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04 Deja Review-Micro Herpesvirus
Terms in this set (66)
Name the medically important herpesviruses and one or two important diseases they cause:
Herpes simplex virus type 1 (HSV-1): gin- givostomatitis and encephalitis
Herpes simplex virus type 2 (HSV-2): herpes genitalis and neonatal herpes Varicella-zoster virus (VZV): varicella (chickenpox) and zoster (shingles) Epstein-Barr virus (EBV): infectious mono- nucleosis and associated with various cancers (eg, nasopharyngeal carcinoma and Burkett lymphoma)
Cytomegalovirus (CMV): cytomegalic inclu- sion disease, mononucleosis, various diseases in immunocompromised
Human herpesvirus 6 (HHV6): roseola in- fantum
Human herpesvirus 8 (HHV8): associated with Kaposi's sarcoma
Mnemonic: Herpes Viruses Cause Harmful Effects (HSV, VZV, CMV, HHV, EBV).
Describe the morphology of the herpesviruses:
Enveloped icosahedral nucleocapsids with linear double-stranded DNA genome
Where are the viral proteins and DNA synthesized?
DNA and viral proteins are synthesized in the host nucleus.
What is unique about the herpesvirus envelope?
Envelope is derived from the host nuclear membrane. All other enveloped viruses obtain their membrane from the cell membrane.
Why do herpesviruses form Cowdry type A intranuclear inclusion bodies?
The virus transports structural viral proteins into the nucleus where it assembles. These structural proteins form eosinophilic bodies
surrounded by a clear halo that displaces the nucleolus. However, Cowdry type A are not specific for herpesvirus infection as it also occurs in yellow fever virus.
Which herpesviruses infect primarily epithelial cells, have relatively short reproductive cycle, and cause latent infections in neurons?
Alpha herpesviruses which include HSV-1, HSV-2, and VZV
Which herpesviruses have a relatively long reproductive cycle, often causing infected cells to become enlarged and become latent in a variety of tissue?
Beta herpesviruses, which include CMV and HHV6
Which herpesviruses infect and become latent in primarily lymphoid tissue?
Gamma herpesviruses, which include EBV and HHV8
Name all of the diseases that HSV-1 can cause:
Gingivostomatitis (vesicular lesions, fever, tender regional lymphadenopathy), pharyngotonsillitis (fever, sore throat, ulcerative lesions with grayish exudates on tonsils an- dpharynx), herpes labialis (prodromal pain/ tingling, vesicles), keratoconjunctivitis (corneal ulcers), encephalitis (fever, hemorrhagic lesion in temporal lobe), and genital herpes (less common than HSV-2)
How is HSV-1 transmitted?
Most people acquire HSV-1 through direct contact or oral secretions during childhood
Where does HSV-1 usually become latent?
How does primary infection with HSV-1 typically present?
Primary infection usually occurs in childhood and is asymptomatic
How does HSV-1 reactivation usually present?
Vesicular lesions in oral, labial, and ocular mucosae that is preceded by pain, burning, itching, and paresthesia. Viral shedding of HSV-1 occurs up to 96 hours after onset of symptoms.
How is HSV-1 encephalitis diagnosed clinically? What tests are ordered?
Clinically: fever, confusion, headache Magnetic resonance imaging (MRI): hemorrhagic lesion in the temporal lobe Cerebrospinal fluid(CSF): increased red blood cells (RBCs) and viral DNAby poly- merase chain reaction (PCR) Electroencephalogram (EEG): diffuse slowing
Mnemonic: In the ER, TaP CsF (EEG, RBCs, Temporal lobe, PCR CSF, Confu- sion, Fever)
What is the prognosis for untreated and treated HSV-1 encephalitis?
Untreated patients have up to 70% mortality. Treated patients often have neurological sequelae and 20% mortality.
Is HSV-1 encephalitis common?
Yes, it is the most common cause of sporadic, acute necrotizing encephalitis in the United States. Up to 10% to 20% of all cases of encephalitis are caused by HSV-1.
Traumatic implantation of herpesvirus into the hands, as commonly seen in dentists, causes what painful condition?
Name three diseases that HSV-2 can cause:
2. Genital herpes, neonatal herpes
3. Less commonly oral herpes
How is HSV-2 usually transmitted?
Through sexual contact. Lifetime sero- prevalence estimates range from 20% to 80%.
