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 lipsthatspontaneously 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