Herpes simplex virus: Difference between revisions
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| + | * Comprises herpes simplex virus 1 (HSV-1) and HSV-2, which are members of the [[Human herpesvirus]] family |
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| + | * Cause typical painful vesicular lesions on labia or external genitals |
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| + | * Occasionally cause a viral encephalitis |
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| + | |||
== Background == |
== Background == |
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=== Microbiology === |
=== Microbiology === |
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| − | * |
+ | * Enveloped, double-stranded DNA virus |
| + | * HSV-1 and HSV-2 are morphologically and genetically distinct viruses |
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| + | * Can be infected with both |
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=== Epidemiology === |
=== Epidemiology === |
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| + | * Worldwide distribution, and only found in humans |
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| + | * Most common cause of genital lesions |
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| + | * Spread through person-to-person contact with skin or mucosa; not spread via fomits |
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| + | * HSV-1 is more common, with 90% of adults having antibodies by age 40 |
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| + | ** Often acquired in childhood in Asia and Africa |
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| + | ** More common in lower SES populations |
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| + | * HSV-2 has seroprevalence of 15-20% in US |
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| + | ** More common in women than men, in HIV-infected people, and in MSM |
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| + | ** May be subclinical if already infected with HSV-1 |
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=== Pathophysiology === |
=== Pathophysiology === |
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| + | * Fusion of envelope and cell membrane is mediated by viral glycoproteins B, C, and D and host cell proteins cellular heparin sulfate, TNF receptors, and immunoglobulins |
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| + | * Internal capsid is released, which makes its way to the nucleus |
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| + | * Viral DNA polymerase enzyme and viral DNA helicase are targets of antivirals |
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| + | * Viral DNA may remain latent in about 10% of nearby neurons, characterized by latency-associated transcripts (LATs) |
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| + | ** Despite being latent, virus can still be shed in mucosa anywhere from 1/10 to 3/4 of days |
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| + | * HSV-1 prefers trigeminal ganglia as well as cervical ganglia, or sacral nerve root ganglia if genital |
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== Clinical Presentation == |
== Clinical Presentation == |
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| + | * Incubation period usually within 5 days for primary infection |
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== Diagnosis == |
== Diagnosis == |
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Revision as of 11:32, 16 October 2019
- Comprises herpes simplex virus 1 (HSV-1) and HSV-2, which are members of the Human herpesvirus family
- Cause typical painful vesicular lesions on labia or external genitals
- Occasionally cause a viral encephalitis
Background
Microbiology
- Enveloped, double-stranded DNA virus
- HSV-1 and HSV-2 are morphologically and genetically distinct viruses
- Can be infected with both
Epidemiology
- Worldwide distribution, and only found in humans
- Most common cause of genital lesions
- Spread through person-to-person contact with skin or mucosa; not spread via fomits
- HSV-1 is more common, with 90% of adults having antibodies by age 40
- Often acquired in childhood in Asia and Africa
- More common in lower SES populations
- HSV-2 has seroprevalence of 15-20% in US
- More common in women than men, in HIV-infected people, and in MSM
- May be subclinical if already infected with HSV-1
Pathophysiology
- Fusion of envelope and cell membrane is mediated by viral glycoproteins B, C, and D and host cell proteins cellular heparin sulfate, TNF receptors, and immunoglobulins
- Internal capsid is released, which makes its way to the nucleus
- Viral DNA polymerase enzyme and viral DNA helicase are targets of antivirals
- Viral DNA may remain latent in about 10% of nearby neurons, characterized by latency-associated transcripts (LATs)
- Despite being latent, virus can still be shed in mucosa anywhere from 1/10 to 3/4 of days
- HSV-1 prefers trigeminal ganglia as well as cervical ganglia, or sacral nerve root ganglia if genital
Clinical Presentation
- Incubation period usually within 5 days for primary infection
Diagnosis
Management
References
- a b M. Howard, J. W. Sellors, D. Jang, N. J. Robinson, M. Fearon, J. Kaczorowski, M. Chernesky. Regional Distribution of Antibodies to Herpes Simplex Virus Type 1 (HSV-1) and HSV-2 in Men and Women in Ontario, Canada. Journal of Clinical Microbiology. 2003;41(1):84-89. doi:10.1128/jcm.41.1.84-89.2003.