Where does HSV-2 usually become latent?
Sacral root ganglia
How does primary infection with HSV-2 typically present?
Primary infections are typically more severe than recurrent outbreaks. Primary episode of
genital herpes may last 2 to 3 weeks with painful erythematous, vesicular lesions. Patients may also have asymptomatic primary infections and develop recurrent disease months to years later.
How does HSV-2 reactivation usually present?
Milder outbreak with prodrome of pain, itching, tingling, burning, or paresthesia followed by vesicular lesions. Note that half of HSV-2 seropositive individuals do not have clinically apparent outbreaks but still have episodes of viral shedding and can transmit disease.
Is neonatal herpes a serious infection?
Yes. Cases range from asymptomatic to severe disseminated disease or encephalitis. Ninety percent of neonatal herpes is transmitted perinatally (especially if mother's primary infection was during the pregnancy) and 70% of mothers are asymptomatic. Without therapy, mortality can approach 65%.
How can neonatal herpes be prevented?
Cesarean section, although its routine prophylactic use remains controversial
What is the Tzanck smear?
A rapid test with Giemsa stain to show multinucleated giant cells. Tzanck smear cannot distinguish between HSV-1, HSV-2, and VZV
Is it possible to distinguish between HSV-1 and HSV-2?
Yes, with fluorescent antibody or with restriction enzyme cleavage to yield distinct DNA patterns
What is HSV thymidine kinase? How is this important for latency?
Enzyme synthesized by HSV that allows the virus to grow in cells lacking high concentrations of phosphorylated nucleic acid precursors. It converts the nucleotide thymidine to the substance thymidine 5'-phosphate. Neural cells usually do not replicate their genome so they naturally have very low concentrations of these precursors.
How is thymidine kinase pharmacologically important?
Thymidine kinase is necessary to phos- phorylate acyclovir into its active form. This is how acyclovir achieves its specificity for HSV.
What diseases does VZV cause?
Varicella (chickenpox) and zoster (shingles)
How is chickenpox differentiated from smallpox?
Chickenpox has asynchronous vesicles, occurs primarily on the trunk, and the lesions are more superficial. Smallpox has vesicles that are all at the same stage, occurs primarily on the face, arms, and hands, and the mucus membranes of the nose and mouth. Chickenpox is contagious before symptoms appear and smallpox is most contagious after symptoms appear.
What is zoster?
Painful vesicular rash that occurs along a dermatome as a result of reactivation of VZV that lies dormant in the nerve tissue. Zoster can occur in any patient infected with varicella-zoster. The risk of zoster increases with age and impaired immune function.
How might varicella-zoster present in immunocompromised patients?
Immunocompromised patients might develop zoster multiplex (zoster in more than one dermatome), zoster sine herpete (dermatome pain without cutaneous vesicles), myelitis (central nervous system [CNS] deficits), or keratitis (zoster in the ophthalmic division of the trigeminal nerve).
What complication is associated with asprin administration following influenza B or varicella-zoster virus infection?
Reye syndrome: coma, microvesicular fatty liver, encephalopathy
Where does varicella-zoster usually become latent?
Dorsal root ganglia
What is the treatment of varicella-zoster infections?
Acyclovir is used for active cases and for prophylaxis in immunocompromised patients.
Is there a vaccine available against chicken-pox?
Yes. Both live-attenuated VZV vaccine and VZV immune globulin are available.
Name all the diseases that CMV can cause:
Heterophile-negativemononucleosis syndrome, cytomegalic inclusion disease, and a range of diseases in immunocompromised patients (pneumonia, hepatitis, encephalitis, retinitis, neuropathy, and CMV syndrome)
How common is CMV infection?
More than 80% of adults have antibodies to CMV.
What is cytomegalic inclusion disease?
Congenital clinical syndrome from CMV infection with multinucleated giant cells, resulting in jaundice, splenomegaly, thrombocytopenia, mental retardation, and microcephaly. Congenital CMV infections do not
always develop into inclusion disease.
Is congenital CMV infection common?
Yes. It is the most common cause of congenital abnormalities. Neurological problems such as mental retardation may be present without other signs of CMV infection.
During what trimester of pregnancy is the fetus most at risk for congenital abnormalities from CMV infection?
