HHV-6 and HHV-8

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Questions and Answers

HHV-6 establishes latency in monocytes. What is the primary risk associated with this latent state, especially in immunocompromised individuals?

  • Reactivation leading to serious infections such as encephalitis. (correct)
  • Development of Kaposi's sarcoma due to HHV-6 induced immunosuppression.
  • The immediate progression to roseola infantum, regardless of prior infection history.
  • An increased susceptibility to bacterial infections due to monocyte dysfunction.

Why is Kaposi's sarcoma-associated herpesvirus (KSHV/HHV-8) classified as an oncovirus?

  • It integrates its viral DNA into the host genome, causing genomic instability and cancer.
  • Its lytic cycle aggressively destroys immune cells, indirectly promoting tumor development.
  • It inhibits tumor suppressor proteins like p53, preventing apoptosis and promoting uncontrolled cell proliferation. (correct)
  • It directly induces mutations in host DNA, leading to uncontrolled cell growth.

What is the most critical factor that differentiates the clinical management of HHV-6 versus HHV-8 infections?

  • HHV-6 is primarily managed with chemotherapy, while HHV-8 is treated with antiviral medications.
  • HHV-6 requires aggressive treatment with radiation therapy, while HHV-8 is managed with supportive care only.
  • HHV-6 management focuses on symptom relief, while HHV-8 treatment aims to halt tumor progression, using local and systemic therapies. (correct)
  • HHV-6 infections are treated with antibiotics to prevent secondary bacterial infections, while HHV-8 requires no intervention.

In immunocompromised individuals, how does the reactivation of HHV-6 typically manifest, and what cell types are primarily involved in this process?

<p>As encephalitis, with the virus replicating in glial cells and astrocytes. (B)</p> Signup and view all the answers

What feature of HHV-8's lytic phase contributes most significantly to the pathogenesis of Kaposi's sarcoma?

<p>The production of cytokines and growth factors that stimulate angiogenesis and cell proliferation. (D)</p> Signup and view all the answers

How do the modes of transmission of HHV-6 and HHV-8 most critically influence the epidemiology and at-risk populations for the associated diseases?

<p>HHV-6, transmitted through respiratory secretions, primarily affects infants and young children, while HHV-8, transmitted sexually, mainly affects adults, particularly those with compromised immune systems. (A)</p> Signup and view all the answers

How does the mechanism of HHV-8's latency differ fundamentally from that of HHV-6, regarding their impact on cellular function and potential for oncogenesis?

<p>HHV-8's latency involves the expression of LANA-1, which interferes with tumor suppressor proteins, promoting cell survival and proliferation, while HHV-6 does not have a similar mechanism. (A)</p> Signup and view all the answers

In diagnosing roseola infantum, which clinical feature is most critical in differentiating it from other common childhood exanthems, such as measles or rubella?

<p>The characteristic pattern of fever preceding the rash, followed by resolution of fever with the onset of the rash. (A)</p> Signup and view all the answers

How does the role of dendritic cells in HHV-6 infection contribute to the virus's ability to disseminate within the host?

<p>Dendritic cells transport HHV-6 to lymph nodes, where the virus can efficiently infect CD4+ T lymphocytes. (C)</p> Signup and view all the answers

What is the primary reason why antiviral treatments like acyclovir or ganciclovir are selectively used in severe cases of HHV-6 infection in immunocompromised individuals?

<p>These drugs specifically target the viral DNA polymerase, inhibiting viral replication and reducing the viral load during active infection. (C)</p> Signup and view all the answers

Flashcards

Human Herpes Virus 6 (HHV-6)

Double-stranded linear DNA virus belonging to the Herpesviridae family, subfamily Betaherpesvirinae, genus Roseolovirus, transmitted via respiratory secretions.

Roseola Infantum

Common childhood disease caused by primary HHV-6 infection, characterized by high fever followed by a maculopapular rash.

HHV-6 Pathogenesis

Through respiratory secretions, the virus attaches to dendritic cells, presents antigens to T cells, migrates to lymph nodes, infecting CD4+ T lymphocytes. Can enter a latent state in monocytes.

Human Herpes Virus 8 (HHV-8/KSHV)

A human gammaherpesvirus also known as Kaposi's sarcoma-associated herpesvirus (KSHV). It is one of the seven known oncoviruses causing Kaposi's sarcoma (KS).

