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HERPES VIRUSES

HERPES VIRUSES. Level 8 LECTURE 8. Introduction. Herpes viruses are a leading cause of human viral disease, second only to influenza and cold viruses. Hv are everywhere in nature. Hv have large, enveloped an icosahedral capsids containing ds dna genomes.

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HERPES VIRUSES

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  1. HERPES VIRUSES Level 8 LECTURE 8

  2. Introduction • Herpes viruses are a leading cause of human viral disease, second only to influenza and cold viruses. • Hv are everywhere in nature. • Hv have large, enveloped an icosahedral capsids containing ds dna genomes. • Dna replication and capsid assembly occurs in the nucleus. • Virus is released by exocytosis, cell lysis, and through cell-cell bridges. • Hv can cause lytic, persistent, latent, and, for EBV, immortalizing infections. • Cell-mediated immunity is required for control.

  3. Herpesvirus Particle HSV-2 virus particle. Note that all herpesviruses have identical morphology and cannot be distinguished from each other under electron microscopy. (Linda Stannard, University of Cape Town, S.A.)

  4. - Properties of Herpes viruses

  5. HERPES VIRUS STRUCTURE - GENERAL • EnvelopeHerpes viruses are enveloped viruses. They bud from the inner nuclear membrane The viral membrane is quite fragile and a virus with a damaged envelope is not infectious (This means that the virus readily falls apart and so the virus can only be obtained by direct contact with mucosal surfaces or secretions of an infected person - it cannot be caught from toilet seats). Besides drying, the virus is also sensitive to acids, detergents and organic solvents as might be expected for an virus with a lipid envelope. • TegumentThe space between the envelope and the capsid is the tegument. This contains virally-encoded proteins and enzymes involved in the initiation of replication • CapsidThese viruses have a doughnut shaped capsomere of about 100-200 nm in diameter with an icosahedral nucleocapsid. The latter contains 162 capsomeres • GenomeThese viruses have double stranded DNA. The size of the genomes differs with cytomegalovirus having the largest genome

  6. Herpes Simplex Virus (HSV) • The first human herpesvirus to be recognized. • The name "herpes" is derived from a Greek word meaning to creep. • The two types of herpes simplex virus, HSV-1 and HSV-2, share many characteristics, including DNA homology, antigenic determinants, tissue tropism, and disease symptoms. • Man is the only natural host for HSV.

  7. PATHOGENESIS AND IMMUNITY • HSV initiates infection through mm or skin breaks . • HSV replicates in cells at the base of lesion and infects the innervating neuron, traveling by \retrograde transport to its ganglion • HSV then returns to the initial site of infection and may be inapparent or may produce vesicular lesions. • The vesicle fluid contains infectious virions. • Tissue damage is caused by a combination of viral pathology and immunopathology. The lesion generally heals without producing a scar. • HSV-2 has a greater potential to cause viremia. • HSV is reactivated from latency by stress .

  8. HSV can cause lytic infections of most cells, persistentinfections of lymphocytes and macrophages, and latent infection of neurons.

  9. Recurrence of HSV infection • Triggers of HSV Recurrence: • UV (medium wave) radiation • Fever • Emotional stress • Physical stress • Menstruation • Foods: Spicy, acidic, allergies • Immunosuppression, and HIV. • Chemotherapy, radiotherapy • These events trigger virus replication in an individual nerve cell within the bundle and allow the virus to travel back down the nerve to develop lesions at same dermatome and location each time.

  10. Stress triggers reactivation either by; • Promoting replication of the virus in the nerve, • Transiently depressing cell-mediated immunity, or, • Inducing both processes. • HSV can be reactivated in spite of the presence of antibody. • However, recurrent infections are generally less severe, more localized, and of shorter duration than the primary infection.

  11. Epidemiology of HSV • HSV Virus causes lifelong infection. • HSV inactivated by drying, detergents, and GIT juices. • Virus may cause asymptomatic shedding. • Virus is found worldwide; There is no seasonal incidence. • Both types of HSV can cause oral and genital lesions. 2) Transmission • Virus is found in saliva, vaginal secretion, lesion fluid. • Virus is transmitted orally and sexually and by placement into eyes and breaks in skin. • "mixing and matching of mucous membranes“ • Autoinoculation • More than 90% of people living in underdeveloped areas have the antibody to HSV-1 by 2 years of age.

  12. Genital herpesis usually caused by HSV-2 but can also be caused by HSV-1(10%) • In male: lesions typically develop on glans or shaft of penis and occasionally in the urethra. • In female: lesions may be seen on the vulva, vagina, cervix, perianal area, or inner thigh and are frequently accompanied by itching and a mucoid vaginal discharge. The lesions are usually painful. • primary infection may be accompanied by fever, malaise, myalgia, and inguinal adenitis (transient viremia). • HSV proctitis is a painful disease in which the lesions are found in the lower rectum and anus. • Unfortunately, any infected person may shed virus asymptomatically. Such individuals may be important vectors for spread of this virus.