First trimester, when organs are still developing. The fetus is more at risk if mother has primary infection with CMV during preg- nancy.
Why is CMV important in transplant patients?
CMV can cause devastating disease to the immunocompromised transplant patient both directly and by increasing degree of immunodeficiency. CMV pneumonia once had a mortality rate of 85% in marrow transplant patients. It is still one of the most common causes of death in bone marrow transplant patients.
What is the most common manifestation of CMV in human immunodeficiency virus (HIV) patients?
CMV retinitis occurs in 20% to 30% of patients with CD4 count lower than 50 cells/ μL.
What is the characteristic finding in cell culture and infected tissue that shows CMV infections?
Owl's-eye nuclear inclusion bodies
What head imaging finding suggests CMV infection?
How are CMV infections treated?
The drug of choice is ganciclovir (nucleoside analogue that inhibits DNA synthesis). Also available are foscarnet (DNA chain inhibitor of phosphorylation) and cidofovir (nucleoside analogue that inhibits DNA replication)
Name the disease caused by HHV6:
Roseola infantum (sixth disease)
What is roseola infantum?
Clinical syndrome of abrupt onset of high fever for 3 to 5 days followed by an erythematous maculopapular rash that appears with the return of normal temperature
Who does HHV6 affect? How is it usually transmitted?
Ninety percent seropositivity is reported in children older than 2 years of age and is transmitted via the saliva of the parents.
What other complications are associated with HHV6?
HHV6 is also the most common cause of febrile seizures in childhood. Also, HHV6 plays a role in HIV patients as it accelerates progression toward AIDS.
Name the diseases that EBV causes:
EBV causes infectious mononucleosis. It is also linked to lymphoproliferative disorders and tumors such as nasopharyngeal carcinoma and Burkitt lymphoma.
What type of cells does EBV primarily infect?
B cells. EBV also remains latent in B cells.
What is infectious mononucleosis? What patient population is often affected?
Self-limiting syndrome of fever, pharyngitis, generalized lymphadenopathy, and hep- atosplenomegaly. More frequently affects adolescents and young adults
Mnemonic: Herpesvirus Gotten From Puckering (Hepatosplenomegaly, General- ized lymphadenopathy, Fever, Pharyngitis)
What other infectious agents cause infectious mononucleosis-like illness?
CMV, HHV6, acute HIV, toxoplasmosis,
viral hepatitis, and syphilis
How is EBV infectious mononucleosis differ- entiated from other mononucleosis?
EBV infections generate immunoglobulin M (IgM) antibodies that agglutinate sheep and horse RBC (heterophile positive). Other mononucleosis-like illnesses are heterophile negative.
What congenital immunodeficiencies are asso-ciated with development of EBV-associated lymphoproliferative disorders?
Wiskott-Aldrich syndrome, Ataxia-tel- angiectasia, Chédiak-Higashi syndrome, and common variable immunodeficiency (CVID)
Mnemonic: Worry About Congenital
Causes of EBV infections
What disease does EBV cause in immunocompromised patients?
Hairy cell leukoplakia, a nonmalignant lesion of the tongue
Which population has the highest incidence of nasopharyngeal carcinoma?
People from southern China and less common in North American Inuits
How are EBV infections diagnosed?
Classically three criteria:
1. Lymphocytosis (at least 10% atypical lymphocytes)
2. Heterophile test
3. Positive serologic test for EBV
What are atypical lymphocytes?
Infected B cells are not the atypical ones; they are actually uninfected activated T cells responding to the EBV infection.
Is there treatment of EBV infections?
No antiviral drugs or vaccines are available.
What neoplasm is associated with HHV8?
What is Kaposi sarcoma?
Kaposi sarcoma is a vascular neoplasm that manifests in the skin and other organs. It usually begins as a red/purple patch that becomes nodular and plaque like. It is the most common malignancy in AIDS patients.
Does HHV8 definitively cause Kaposi sarcoma?
No, HHV8 is necessary but not sufficient for the development of Kaposi sarcoma. HHV8 inactivates the tumor suppressor gene retinoblastoma protein (RB).
What is the prognosis for Kaposi sarcoma?
Patients usually do not die of Kaposi sarcoma; however, it is usually present at death. Most patients die from associated opportunistic infections.
How is Kaposi sarcoma diagnosed?
Biopsy, HHV8 DNA/RNA detection
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