Which genome type is characteristic of herpesviruses?
_______-stranded _______
Double-stranded DNA
Which capsid structure characterizes herpesviruses?
A. Helical
B. Complex
C. Icosahedral
D. Filamentous
C. Icosahedral
Which layer surrounds the herpesvirus nucleocapsid?
A. Tegument
B. Matrix capsule
C. Peptidoglycan
D. Lipid core
A. Tegument
Which component predominates in herpesvirus envelopes?
A. Host cholesterol
B. Cellular enzymes
C. Viral phospholipids
D. Viral glycoproteins
D. Viral glycoproteins
The herpesvirus outer envelope originates from what?
A. Viral capsid
B. Cell membrane
C. Host chromosome
D. Nuclear matrix
B. Cell membrane
A patient recovers from primary HSV infection. Which property allows lifelong persistence?
A. Continuous viremia
B. Chromosomal integration
C. Latent infection
D. Persistent extracellular replication
C. Latent infection
Under which circumstance can herpesvirus latency develop?
A. Only after severe disease
B. Only after vesicular disease
C. Only after recurrent disease
D. Without evident primary disease
D. Without evident primary disease
Why may HSV shedding go unnoticed?
A. Viremia masks lesions
B. Lesions may be inapparent
C. Latency blocks inflammation
D. Antibodies prevent symptoms
B. Lesions may be inapparent
Which environmental condition readily damages herpesviruses?
A. High humidity
B. Neutral pH
C. Drying
D. Isotonic saline
C. Drying
Which treatment readily inactivates herpesviruses?
A. Heat
B. Refrigeration
C. Visible light
D. Hypertonic saline
A. Heat
Which substance can readily inactivate herpesviruses?
A. Glucose
B. Albumin
C. Bicarbonate
D. Mild detergent
D. Mild detergent
Herpesviruses are particularly susceptible to which agents?
A. Amino acids
B. Solvents
C. Electrolytes
D. Nucleotides
B. Solvents
Why does normal skin resist HSV infection?
A. It blocks viral penetration
B. It produces antiviral IgG
C. It destroys viral DNA
D. It prevents ganglionic latency
A. It blocks viral penetration
Alphaherpesvirus glycoproteins initially bind which host structure?
A. Integrin receptors
B. Sialic acid
C. MHC class I
D. Heparan sulfate chains
D. Heparan sulfate chains
Heparan sulfate used by HSV is found on:
A. Nuclear histones
B. Cell-surface proteoglycans
C. Cytoplasmic ribosomes
D. Mitochondrial proteins
B. Cell-surface proteoglycans
Binding of HSV glycoprotein to entry receptor triggers:
A. Viral transcription
B. DNA replication
C. Membrane fusion
D. Capsid assembly
C. Membrane fusion
HSV envelope fusion can occur directly with the:
A. Plasma membrane
B. Nuclear membrane
C. Golgi membrane
D. Mitochondrial membrane
A. Plasma membrane
HSV envelope fusion may alternatively occur within the:
A. Lysosome
B. Peroxisome
C. Nucleolus
D. Endosome
D. Endosome
After nucleocapsid transport to nuclear pores, HSV DNA enters the:
A. Cytoplasm
B. Nucleus
C. Golgi
D. Endosome
B. Nucleus
HSV reaches latency after entering which structures?
A. Blood vessel endings
B. Lymphatic channels
C. Nerve cell endings
D. Sweat gland ducts
C. Nerve cell endings
HSV travels from peripheral nerve endings toward:
A. Ganglion cell bodies
B. Epidermal keratinocytes
C. Regional lymph nodes
D. Bone marrow cells
A. Ganglion cell bodies
HSV latency is established primarily within which site?
A. Epidermal basal cells
B. Hepatic macrophages
C. Bone marrow cells
D. Peripheral sensory ganglia
D. Peripheral sensory ganglia
Besides sensory ganglia, HSV may establish latency in:
A. Germinal centers
B. Autonomic ganglia
C. Splenic sinusoids
D. Renal glomeruli
B. Autonomic ganglia
During lytic (active) infection, the herpesvirus genome enters the cell host nucleus as a linear, double-stranded DNA molecule.