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Kaposi's Sarcoma (KS)

HHV-8 causes vascular lesion characterized by vascular proliferation and dark or violaceous plaques on the skin, mouth, GI tract, or lungs.

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HHV-8 Transmission and Entry

Through sexual contract, HHV-8 enters B cells, endothelial cells, macrophages, and epithelial cells. Exhibits latent and lytic phases.

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HHV-8 Latent Phase

The virus remains in the cell without destroying it and expresses the latency-associated nuclear antigen (LANA-1). LANA-1 inhibits the tumor suppressor protein p53.

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HHV-8 Lytic Phase

The virus replicates, producing new viruses that destroy the cell and infect neighboring cells.

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Kaposi's Sarcoma Types

Classic, endemic, epidemic (AIDS-associated), and immunosuppression therapy-related.

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Kaposi's Sarcoma Diagnosis

Histology of lesions reveals spindle cells, immunohistochemical staining for LANA-1, and PCR for viral DNA.

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Study Notes

  • Human Herpes Virus 6 (HHV-6) and Human Herpes Virus 8 (HHV-8) are double-stranded linear DNA viruses

HHV-6

  • Belongs to the Herpesviridae family, Betaherpesvirinae subfamily, and Roseolovirus genus
  • Transmitted through respiratory secretions
  • Attaches to dendritic cells (skin, nose, lungs, stomach, intestines) which present antigens to T cells
  • Migrates to lymph nodes, infecting CD4+ T lymphocytes where it replicates efficiently
  • Undergoes the lytic cycle within T cells, destroying them and infecting neighboring cells
  • Can also replicate in monocytes, macrophages, NK cells, astrocytes, megakaryocytes, and glial cells, but less efficiently
  • Enters a latent state in monocytes, potentially reactivating in immunocompromised individuals, causing serious infections like encephalitis
  • Primary infection causes roseola infantum (exanthem subitum or sixth disease)
  • Common in children aged 6 months to 2 years.
  • Incubation period: 1-2 weeks
  • Symptoms: High fever (up to 40°C or 104°F) lasting 3-5 days, peri-orbital edema, acute otitis media, rhinorrhea, cough, vomiting, diarrhea, bulging fontanelle, lymphadenopathy, and Nagayama spots
  • After fever subsides, a maculopapular rash appears on the neck, trunk, face, and extremities, lasting a few hours to two days
  • Diagnosis: Clinical findings, PCR to identify viral DNA, and serological tests for IgG antibodies against HHV-6
  • Treatment: Supportive care (antipyretics, increased fluid intake); antivirals in severe cases

HHV-8

  • Also called Kaposi's sarcoma-associated herpesvirus (KSHV)
  • Belongs to the family of human gammaherpesviruses
  • One of the seven known oncoviruses, specifically causing Kaposi's sarcoma (KS)
  • Large, double-stranded linear DNA virus
  • Surrounded by an icosahedral capsid, a protein layer called the tegument, and an envelope with viral glycoproteins
  • Transmitted through sexual contact
  • Enters B cells, endothelial cells, macrophages, and epithelial cells
  • Latent Phase: Virus remains in the cell without destroying it, expresses latency-associated nuclear antigen (LANA-1), inhibiting tumor suppressor protein p53, preventing apoptosis, leading to uncontrolled cellular proliferation
  • Lytic Phase: Virus replicates, producing new viruses that destroy the cell and infect neighboring cells
  • Healthy immune system limits infection due to humoral (antibodies) and cellular (cytotoxic T cells) immune responses
  • Immunocompromised individuals are at higher risk

Clinical Presentation of Kaposi’s Sarcoma

  • Four types: Classic, endemic, epidemic (AIDS-associated), and immunosuppression therapy-related
  • Characterized by vascular proliferation and dark or violaceous plaques on the skin, mouth, GI tract, or lungs
  • Lesions resemble bruises, which can grow into nodules and merge
  • Other symptoms: weight loss, nausea, vomiting, diarrhea, bleeding, malabsorption, shortness of breath, chest pain, cough, hemoptysis

Diagnosis

  • Biopsy of lesions, microscopic examination showing spindle cells, immunohistochemical staining for LANA-1, and PCR for viral DNA

Treatment

  • Aimed at stopping the progression of KS
  • Local treatments (radiation therapy, cryosurgery) for skin lesions
  • Chemotherapy (doxorubicin, daunorubicin, thalidomide, paclitaxel) for widespread disease

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