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WorksheetsHerpesviridae
Total questions: 55
Worksheet time: 2hrs 50mins
The family Herpesviridae consists of
more than 10 viruses that infect vertebrates and invertebrates.
more than 100 viruses that infect vertebrates and invertebrates.
more than 10 viruses that do not infect vertebrates and invertebrates.
more than 100 viruses that do not infect vertebrates and invertebrates.
The family Herpesviridae is divided in
2 subfamlies : Alphaherpesvirinae, Betaherpesvirinae
3 subfamlies : Alphaherpesvirinae, Betaherpesvirinae, Gammaherpesvirinae
4 subfamlies : Alphaherpesvirinae, Betaherpesvirinae, Gammaherpesvirinae, Deltaherpesvirinae
The family is not divided in subfamilies.
Genus Herpes simplex virus is in
Alphaherpesvirinae
Betaherpesvirinae
Gammaherpesvirinae
Deltaherpesvirinae
Genus Varicella-zoster is in
Alphaherpesvirinae
Betaherpesvirinae
Gammaherpesvirinae
Deltaherpesvirinae
Genus Cytomegalovirus is in
Alphaherpesvirinae
Betaherpesvirinae
Gammaherpesvirinae
Deltaherpesvirinae
Genus Roseolovirus is in
Alphaherpesvirinae
Betaherpesvirinae
Gammaherpesvirinae
Deltaherpesvirinae
Genus Lymphocryptovirus is in
Alphaherpesvirinae
Betaherpesvirinae
Gammaherpesvirinae
Deltaherpesvirinae
Human herpes virus (HHV-6 and HHV-7) are in genus
Herpes simplex virus
Varicella-zoster
Roseolovirus
Lymphocryptovirus
Epstein Barr virus (EBV) and HHV-8 are in genus
Herpes simplex virus
Varicella-zoster
Roseolovirus
Lymphocryptovirus
General structure of the family Herpesviridae
Non-enveloped, helical capsid
Non-enveloped, icosahedral capsid
Enveloped, helical capsid
Enveloped, icosahedral capsid
General structure of the family Herpesviridae
120 - 200 nm of diameter, dsDNA, 152 kbp
120 - 200 nm of diameter, ssRNA, 152 kbp
120 - 300 nm of diameter, dsDNA, 152 kbp
120 - 200 nm of diameter, dsDNA, 162 kbp
Virus in the subfamily Alphaherpesvirinae is latent in
Sensory ganglia
Blood, lymphoid tissue, secretory glands and kidneys
Lymphocytes, some epithelial cells and endothelial cells
All answers are possible.
Virus in the subfamily Betaherpesvirinae is latent in
Sensory ganglia
Blood, lymphoid tissue, secretory glands and kidneys
Lymphocytes, some epithelial cells and endothelial cells
All answers are possible.
Virus in the subfamily Gammaherpesvirinae is latent in
Sensory ganglia
Blood, lymphoid tissue, secretory glands and kidneys
Lymphocytes, some epithelial cells and endothelial cells
All answers are possible.
Herpes simplex virus is latent in
Sensory ganglia
Trigeminal ganglia
Sacral ganglia
All answers are correct.
The initial virus-cell interaction for penetration of the herpes simplex virus occurs when
2 viral envelope glycoproteins : glycoprotein C (gC) and glycoprotein B (gB) bind to a cell surface particle called herparan sulfate.
the major receptor-binding protein, glycoprotein D (gD), binds to at least one of 3 known entry receptors : herpesvirus entry mediator (HVEM), nectin-1 and 3-O sulfated heparan sulfate
the nectin receptors produce cell-cell adhesion, to provide a strong point of attachment for the virus to host cell.
glycoprotein D (gD) changes its conformation and interacts with viral glycoprotein H (gH) and L (gL), which form a gH/gL complex.
The initial virus-cell interaction for penetration of the herpes simplex virus occurs when
2 viral envelope glycoproteins : glycoprotein C (gC) and glycoprotein B (gB) bind to a cell surface particle called herparan sulfate.
the major receptor-binding protein, glycoprotein D (gD), binds to at least one of 3 known entry receptors : herpesvirus entry mediator (HVEM), nectin-1 and 3-O sulfated heparan sulfate
the nectin receptors produce cell-cell adhesion, to provide a strong point of attachment for the virus to host cell.
glycoprotein D (gD) changes its conformation and interacts with viral glycoprotein H (gH) and L (gL), which form a gH/gL complex, once bounds to HVEM.