However, to establish stable long-term latency without integrating into human DNA, the viral genome undergoes significant conformational and chromatin _______.
modifications
Latent herpesvirus DNA persists in the nucleus as an:
A. Episome
B. Provirus
C. Transposon
D. Viroid
A. Episome
A herpesvirus episome is most analogous to a:
A. Ribosome
B. Chromosome
C. Prion
D. Plasmid
D. Plasmid
Viral gene transcription during herpesvirus latency is generally:
A. Extensive
B. Minimal
C. Continuous
D. Unregulated
B. Minimal
Immediate-early HSV transcription is assisted by factors carried in the:
A. Tegument
B. Envelope lipids
C. Host nucleus
D. Viral DNA
A. Tegument
Where is the herpesvirus tegument located?
A. Inside viral genome
B. Outside viral envelope
C. Within host nucleus
D. Between capsid and envelope
D. Between capsid and envelope
Immediate-early HSV proteins primarily activate expression of:
A. Late genes
B. Early genes
C. Host genes
D. Latency genes
B. Early genes
HSV early-gene products are primarily required for:
A. Viral DNA replication
B. Virion attachment
C. Axonal transport
D. Membrane fusion
A. Viral DNA replication
Which event occurs before HSV late-gene expression?
A. Capsid release
B. Neuronal transport
C. Envelope fusion
D. Viral DNA synthesis
D. Viral DNA synthesis
Following viral DNA synthesis, which genes are expressed?
A. Immediate-early genes
B. Viral late genes
C. Latency genes
D. Host repair genes
B. Viral late genes
Which proteins are included among HSV late products?
A. Host transcription factors
B. Cellular proteoglycans
C. Viral glycoproteins
D. Heparan sulfate
C. Viral glycoproteins
Herpesvirus late glycoproteins are inserted into:
A. Cell membranes
B. Viral DNA
C. Host ribosomes
D. Nuclear chromatin
A. Cell membranes
Acyclovir blocks HSV DNA synthesis. Which downstream process is most directly reduced?
A. Immediate-early transcription
B. Viral attachment
C. Tegument entry
D. Late-gene expression
D. Late-gene expression
How does herpesvirus acquire its final glycoprotein-rich envelope?
A. Nuclear membrane disruption
B. Budding into cytoplasmic vacuoles
C. Direct plasma membrane synthesis
D. Capsid-mediated membrane fusion
B. Budding into cytoplasmic vacuoles
The vacuoles used for herpesvirus envelopment arise from the:
A. Rough endoplasmic reticulum
B. Nuclear envelope
C. Lysosomal membrane
D. Golgi apparatus
D. Golgi apparatus
After final envelopment, mature herpesvirions reach the cell surface through:
A. Cytoplasmic vacuoles
B. Nuclear pores
C. Axonal vesicles
D. Ribosomal transport
A. Cytoplasmic vacuoles
How are mature herpesvirions ultimately released from infected cells?
A. Cell lysis
B. Endocytosis
C. Exocytosis
D. Transcytosis
C. Exocytosis
The effectiveness of cellular immunity against herpesviruses varies primarily with:
A. Sex
B. Blood type
C. Age
D. Body mass
C. Age
Developing neonatal organs may worsen HSV disease because their cells have greater:
A. Adaptive resistance
B. Antibody production
C. Interferon secretion
D. Innate viral susceptibility
D. Innate viral susceptibility
Why does herpes zoster become more common with aging?
A. Increased viral replication
B. Antiviral immune senescence
C. Increased epithelial turnover
D. Enhanced antibody affinity
B. Antiviral immune senescence
HSV and VZV primarily destroy which cells during mucocutaneous replication?
A. Epithelial cells
B. Fibroblasts
C. Endothelial cells
D. Macrophages
A. Epithelial cells
HSV and VZV epithelial destruction initially produces which lesion?
A. Papule
B. Pustule
C. Vesicle
D. Nodule
C. Vesicle
What typically happens to herpesvirus vesicular lesions?
A. They calcify
B. They rupture
C. They become nodules
D. They undergo fibrosis
B. They rupture
After herpesvirus vesicles rupture, what remains?
