Properties o Belong to the alphaherpesvirus subfamily of herpesviruses ds dna enveloped virus with a genome of around 150kb o The genome of HSV-1 and HSV-2 share 50-70% h homolog o They also share several cross-reactive epitopes with each other. There is also antigenic cross reaction with VZV o Man is the only natural host for HsV
Properties ⚫ Belong to the alphaherpesvirus subfamily of herpesviruses ⚫ ds DNA enveloped virus with a genome of around 150 kb ⚫ The genome of HSV-1 and HSV-2 share 50 - 70% homology. ⚫ They also share several cross-reactive epitopes with each other. There is also antigenic crossreaction with VZV. ⚫ Man is the only natural host for HSV
Epidemiology (1) o HSV is spread by contact, as the virus is shed in saliva, tears genital and other secretions o by far the most common form of infection results from a kiss given to a child or adult from a person shedding the virus Primary infection is usually trivial or subclinical in most individuals. It is a disease mainly of very young children ie those below 5 years o There are 2 peaks of incidence, the first at0-5 years and the second in the late teens, when sexual activity commence o About 10% of the population acquires HSV infection through the genital route and the risk is concentrated in young adulthood
Epidemiology (1) ⚫ HSV is spread by contact, as the virus is shed in saliva, tears, genital and other secretions. ⚫ By far the most common form of infection results from a kiss given to a child or adult from a person shedding the virus. ⚫ Primary infection is usually trivial or subclinical in most individuals. It is a disease mainly of very young children ie. those below 5 years. ⚫ There are 2 peaks of incidence, the first at 0 - 5 years and the second in the late teens, when sexual activity commences. ⚫ About 10% of the population acquires HSV infection through the genital route and the risk is concentrated in young adulthood
Epidemiology(2) o Generally Hs V-I causes infection above the belt and HSV-2 below the belt. In fact. 40% of clinical isolates from genital sores are hsv-1, and 5%o of strains isolated from the facial area are hsv-2. This data is complicated by oral sexual practices o Following primary infection, 45%0 of orally infected individuals and 60% of patients with genital herpes will experience recurrences o The actual frequency of recurrences varies widely between individuals
Epidemiology (2) ⚫ Generally HSV-1 causes infection above the belt and HSV-2 below the belt. In fact, 40% of clinical isolates from genital sores are HSV-1, and 5% of strains isolated from the facial area are HSV-2. This data is complicated by oral sexual practices. ⚫ Following primary infection, 45% of orally infected individuals and 60% of patients with genital herpes will experience recurrences. ⚫ The actual frequency of recurrences varies widely between individuals
Herpes Simplex Virus Herpes simplex Virus 2 encephalitis meningIts conjuncts gingivostomatitis tonsilitis labialis gingivostomatitis tonsilitis labialis pharyngitis esophagitis pharyngitis herpes gladiatorum tracheobronchitis i penanal herpes gental herpes genital herpes herpes whitlow herpes whitlow
Pathogenesis o During the primary infection, HSV spreads locally and a short-lived viraemia occurs, whereby the virus is disseminated in the body. Spread to the to craniospinal ganglia occurs. o The virus then establishes latency in the craniospinal ganglia. o The exact mechanism of latency is not known, it may be true latency where there is no viral replication or viral persistence where there is a low level of viral replication. o Reactivation-It is well known that many triggers can provoke a recurrence. These include physical or psychological stress, infection; especially pneumococcal and meningococcal, fever, irradiation; including sunlight, and menstruation
Pathogenesis ⚫ During the primary infection, HSV spreads locally and a short-lived viraemia occurs, whereby the virus is disseminated in the body. Spread to the to craniospinal ganglia occurs. ⚫ The virus then establishes latency in the craniospinal ganglia. ⚫ The exact mechanism of latency is not known, it may be true latency where there is no viral replication or viral persistence where there is a low level of viral replication. ⚫ Reactivation - It is well known that many triggers can provoke a recurrence. These include physical or psychological stress, infection; especially pneumococcal and meningococcal, fever, irradiation; including sunlight, and menstruation