  13. Herpes encephalitis • HSV is the most common viral cause of sporadic encephalitis and results in significant morbidity and mortality, even in patients who receive appropriate treatment. • Herpes encephalitis is usually caused by HSV-1. • HSV meningitis is most often a complication of genital HSV-2 infection; symptoms resolve by themselves.

  14. HSV infection in the neonate • a damaging and often fatal disease caused most often by HSV-2. • The baby initially appears septic, and vesicular lesions may be present. • Because the cell-mediated immune response is not yet developed in the neonate, HSV disseminates to the liver, lung, and other organs, as well as to the central nervous system (CNS). • Progression of the infection to the CNS results in death, mental retardation, or neurologic disability, even with treatment.

  15. Lab Diagbnosis of HSV • Direct microscopic examination of cells from base of lesion (see histopathology) • Cell culture: detects identifiable cytopathologic effect in most cell cultures. • Assay of tissue biopsy, smear, cerebrospinal fluid, or vesicular fluid for HSV antigen or genome by: 1- Enzyme immunoassay, 2- immunofluorescent stain, 3- in situ DNA probe analysis 4- polymerase chain reaction (PCR).

  16. Human Herpesvirus (Varicella-Zoster Virus) Infections • Causes two diseases • Varicella • Often called chicken pox • Typically occurs in children • Herpes zoster • Also called shingles • Usually occurs in adults

  17. Herpesviridae • Human Herpesvirus 3 (Varicella-Zoster Virus) Infections • Epidemiology and pathogenesis of VZV infections • Chicken pox is highly infectious disease • Virus enters skin through the respiratory tract or eyes • Virus travels via the blood from infection site throughout body • Characteristic skin lesions appear 2–3 weeks after infection • The disease is usually mild in children • Chicken pox in adults is typically more severe • Latent virus can reactivate producing a rash known as shingles

  18. Characteristic chicken pox lesions Figure 24.9

  19. Shingles Figure 24.11

  20. Human Herpesvirus 3 (Varicella-Zoster Virus) Infections • Diagnosis, treatment, and prevention • Diagnosis • Chicken pox is diagnosed from the characteristic lesions • Shingles lesions can be more difficult to diagnose • Treatment • Chicken pox is usually self-limiting • Shingles treatment involves management of symptoms • Prevention • Difficult because virus is shed before clear signs appear

  21. Human Herpesvirus 4 (Epstein-Barr Virus) Infections • Also referred to as EBV • Can cause a number of different diseases

  22. Herpesviridae • Human Herpesvirus 4 (Epstein-Barr Virus) Infections • Epidemiology and pathogenesis of HHV-4 infections • Transmission usually occurs via saliva • Initially infect epithelium of pharynx and parotid salivary glands • Virus enters the bloodstream and invades B lymphocytes • Become latent and suppress apoptosis of B cells • Immune response causes infectious mononucleosis symptoms • Cytotoxic T cells kill virus-infected B lymphocytes • Cancer development appears to depend on various cofactors • Extreme diseases arise in individuals with T cell deficiency

  23. Human Herpesvirus 4 (Epstein-Barr Virus) Infections • Diagnosis, treatment, and prevention • Diagnosis • Some diseases diagnosed by their characteristic signs • Treatment • Burkitt’s lymphoma responds well to chemotherapy • Mono patients are treated to relieve the symptoms • Other conditions have no effective treatment • Prevention • Hard because virus is widespread and transmitted by saliva

  24. Human Herpesvirus 5 (Cytomegalovirus) Infections • Infected cells become enlarged • One of the more common infections of humans • Transmission occurs through bodily secretions • Requires close contact and a large exchange of secretion • Usually occurs via sexual intercourse • Also transmitted by in utero exposure, vaginal birth, blood transfusions, and organ transplants • Most CMV infections are asymptomatic • Complications in fetuses, newborns, and immunodeficient patients

  25. Human Herpesvirus 5 (Cytomegalovirus) Infections • Diagnosis, treatment, and prevention of HHV-5 infections • Diagnosis • Detection of enlarged cells and cellular inclusions • Treatment • Treatment of fetuses and newborns is difficult • Damage usually occurs before infection is discovered • Fomiversen is used to treat CMV eye infections • Prevention • safe sex can reduce chance of infection

  26. An owl’s eye cell diagnostic for cytomegalovirus infection Figure 24.14

  27. Other Herpesvirus Infections • Human herpesvirus 6 (HHV-6) • In the genus Roseolovirus • Causes roseola • Characterized by pink rash on face, neck, trunk, and thighs • May be linked to multiple sclerosis • Can cause mononucleosis-like symptoms • Human herpesvirus 8 (HHV-8, Rhadinovirus) • Associated with Kaposi’s sarcoma

  28. Roseola Figure 24.15

  29. Kaposi’s sarcoma Figure 24.16

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