A. Deep necrotic ulcers
B. Painless black eschars
C. Raised verrucous plaques
D. Shallow gray-white ulcers
D. Shallow gray-white ulcers
Herpetic ulcers typically occur on which background?
A. Pale base
B. Necrotic base
C. Purpuric base
D. Erythematous base
D. Erythematous base
Which environmental exposure can reactivate latent HSV?
A. Cold weather
B. Sunburn
C. High humidity
D. Mild exercise
B. Sunburn
Which physiologic event can trigger HSV reactivation?
A. Ovulation
B. Pregnancy
C. Menstruation
D. Lactation
C. Menstruation
Which infectious event can trigger latent HSV reactivation?
A. Systemic infection
B. Local colonization
C. Asymptomatic bacteriuria
D. Remote vaccination
A. Systemic infection
Which host condition can promote HSV reactivation?
A. Hyperlipidemia
B. Hypertension
C. Immune impairment
D. Iron deficiency
C. Immune impairment
Which psychological factor may reactivate HSV?
A. Mild boredom
B. Sleep duration
C. Social isolation
D. Emotional stress
D. Emotional stress
Reactivated HSV reaches peripheral epithelial cells by traveling down:
A. Axonal processes
B. Lymphatic vessels
C. Capillary beds
D. Epidermal ducts
A. Axonal processes
After reactivation, HSV infects which nearby cells?
A. Ganglion neurons
B. Mucocutaneous epithelial cells
C. Circulating lymphocytes
D. Vascular endothelial cells
B. Mucocutaneous epithelial cells
HSV-1 can spread from peripheral nerves into the CNS and cause:
A. Transverse myelitis
B. Encephalitis
C. Cerebellar abscess
D. Bacterial meningitis
B. Encephalitis
HSV-1 encephalitis characteristically produces what inflammatory pattern?
A. Unilateral focal inflammation
B. Symmetric diffuse inflammation
C. Multifocal spinal inflammation
D. Predominantly meningeal inflammation
A. Unilateral focal inflammation
HSV-1 encephalitis is notable for being unusually:
A. Self-limited and mild
B. Relapsing and painless
C. Slowly reversible
D. Progressive and destructive
D. Progressive and destructive
A healthy child develops neurologic symptoms after chickenpox. Which complication is most characteristic?
A. Peripheral neuropathy
B. Temporal lobe necrosis
C. Cerebellar ataxia
D. Spinal cord infarction
C. Cerebellar ataxia
A clinician scrapes a suspected HSV lesion. Which test can directly detect viral DNA?
A. Gram stain
B. Viral culture
C. Heterophile antibody test
D. Polymerase chain reaction
D. Polymerase chain reaction
Direct fluorescent testing of an HSV lesion uses antibodies targeting:
A. Host DNA
B. Viral antigens
C. Cellular enzymes
D. Viral RNA
B. Viral antigens
Which combination establishes a definitive HSV diagnosis?
A. PCR and Gram stain
B. Culture and serology
C. Cytopathic changes and immunofluorescence
D. Biopsy and heterophile testing
C. Cytopathic changes and immunofluorescence
Which antiviral is especially useful against several herpesviruses?
A. Acyclovir
B. Ribavirin
C. Oseltamivir
D. Remdesivir
A. Acyclovir
Acyclovir is structurally an analog of which molecule?
A. Adenosine
B. Cytidine
C. Thymidine
D. Guanosine
D. Guanosine
Acyclovir is initially phosphorylated primarily by:
A. Host ribosomal enzymes
B. Herpesvirus enzymes
C. Cellular mitochondrial enzymes
D. Host nuclear polymerases
B. Herpesvirus enzymes
Why is acyclovir selectively active in infected cells?
A. Host enzymes rapidly activate it
B. It enters only infected cells
C. Viral enzymes phosphorylate it
D. Uninfected cells lack DNA
C. Viral enzymes phosphorylate it
After activation, acyclovir is incorporated into:
A. Viral DNA
B. Host RNA
C. Viral proteins
D. Cellular membranes
A. Viral DNA
Once incorporated into viral DNA, acyclovir acts as a:
A. Polymerase activator
B. Base-pair stabilizer
C. Proofreading inhibitor
D. Chain-terminating nucleotide
D. Chain-terminating nucleotide
Why does acyclovir have little toxicity in uninfected cells?
