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    Cards (200)

    • Herpes viruses that commonly infect humans

      • Herpes simplex viruses type 1&2
      • Varicella-Zoster virus
      • Cytomegalovirus(CMV)
      • Epstein-Barr viruses
      • Human herpes viruses 6,7
      • Kaposi's sarcoma virus or human herpesvirus 8
      • Herpes B virus of monkey
    • Virion
      • Spherical
    • Genome
      • dsDNA, Linear
    • Protein
      • More than 35 proteins in virion
    • Envelope
      • Contains viral glycoprotein and Fc receptor
    • Replication
      • In the nucleus and bud from the nuclear membrane
    • Structural components of all Herpes viruses
      • Genome
      • Capsid
      • Envelope
      • Tegument
    • Herpes virus subfamilies
      • Alpha Herpes
      • Beta Herpes
      • Gamma Herpes
    • Alpha Herpes
      Rapid replication cycle (12-18 hrs), variable host range, tendency to form latency in sensory ganglia, produce rapid CPE & release virus from infected cells
    • Beta Herpes

      Narrow host range, slow replication cycle (more than 24 hrs)
    • Gamma Herpes
      Infect lymphoid tissue & cause latency in lymphocyte
    • Herpes simplex viruses (HSV)

      Wide spread in human, wide host range, two types (1&2) with similar genome organization and 50-70% homology
    • HSV-1 transmission
      Direct contact with infected saliva, skin lesions or respiratory secretions
    • HSV-2 transmission
      Sexually (Venereal disease) and from maternal genital to newborn (Perinatal)
    • HSV pathology
      Cytolytic, leads to ballooning of infected cells and formation of intracellular inclusion bodies
    • HSV pathogenesis - primary infection
      Virus enters through defects/broken skin or mucous membranes, multiplies locally with cell-to-cell spread, enters cutaneous nerve fibres and transported intra-axonally to dorsal root ganglia where it replicates, migrates from ganglia to skin/mucosa to cause lesions
    • HSV latent infection
      Virus stays latent in infected cells for lifetime, can be reactivated by stimuli like axonal injury, fever, stress, UV/sunlight exposure, infection
    • HSV-1 clinical features
      Herpes Labialis - Painful ulcerating vesicles on lips that spontaneously resolve in <2 weeks
    • HSV-2 clinical features
      Genital herpes - Painful vesicular lesions in genital area, Neonatal herpes from contact with maternal genital to newborn
    • HSV laboratory diagnosis
      • Direct detection (Giemsa stain, EM, Immunofluorescence)
      • PCR
      • Virus isolation
      • Serology (IgM & IgG ELISA)
    • Varicella-Zoster Virus (VZV)
      Causes two diseases: Varicella (Chickenpox) and Zoster (Shingles)
    • VZV pathogenesis - Varicella
      Infection occurs through mucosa of conjunctiva and upper respiratory tract, initial replication in regional lymph nodes, then primary and secondary viremia transports virus to skin causing vesicles
    • VZV pathogenesis - Zoster
      Reactivation of latent VZV in neurons of sensory ganglia, virus travels down nerve to skin inducing vesicle formation
    • VZV laboratory diagnosis
      • Direct detection (multinucleate giant cells)
      • Virus isolation
      • Serology (IgG, IgM)
    • Epstein-Barr Virus (EBV)
      Latency in B lymphocytes, associated with Infectious Mononucleosis, Nasopharyngeal Carcinoma, Burkitt Lymphoma, Oral hairy leukoplakia
    • EBV pathogenesis - primary infection
      Transmitted by saliva, infects B lymphocytes by binding to CD21 receptor, integrates viral DNA into cell genome, establishes latent infection
    • EBV viral antigens
      • Viral capsid antigen (VCA)
      • Early antigen (EA)
      • Epstein-Barr nuclear antigen (EBNA)
      • Viral membrane antigen (VMA)
    • EBV laboratory diagnosis
      • Monospot test for heterophil antibody
      • Serology for VCA IgM, VCA IgG, EBNA IgG
      • Histology for Burkitt's lymphoma and Nasopharyngeal Carcinoma
    • No vaccine available for EBV, Acyclovir reduces EBV shedding but has no effect on symptoms
    • Cytomegalovirus (CMV)
      Ubiquitous herpes virus, causes characteristic cytopathic effect and nuclear inclusion bodies
    • CMV transmission
      Direct contact with infected saliva, blood, urine, semen, cervical/vaginal secretions or breast milk, Perinatal
    • CMV pathogenesis - normal host
      Transmitted by close contact, causes systemic infection after 4-8 weeks, primary infection usually asymptomatic but can cause Infectious Mononucleosis
    • CMV pathogenesis - immunocompromised host
      Primary infection more severe, can cause pneumonia, leukopenia, transplant rejection
    • CMV pathogenesis - congenital/perinatal infection
      Can cause severe fetal/newborn disease, developmental defects, mental retardation, deafness, high mortality
    • CMV laboratory diagnosis
      • Direct detection (histology, pp65 antigenemia, PCR)
      • Virus isolation
      • Serology (IgG, IgM)
    • Human Herpes virus 6
      Two forms (A and B), associated with exanthema subitum (roseola infantum), rejection of transplanted kidneys, fulminant hepatitis, CNS infections
    • Human Herpes virus 7
      Associated with some cases of exanthema subitum, found in saliva of majority of adults
    • Human Herpes virus 8

      Associated with Kaposi's sarcoma in AIDS patients and intra-abdominal solid tumors
    • Shingles is caused by Varicella-Zoster Virus (VZV)
    • pp65 antigenemia is found in Cytomegalovirus (CMV) infection
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