Herpes simplex virus enters the cell through its capsid entry pore, which is produced by
interaction between glycoprotein D (gD) with at least one of known substances : herpesvirus entry mediator (HVEM), nectin-1 and 3-O sulfated heparan sulfate
interaction between glycoprotein B and C with heparan sulfate
interaction between glycoprotein B with gH/gL complex
12 copies of portal protein, UL6, arranged as a ring adhered to each other due to a leucine zipper sequence of amino acids
Herpes simplex virus releases its genome into the host cell nucleus via its capsid portal, which is formed by
interaction between glycoprotein D (gD) with at least one of known substances : herpesvirus entry mediator (HVEM), nectin-1 and 3-O sulfated heparan sulfate
interaction between glycoprotein B and C with heparan sulfate
interaction between glycoprotein B with gH/gL complex
12 copies of portal protein, UL6, arranged as a ring adhered to each other due to a leucine zipper sequence of amino acids
During herpes simplex virus enters "replication" stage, protein synthesis of the host is shut off by
HVEM (Herpesvirus entry mediator)
UL6
VHS or UL46
α-TSF
Which of the following herpes virus proteins form the capsid and the receptors on the surface of the virus?
Immediate-early proteins
Early proteins
Late proteins
All answers are correct.
Which of the following herpes virus proteins regulate the genetic replication of the virus?
Immediate-early proteins
Early proteins
Late proteins
All answers are correct.
Viral assembly of herpes simplex virus occurs in which part of the host cell?
Cytoplasm
Nucleus
Cytoplasm and nucleus
Golgi apparatus
Release of herpes simplex virus :
A. Primary envelopment : acquired by budding into the inner nuclear membrane of the host cell. This then fuses with the outer nuclear membrane, releasing a naked capsid into the cytoplasm.
B. Secondary envelopment : the virus acquires its final envelope by budding into cytoplasmic vesicles.
A and B are correct.
None of which is correct.
Clinically, pathogenic herpes simplex virus includes
Oral herpes
Genital herpes
Ocular herpes
Otic herpes
Vascular herpes
Oral herpes includes gingivostomatitis and recurrent labial herpes :
is often caused by HSV-1
is often caused by HSV-2
is often caused by HSV-1, rarely by HSV-2
is often caused by HSV-2, rarely by HSV-1
Genital herpes :
is often caused by HSV-1
is often caused by HSV-2
is often caused by HSV-1, sometimes by HSV-2
is often caused by HSV-2, sometimes by HSV-1
Ocular herpes :
is often caused by HSV-1
is often caused by HSV-2
is often caused by HSV-1, rarely by HSV-2
is often caused by HSV-2, rarely by HSV-1
Severe forms of herpes simplex virus infection (neonatal herpes, herpes encephalitis, retinitis, necrosis, herpes hepatitis) are treated using
Acyclovir
Epivir
Amodiaquine
Metronidazole
Primary infection of varicella-zoster virus is
Chickenpox
Shingles
AIDS
Epilepsy
Reactivated infection of varicella-zoster virus is
Chickenpox
Shingles
AIDS
Epilepsy
Varicella-zoster virus is cultivated in
Human embryonic fibroblasts
Human embryonic lung cells
Murine kidney cells
Embryonated egg
Transmission of varicella-zoster virus :
By aerosol
By respiratory droplets
Mother-to-fetus transmission
By eye contact with infected patients
By talking to each other on phone
Mother-to-fetus transmission of varicella-zoster virus occurs
before the 24th week of pregnancy
during the 24th week of pregnancy
after the 24th week of pregnancy
All answers are correct.