A. It cannot enter cells
B. Cell enzymes poorly phosphorylate it
C. Host DNA excludes guanosine
D. Cellular polymerases destroy it
B. Cell enzymes poorly phosphorylate it
Which drug is a guanosine analog related to acyclovir?
A. Ganciclovir
B. Valacyclovir
C. Penciclovir
D. Foscarnet
C. Penciclovir
Which route is particularly useful for penciclovir?
A. Topical
B. Intramuscular
C. Inhaled
D. Intrathecal
A. Topical
Why is penciclovir poorly suited for oral therapy?
A. Excessive nephrotoxicity
B. Rapid viral resistance
C. Severe marrow suppression
D. Poor oral bioavailability
D. Poor oral bioavailability
Valacyclovir is a prodrug of which antiviral?
A. Penciclovir
B. Acyclovir
C. Ganciclovir
D. Cidofovir
B. Acyclovir
Famciclovir is a prodrug of which antiviral?
A. Acyclovir
B. Ganciclovir
C. Penciclovir
D. Foscarnet
C. Penciclovir
Valacyclovir and famciclovir are commonly used to treat:
______ or ______ disease
HSV or VZV disease
Which herpesvirus subfamily includes cytomegalovirus?
A. Alphaherpesvirus
B. Betaherpesvirus
C. Gammaherpesvirus
D. Deltaherpesvirus
B. Betaherpesvirus
Which virus is the prototype gammaherpesvirus?
A. Cytomegalovirus
B. HHV-6
C. Epstein-Barr virus
D. Varicella-zoster virus
C. Epstein-Barr virus
Community-acquired CMV and EBV initially contact which surfaces?
A. Keratinized surfaces
B. Mucosal surfaces
C. Serosal surfaces
D. Synovial surfaces
B. Mucosal surfaces
Which mucosal site commonly permits CMV acquisition?
A. Conjunctiva
B. Nasopharynx
C. Oropharynx
D. Rectum
C. Oropharynx
Which additional mucosal site permits community CMV acquisition?
A. Genital tract
B. Bronchial tree
C. Middle ear
D. Urinary bladder
A. Genital tract
In many populations, infants most commonly acquire CMV through:
A. Placental blood
B. Respiratory droplets
C. Breast milk
D. Skin contact
C. Breast milk
Which behavior also commonly transmits CMV during adolescence?
A. Shared utensils
B. Sexual contact
C. Casual touching
D. Aerosol inhalation
B. Sexual contact
CMV is best classified epidemiologically as which infection?
A. Vector-borne infection
B. Foodborne infection
C. Sexually transmitted infection
D. Zoonotic infection
C. Sexually transmitted infection
CMV crosses which structure to infect a fetus?
A. Amnion
B. Placenta
C. Chorion
D. Cervical epithelium
B. Placenta
Transplacental CMV infection produces which condition?
A. Neonatal HSV
B. Congenital CMV
C. Acquired EBV
D. Zoster infection
B. Congenital CMV
A newborn with congenital CMV is at risk for permanent:
A. Hearing loss
B. Cataracts only
C. Renal agenesis
D. Limb defects
A. Hearing loss
Congenital CMV can cause severe disease involving primarily which system?
A. Musculoskeletal system
B. Nervous system
C. Endocrine system
D. Gastrointestinal system
B. Nervous system
Besides community exposure, which patients are at special CMV and EBV risk?
A. Hospitalized patients
B. Healthy athletes
C. Schoolchildren
D. Outdoor workers
A. Hospitalized patients
CMV and EBV attachment involves which host molecules?
A. Integrins
B. Glycosaminoglycans
C. Cadherins
D. Selectins
B. Glycosaminoglycans
One CMV/EBV entry pathway involves receptor binding followed by:
A. Plasma membrane fusion
B. Nuclear membrane fusion
C. Direct DNA injection
D. Ribosomal entry
A. Plasma membrane fusion
The second CMV/EBV entry pathway begins with receptor binding followed by:
A. Budding
B. Internalization
C. Exocytosis
D. Nuclear import
B. Internalization
After internalization, CMV/EBV fusion requires what condition?
