1, 2, 3A, 3B, & 3C)
  • Latent proteins (LP)
  • Latent membrane proteins (LMP 1 & 2)
  • 2 small Epstein-Barr-encoded RNA molecules (EBER1 & 2)
47
Q

Outcomes of infection with EBV (chart)

A
48
Q

Infectious mononucleosis

A
  1. T cell response to EBV-immortalized B cells
  • B cells are stimulated to divide & secrete antibody (polyclonal activation)
  • Heterophile antibodies
    • IgM which recognizes Paul-Bunnell antigen on sheep, horse & bovine erythrocytes
  1. EBV-activated B cells are eliminated by T cells
  • Activation & proliferation of T cells
  • Large, atypical T cells (Downey cells)
  1. Reactivation is common in tonsils & oropharynx
    * Asymptomatic, but virus is shed in saliva
49
Q

Serology for EBV

A
  1. Acute infection is confirmed by detection of :
  • IgM to VCA
  • VCA antibody, but no EBNA antibody
  • EA antibody (not everyone makes antibody to EA)
  1. α-EBNA antibody requires lysis of infected cells
  • occurs as T cells clear the infection
  • associated with convalescence/resolution of infection
  1. Detection of both VCA IgG & EBNA antibodies indicates previous infection

Note:

  • Anti-VCA IgM remains elevated for 2-3 months
  • Anti-VCA IgG in the absence of IgM indicates past exposure; IgG persists for life
  • Anti-EBNA becomes detectable 3-6 weeks after onset of symptoms; persists for life
  • Anti-EA – less useful in diagnosis of mono; detectable 3-4 weeks after onset of symptoms; persist for 3-6 months
50
Q

EBV-associated cancers &HIV associated productive infection

A

Productive infection of epithelial cells occurring in AIDS patients:

Hairy oral leukoplakia – raised, white lesions on the tongue

51
Q

Gamma Herpesviruses–Human herpesvirus 8 (HH8)

A
  • 1994: sequencing data indicated a herpesvirus was present in Kaposi sarcoma tumor cells (KSHV)
  • Infects B cells, endothelial cells, epithelial cells, monocytes
  • Transmission – sexual; possibly saliva, organ transplants, iv drug use
  • Primary infection
    • Immunocompetent – usually asymptomatic
    • Immunocompromised – fever, splenomegaly, lymphoid hyperplasia
  • Transformation
    • Virus expresses proteins with homology to cellular proteins that promote growth & inhibit apoptosis
52
Q

HHV8–clinical diseases

A
  1. Kaposi sarcoma(seen in image)
  • A cancer of the lymphatic endothelial lining
  • bluish-red cutaneous nodules
  1. Primary effusion lymphoma
  • Also called body cavity-based lymphomas
  • Often co-infected with EBV
  1. Multicentric Castleman’s disease
  • Lymphoproliferative disease
  • Fever, splenomegaly, hepatomegaly, generalized lymphadenopathy
  • image details:*
  • This is a view of the medial side of a Kaposi sarcoma (KS) patient’s right heel, displaying the familiar, characteristic violaceous cutaneous plaques indicative of this disease. KS is a malignant tumor of the lymphatic endothelium caused by the human herpesvirus 8 (HHV8), also known as Kaposi’s sarcoma-associated herpesvirus (KSHV), and arises from a cancer of the lymphatic endothelial lining. It is characterized by bluish-red cutaneous nodules. Kaposi’s sarcoma is thought of as an opportunistic infection, affecting patients whose immune systems have been compromised, as in the case of patients with HIV/AIDS.*
53
Q

What are soem properties of Hepadnavirus?

“think Hepatitis”

A
  1. Enveloped, partially ds DNA
  2. DNA virus that replicates through an RNA intermediary
  3. Small spherical; large spherical (Dane particle); or long filamentous particles
  • Dane particle contains the nucleocapsid & is the infectious virus
  • Small & filamemtous particles are empty envelops
54
Q

Hepatitis B virus & Subviral particles

A
  1. HBsAg indicates active infection
    * Acute & chronic
  2. Antibody to HBsAg indicates immunity to HBV
    * Anti-HBsAg recognizes virus & empty particles
55
Q

Describe the HBV Genome:

A
  1. Partially double stranded DNA genome
    • strand – complete
    • strand – partial
  1. P protein:
    * RNA-dependent DNA polymerase with RNase H activity
  2. HBV is a DNA virus that replicates through an RNA intermediate
56
Q

Importance of Gene S and Gene C of HBV genome

A

Gene S – surface glycoprotein (HBsAg)

  • 3 initiation codons ==> small, medium & large HBsAg
  • Particles are composed of different ratios of S, M & L HBsAg

Gene C

  • 2 initiation codons
  • HBcAg = core protein (capsid)
  • HBeAg = secreted protein

Note:

HBsAg, HBcAg & HBeAg – important for interpreting HBV serology

57
Q

HBV replication

Entry & uncoating

A

Entry & uncoating

  • Core particle migrates to the nucleus
  • Partial ds DNA is completed (cccDNA)
    • covalently closed circular DNA
    • stable minichromosome in the nuclei of infected hepatocytes
58
Q

HBV replication

transcription& translation of mRNA

A

Transcription & translation of mRNA

  • Largest mRNA = pre-genome RNA
  • Encapsidated within core along with RT
  • Reverse transcribed into – strand DNA
  • RNase H cleaves RNA
  • Partial + strand DNA made from – strand DNA template
59
Q