Incubation period of varicella-zoster virus :
7 days
14 days
21 days
28 days
General symptoms of chickenpox :
Fever, sometimes abdominal pain, rash all over the body
Localized, unilateral infection (limited in 1 area innervated by 1 sensory ganglion, with neuralgia)
Prostatitis, urethritis, genital discharges, dysuria
Lactose intolerance, malabsorption
General symptoms of shingles :
Fever, sometimes abdominal pain, rash all over the body
Localized, unilateral infection (limited in 1 area innervated by 1 sensory ganglion, with neuralgia)
Prostatitis, urethritis, genital discharges, dysuria
Lactose intolerance, malabsorption
Treatment of varicella-zoster virus :
Antiseptic, acyclovir, famciclovir, foscavir, cidofovir
Antiseptic, antibiotics, acyclovir
Chloroquine, doxycycline, atovaquone/proguanil, mefloquine
Metronidazole, tinidazole, tenoquinol
Vaccines of varicella-zoster virus :
Live-attenuated vaccine (1 dose = 0.5 mL) : SC or IM
Convalescent zoster immunoglobulin
Interferon α and ribavirin
Antiseptics, acyclovir, famciclovir, foscavir and cidofovir
Genome structure of cytomegalovirus :
Double-stranded linear DNA
Double-stranded circular DNA
Single-stranded linear RNA
Double-stranded circular RNA
Incubation period of cytomegalovirus :
14 days
21 days
30 days
50 days
Cytopathic effect (CPE) of cytomegalovirus appears in
1 week
1 - 5 weeks
5 - 10 weeks
10 - 15 weeks
Cytomegalovirus is excreted through
saliva
pharyngeal secretions
tears
urine
cervicovaginal secretions, semen
Clinical signs of primary cytomegalovirus infection :
Prolonged fever, headache, myalgia, splenomegaly and hepatomegaly (rare), mononucleosis with lymphocytosis, elevations of serum transaminases (hypertransaminasemia), frequent moderate thrombocytopenia
Acute hepatitis, meningoencephalitis, pneumonitis, colitis
Severe anemia, hemoglobinuria, oliguria, pulmonary edema, hypoglycemia, acute kidney failure, metabolic acidosis, low blood pressure, acute respiratory distress syndrome (ARDS), cerebral malaria, hyperparasitemia, abnormalities in blood coagulation
Lymphadenopathy, fever, rash, headache, diarrhea, sore throat, fatigue, neurological manifestation, loss of appetite, weight loss
Complications of primary cytomegalovirus infection :
Prolonged fever, headache, myalgia, splenomegaly and hepatomegaly (rare), mononucleosis with lymphocytosis, elevations of serum transaminases (hypertransaminasemia), frequent moderate thrombocytopenia
Acute hepatitis, meningoencephalitis, pneumonitis, colitis
Severe anemia, hemoglobinuria, oliguria, pulmonary edema, hypoglycemia, acute kidney failure, metabolic acidosis, low blood pressure, acute respiratory distress syndrome (ARDS), cerebral malaria, hyperparasitemia, abnormalities in blood coagulation
Lymphadenopathy, fever, rash, headache, diarrhea, sore throat, fatigue, neurological manifestation, loss of appetite, weight loss
Laboratory diagnoses of cytomegalovirus infection :
Cytology
Viral isolation and culture
Detection of viral antigens
PCR test for viral DNA
Serology
Structure of EBV (Epstein Barr virus) :
Capsid : 100 nm, Envelop : 200 nm
Capsid : 125 nm, Envelop : 200 nm
Capsid : 150 nm, Envelop : 250 nm
Capsid : 200 nm, Envelop : 300 nm
Envelop of the EBV derives from
Nuclear membrane
Golgi apparatus
Mitochondria
Ribosomes
Endoplasmic reticulum
Replication of the EBV occurs in
Nucleus
Golgi apparatus
Mitochondria
Endoplasmic reticulum
Tropism of Epstein Barr virus :
Sensory ganglia
Salivary glands
B-lymphocytes
Epithelial cells
Endothelial cells
Latency of Epstein Barr virus :
Sensory ganglia
Salivary glands
B-lymphocytes
Epithelial cells
Endothelial cells
Latency of Epstein Barr virus :
Sensory ganglia
Salivary glands
B-lymphocytes
Epithelial cells
Endothelial cells
Epstein Barr virus primarily infects :
Endothelial cells
Salivary glands
B-lymphocytes
Oropharyngeal epithelial cells
Epstein Barr virus is released through
Endothelial cells
Saliva
B-lymphocytes
Oropharyngeal epithelial cells
Kaposi's sarcoma lesions contain :
HSV-1 and HSV-2
Cytomegalovirus
Epstein Barr virus
HHV-8