A. Neutral pH
B. Alkaline pH
C. Acidic pH
D. Hypertonic pH
C. Acidic pH
Acid-dependent fusion releases which structures from endocytic vesicles?
A. Ribosomes and RNA
B. Nucleocapsid and tegument
C. Glycoproteins and lipids
D. Histones and enzymes
B. Nucleocapsid and tegument
EBV gp350/220 binds which B-cell receptor?
A. CD4
B. CD8
C. CD21
D. CD28
C. CD21
EBV enters epithelial cells optimally at which pH?
A. Neutral pH
B. Acidic pH
C. Alkaline pH
D. Variable pH
A. Neutral pH
EBV entry into epithelial cells requires which process?
A. Clathrin endocytosis
B. Macropinocytosis
C. Phagocytosis
D. No endocytosis
D. No endocytosis
Which proteins are sufficient for EBV membrane fusion?
A. gB, gH, gL
B. gp42, gp120, gp41
C. gB, gp42, CD21
D. gp350, gL, CD4
A. gB, gH, gL
Virions lacking gp42 infect which cells more efficiently?
A. B lymphocytes
B. Epithelial cells
C. T lymphocytes
D. Monocytes
B. Epithelial cells
Compared with gp42-containing virions, gp42-deficient EBV shows enhanced infection of:
A. Neurons
B. Hepatocytes
C. Epithelial cells
D. Macrophages
C. Epithelial cells
After CMV or EBV penetrates a cell, the nucleocapsid is transported toward the:
A. Nucleus
B. Golgi apparatus
C. Lysosome
D. Plasma membrane
A. Nucleus
CMV and EBV nucleocapsid transport likely depends on:
A. Actin depolymerization
B. Ribosomal movement
C. Microtubular transport
D. Nuclear diffusion
C. Microtubular transport
Herpesvirus assembly occurs in which cellular compartments?
A. Nucleus and golgi
B. Cytoplasm and golgi
C. Nuclear and cytoplasmic
D. Golgi and cytoplasmic
C. Nuclear and cytoplasmic
During replication, CMV and EBV DNA initially forms long:
A. Concatemers
B. Episomes
C. Proviruses
D. Plasmids
A. Concatemers
A concatemer consists of repeated copies of:
A. Viral proteins
B. Host chromosomes
C. Viral transcripts
D. Genome-length viral DNA
D. Genome-length viral DNA
During capsid maturation, concatemers are cleaved into:
A. Short RNA fragments
B. Unit-length genomes
C. Episomal circles
D. Host-sized chromosomes
B. Unit-length genomes
Unit-length herpesvirus genomes are generated during:
A. Initial attachment
B. Viral penetration
C. Immediate-early transcription
D. Packaging and capsid maturation
D. Packaging and capsid maturation
Nucleocapsids initially exit the nucleus by budding through the:
A. Golgi membrane
B. Nuclear membrane
C. Plasma membrane
D. Endosomal membrane
B. Nuclear membrane
After leaving the nucleus, nucleocapsids acquire which layer?
A. Tegument
B. Capsid
C. Glycocalyx
D. Peptidoglycan
A. Tegument
Final CMV and EBV envelopment occurs through the:
A. Nuclear pathway
B. Endocytic pathway
C. Secretory pathway
D. Mitochondrial pathway
C. Secretory pathway
Latent herpesvirus infection is characterized by what gene-expression pattern?
A. Continuous
B. Restricted
C. Unregulated
D. Complete
B. Restricted
During latent infection, Epstein-Barr virus nuclear antigen 1 (EBNA-1) primarily ensures that viral episomes are:
A. Maintained and partitioned
B. Cleaved and packaged
C. Fused and internalized
D. Transcribed and translated
A. Maintained and partitioned
During latent infection and proliferation of host cells, Epstein-Barr virus (EBV) DNA persists primarily as a:
A. Self-replicating episome
B. Integrated linear provirus
C. Host chromosomal insertion
D. Cytoplasmic plasmid
A. Self-replicating episome
Which latent EBV protein provides cellular growth signals?