HBV replication

Assembly & release

A

Assembly & release

  • Core buds into ER or pre-Golgi
    • Picks up envelop with HBsAg
  • Progeny virions released via exocytosis
    • Empty spheres & filaments containing HBsAg also released
  • HBeAg is secreted by infected cells
    • Not incorporated into progeny virions
    • Marker for higher infectivity
60
Q

HBV Hepatitis

Transmission/ Acute vs Chronic infections

A

Transmission

  • sexual, IV drug use, blood, perinatal (mother to baby during birth)

Acute infection

  • Incubation period – 6 weeks to 6 months
  • fever, fatigue, nausea, abdominal discomfort, dark urine, jaundice
  • duration = 1-3 weeks

Chronic infection

  • Persistence of HBsAg for >6 months is considered a chronic infection
  • Anti-HBc will be positive but anti-HBs will be negative
  • Infants with HBV have ~90% chance of developing chronic infection; adults ~5% chance
  • increased risk for cirrhosis or hepatocellular carcinoma
61
Q

HBV Dx

A

1. Clinical signs:

  • Liver function tests (aspartate aminotransferase, alanine aminotransferase)
  • Jaundice (not always present)
  • RUQ (right upper quadrant) discomfort
  1. Serology & antigen detection
  • HBsAg vs anti-HBs
  • Anti-HBc IgM vs anti-HBc IgG
  • HBeAg vs anti-HBe ==> indicates infectivity
  • first 2 points above (Acute vs. Chronic infection)

3. PCR

  • Detects viral DNA
  • Quantifies viral load in serum
62
Q

HBV management & prevention

A

1. Management:

  • HBV immunoglobulin (HBIG) – post exposure
    • Infants born to infected mothers
    • Spouses of infected patients
    • HCW following needle stick injury
  • Antiviral drugs
    • Inhibit the RNA-dependent DNA polymerase (reverse transcriptase)

2. Prevention:

  • Recombinant vaccine
    • Induces response to HBsAg; administered at: 0, 1, 6 months
    • Unvaccinated individuals at risk of exposure (see notes section)
63
Q

Exmaples of individuals at risk of HBV exposure include:

A

Examples of individuals at risk of exposure to HBV:

  1. high risk groups – Alaska Natives, Pacific Islanders, infants of immigrants from countries with a high prevalence of chronic HBV infection
  2. history of other sexually transmitted diseases
  3. multiple sex partners
  4. sex partners of persons with chronic HBV
  5. health care and public safety workers who have exposure to blood in the workplace
  6. injecting drug users
  7. sexually active homosexual and bisexual men
  8. recipients of clotting‑factor concentrates
64
Q

What are some properties of Poxviruses?

A
  1. Enveloped ds DNA viruses with a complex capsid (oval or brick shaped)
    * Core is within a double membrane & surrounded by a viral envelop
  2. Largest & most complex medically significant virus
  3. Replication occurs in the cytoplasm
    * Encodes a DNA-dependent RNA polymerase & all other enzymes needed for RNA & DNA synthesis
  4. Medically significant pox viruses
  • Variola (smallpox)
  • Molluscum contagiosum virus
65
Q

Smallpox

Describe how smallpox is spread within the body:

A
  1. The virus enters and replicates in the respiratory tract without causing symptoms.
  2. The virus infects macrophages, which enter the lymphatic system and carry the virus to regional lymph nodes.
  3. The virus then replicates and initiates a viremia, causing the infection to spread to the spleen, bone marrow, lymph nodes, liver, and all organs, followed by the skin (rash).
  4. A secondary viremia causes the development of additional lesions throughout the host, followed by death or recovery with or without sequelae.
  5. Recovery from smallpox was associated with prolonged immunity and lifelong protection.
66
Q

General information about Smallpox

A
  1. Eradiated (1977) by widespread vaccination but considered a potential bioterrorism agent
  2. Transmission
    * Respiratory route or contact with virus in skin lesions or on fomites
  3. Asymptomatic incubation period
  4. Rash (pox) follows dissemination to skin
67
Q

Smallpox vaccine

A
  • Vaccine = live attenuated vaccinia virus
    • Pox viruses infecting other animals closely related to variola
    • Vaccina is thought to have been derived from cowpox but it may have been a hybrid with other animal poxviruses
  • Vaccination involves scratching live virus into the patient’s skin with a bifurcated needle
  • Development of vesicles & pustules confirms a response to the vaccine
  • discontinued ~ 1980
    • reintroduced for military personnel & first responders in case of bio warfare
68
Q

Molluscum contagiosum

transmission/Dx/Management/clinical Dz

A

1. Transmission

  • Skin-skin contact or exposure to contaminated fomites
    • Usually in children <5
    • Sexually transmitted in adults

2. Diagnosis

  • Clinical presentation
  • Histology: eosinophilic inclusion bodies in epithelial cells

3. Management

  • Nodules can be removed by scraping, or by applying liquid nitrogen or iodine solutions

4. Clinical disease (image)

  • White, pink or flesh colored dome-shaped papules; develops a central depression (umbilicated)
    • Painless; occurs in crops
    • Usually on chest, arms, legs & face
    • Self-resolving (months to years) except lesions can persist in individuals who are immunocompromised
69
Q
A

microbiology (6 decks)

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