A. EBNA-1
B. gp42
C. gp350/220
D. LMP1
D. LMP1
Which additional EBV latent protein promotes growth signaling?
A. gB
B. gH
C. LMP2a
D. EBNA-2
C. LMP2a
LMP1 and LMP2a expression ultimately promotes:
A. Viral DNA cleavage
B. Cellular proliferation
C. Capsid degradation
D. Membrane acidification
B. Cellular proliferation
Restricting Epstein-Barr virus (EBV) gene expression during latency primarily serves to limit:
A. Host lymphocyte recognition
B. Viral DNA replication
C. Episomal genome maintenance
D. Host cell proliferation
A. Host lymphocyte recognition
How frequently does EBV reactivate from latency in vivo?
A. Sporadically
B. Continuously
C. Predictably
D. Never
A. Sporadically
EBV reactivation is especially likely with defective virus-specific:
A. B-cell responses
B. Neutrophil responses
C. NK-cell responses
D. T-lymphocyte responses
D. T-lymphocyte responses
Which treatment can predispose to EBV reactivation?
A. Antacid therapy
B. Antihistamine therapy
C. Antibiotic therapy
D. Cytotoxic therapy
D. Cytotoxic therapy
Which additional therapy increases risk of EBV reactivation?
A. Immunosuppressive therapy
B. Bronchodilator therapy
C. Anticoagulant therapy
D. Antipyretic therapy
A. Immunosuppressive therapy
MicroRNAs involved in herpesvirus regulation are classified as:
A. Coding RNAs
B. Noncoding RNAs
C. Ribosomal RNAs
D. Transfer RNAs
B. Noncoding RNAs
MicroRNAs primarily regulate gene expression at which level?
A. DNA replication
B. Translation initiation only
C. Posttranscriptional regulation
D. Chromosomal segregation
C. Posttranscriptional regulation
Cytomegalovirus (CMV) and Epstein-Barr virus (EBV) disseminate throughout the human host primarily as:
A. Cell-associated virus
B. Free-floating plasma virions
C. Aerosolized viral particles
D. Extracellular naked episomes
A. Cell-associated virus
EBV cellular tropism prominently includes which lymphocytes?
A. T lymphocytes
B. B lymphocytes
C. NK lymphocytes
D. Plasma cells
B. B lymphocytes
Besides B lymphocytes, EBV prominently infects which cells?
A. Hepatocytes
B. Neurons
C. Fibroblasts
D. Epithelial cells
D. Epithelial cells
Anti-TNF antibodies can increase the risk of severe:
A. HSV infection and CMV
B. Influenza and CMV
C. CMV and EBV infections
D. Adenovirus and EBV infections
C. CMV and EBV infections
Anti-TNF antibodies are commonly used to treat:
A. Rheumatologic diseases
B. Viral encephalitis
C. Bacterial meningitis
D. Congenital infections
A. Rheumatologic diseases
CMV encodes a functional homolog of which two cytokines?
IL-____ and IL-____
IL-8 and IL-10
Cytomegalovirus (CMV)-encoded cytokine homologs and chemokine receptors primarily function to promote:
A. Viral persistence
B. Host viral clearance
C. Neutralizing antibody production
D. Complement cascade activation
A. Viral persistence
CMV immune-modulating proteins alter which host response?
A. Inflammatory response
B. Coagulation response
C. Endocrine response
D. Hematopoietic response
A. Inflammatory response
A young adult develops low-grade fever, fatigue, pharyngitis, and cervical adenopathy after primary infection. Which syndrome is most likely?
A. Scarlet fever
B. Acute mononucleosis
C. Serum sickness
D. Viral exanthem
B. Acute mononucleosis
Which physical finding commonly accompanies acute mononucleosis?
A. Hepatic bruit
B. Ascites
C. Splenomegaly
D. Clubbing
C. Splenomegaly
Which lymph node finding commonly occurs in acute mononucleosis?
A. Cervical lymphadenopathy
B. Inguinal lymphadenopathy
C. Hilar lymphadenopathy
D. Mesenteric lymphadenopathy
A. Cervical lymphadenopathy
Which blood finding can accompany acute mononucleosis?
A. Neutropenia
B. Eosinophilia
C. Thrombocytosis
D. Monocytosis
D. Monocytosis
Peripheral blood in acute mononucleosis may contain which lymphocytes?
A. Immature
B. Atypical or reactive
C. Naive only
D. Anergic only
B. Atypical or reactive
A patient has mononucleosis symptoms but a negative heterophile test. Which virus can cause this syndrome?
A. CMV
B. VZV
C. HSV-2
D. HHV-6
A. CMV
CMV infection has been strongly associated with development of:
A. Coronary artery disease
B. Aortic dissection
C. Venous thrombosis
D. Mitral stenosis
A. Coronary artery disease
Persistent CMV and EBV infections are associated with chronic:
A. Endocrine disorders
B. Inflammatory diseases
C. Coagulation disorders
D. Metabolic syndromes
B. Inflammatory diseases
Persistent CMV and EBV infections are also associated with human:
A. Autoantibodies
B. Immunodeficiencies
C. Cancers
D. Hemoglobinopathies
C. Cancers
A transplant recipient develops fever, lymphadenopathy, hepatitis, and hematologic abnormalities. Which infection is most likely?
A. Acute EBV
B. Acute VZV
C. Acute HSV
D. Acute CMV
D. Acute CMV
Which organ involvement commonly accompanies transplant-associated acute CMV?
A. Pancreatitis
B. Hepatitis
C. Nephritis
D. Myocarditis
B. Hepatitis
Late cytomegalovirus (CMV) reactivation and disease in allogeneic stem cell transplant recipients is most strongly associated with an increased severity of:
A. Graft-versus-host disease
B. Host-versus-graft rejection
C. Serum sickness
D. Post-transplant lymphoproliferative disorder
A. Graft-versus-host disease
Late CMV disease increases transplant-related:
A. Fertility
B. Bone density
C. Vaccine response
D. Morbidity
D. Morbidity
EBV reactivation after transplantation can induce marked:
A. Lymphoproliferation
B. Neutropenia
C. Fibrosis
D. Erythrocytosis
A. Lymphoproliferation
Which virus is clearly considered oncogenic?
A. CMV
B. HSV-1
C. VZV
D. EBV
D. EBV
Which malignancy is associated with EBV?
A. Hodgkin lymphoma
B. Follicular lymphoma
C. CLL
D. Multiple myeloma
A. Hodgkin lymphoma
Which lymphoma has a classic EBV association?
A. Mantle cell lymphoma
B. Burkitt lymphoma
C. Marginal zone lymphoma
D. Diffuse follicular lymphoma
B. Burkitt lymphoma
Which epithelial malignancy is strongly associated with EBV?
A. Oral squamous carcinoma
B. Thyroid carcinoma
C. Nasopharyngeal carcinoma
D. Renal cell carcinoma
C. Nasopharyngeal carcinoma
Which additional carcinoma is associated with EBV?
A. Hepatocellular carcinoma
B. Colon carcinoma
C. Pancreatic carcinoma
D. Gastric carcinoma
D. Gastric carcinoma
EBV latent membrane proteins promote carcinogenesis by increasing:
A. Cellular proliferation
B. DNA repair
C. Antigen presentation
D. Interferon secretion
A. Cellular proliferation
EBV latent membrane proteins also promote cancer by limiting:
A. Mitosis
B. Apoptosis
C. DNA synthesis
D. Protein translation
B. Apoptosis
Which method can diagnose CMV or EBV infection?
A. Virus isolation
B. Sweat chloride testing
C. Coombs testing
D. Osmotic fragility testing
A. Virus isolation
CMV and EBV diagnosis can include detection of viral:
A. Hormones
B. Antigens
C. Electrolytes
D. Lipoproteins
B. Antigens
Another diagnostic strategy detects viral:
A. Phospholipids
B. Steroids
C. Nucleic acids
D. Glycogen
C. Nucleic acids
CMV and EBV infection can also be assessed through:
A. Bone density
B. Serological responses
C. Pulmonary function
D. Coagulation studies
B. Serological responses
CMV can readily be isolated from which specimen?
A. Urine
B. Synovial fluid
C. Sweat
D. Hair
A. Urine
CMV can also readily be isolated from
A. Tears
B. Saliva
C. Nail clippings
D. Cerumen
B. Saliva
Which additional specimen can readily yield CMV?
A. CSF
B. Stool
C. Blood
D. Sputum only
C. Blood
CMV can readily be isolated from which additional source?
A. Hair
B. Tissue specimens
C. Bone
D. Skin scrapings
B. Tissue specimens
Which assay is useful for CMV diagnosis in immunocompromised patients?
A. Monospot assay
B. Antigenemia assay
C. Coombs assay
D. Schilling test
B. Antigenemia assay
The CMV antigenemia assay primarily uses:
A. Immunofluorescence
B. Gram staining
C. Acid-fast staining
D. Electron microscopy
A. Immunofluorescence
CMV antigenemia detects viral antigen in circulating:
A. Erythrocytes
B. Platelets
C. Leukocytes
D. Reticulocytes
C. Leukocytes
Which test is highly sensitive and specific for EBV?
A. ELISA
B. Culture
C. PCR
D. Gram stain
C. PCR
Which EBV molecules are detected by in situ hybridization?
A. LMPs
B. EBERs
C. EBNAs
D. gp350
B. EBERs
EBERs are best described as:
A. Viral glycoproteins
B. Capsid proteins
C. Noncoding nuclear RNAs
D. Viral polymerases
C. Noncoding nuclear RNAs
Why does Epstein-Barr virus-encoded RNA (EBER) in situ hybridization exhibit high sensitivity for detecting EBV-infected cells?
A. High intranuclear RNA copy number
B. High affinity antibody-antigen binding
C. Rapid lytic viral replication
D. High concentration in serum
A. High intranuclear RNA copy number
Development of new serologic reactivity is called:
A. Seroprotection
B. Seroconversion
C. Seroreversion
D. Seroadsorption
B. Seroconversion
Seroconversion is a standard method for detecting:
A. Latent infection
B. Reactivation
C. Primary infection
D. Drug resistance
C. Primary infection
Seroconversion can detect primary infection with:
A. CMV and EBV
B. HSV and VZV
A. CMV and EBV
During acute EBV mononucleosis, which antibodies are produced?
A. EBV-specific only
B. Non-EBV-specific antibodies
C. Autoantibodies
D. Antinuclear antibodies
B. Non-EBV-specific antibodies
The non-EBV-specific antibodies of mononucleosis are called:
A. Cold agglutinins
B. Heterophile antibodies
C. Rheumatoid factors
D. Isohemagglutinins
B. Heterophile antibodies
Which test detects heterophile antibodies in acute EBV?
A. Monospot test
B. Coombs test
C. Western blot
D. VDRL
A. Monospot test
The Monospot test is best described as a rapid:
A. Precipitation assay
B. Agglutination test
C. Complement fixation test
D. Neutralization assay
B. Agglutination test
What treatment is indicated for disseminated CMV or EBV in immunocompromised patients?
A. Antiviral therapy
B. Antibacterial therapy
C. Antifungal therapy
D. Antiprotozoal therapy
A. Antiviral therapy
Which drug routinely inhibits CMV replication?
A. Oseltamivir
B. Ganciclovir
C. Ribavirin
D. Zanamivir
B. Ganciclovir
Which additional drug inhibits CMV replication?
A. Acyclovir
B. Valacyclovir
C. Foscarnet
D. Famciclovir
C. Foscarnet
Ganciclovir and foscarnet are routinely used for:
A. CMV prevention and treatment
B. EBV vaccination
C. HSV latency eradication
D. VZV prophylaxis only
A. CMV prevention and treatment
Ganciclovir is best classified as a:
A. Protease inhibitor
B. Nucleoside analog
C. Integrase inhibitor
D. Neuraminidase inhibitor
B. Nucleoside analog
Activated ganciclovir inhibits viral DNA-dependent DNA:
A. Ligase
B. Helicase
C. Topoisomerase
D. Polymerase
D. Polymerase
Ganciclovir also inhibits CMV replication by:
A. Arresting DNA elongation
B. Blocking viral attachment
C. Preventing endocytosis
D. Destroying viral capsids
A. Arresting DNA elongation