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Medicine – Herpes Simplex Virus (HSV): Types, Transmission, Pathogenesis, Clinical Features, Diagnosis and Treatment
1. Introduction to Herpes Simplex Virus
Herpes simplex virus (HSV) is a common viral pathogen responsible for recurrent infections involving the skin, mucous membranes and occasionally the central nervous system.
HSV infection is particularly important in sexually transmitted infections because it is a major cause of painful genital ulceration.
There are two principal types of herpes simplex virus: HSV type 1 (HSV-1) and HSV type 2 (HSV-2). Although HSV-1 is traditionally associated with oral infections and HSV-2 with genital infections, both types can infect either anatomical region.
An important characteristic of HSV is its ability to establish lifelong latent infection within sensory nerve ganglia. Following the initial infection, the virus may remain dormant for months or years before becoming reactivated.
Reactivation may produce recurrent lesions, although these episodes are generally shorter and less severe than the initial symptomatic infection.
Antiviral medications such as aciclovir can reduce the duration and severity of symptoms, but they do not eradicate the latent virus.
2. Classification of Herpes Simplex Virus
Herpes simplex viruses belong to the family Herpesviridae, specifically the alphaherpesvirus subfamily.
They are enveloped viruses containing double-stranded DNA.
The two major types are HSV-1 and HSV-2.
Both types share several biological characteristics, including epithelial infection, neuronal latency and the ability to reactivate after periods of dormancy.
However, they differ in their usual anatomical distribution and patterns of recurrence.
3. Herpes Simplex Virus Type 1 (HSV-1)
HSV-1 is traditionally associated with infections involving the oral cavity, lips and surrounding facial skin.
The most familiar manifestation is herpes labialis, commonly called a cold sore.
HSV-1 may also cause primary gingivostomatitis, keratitis, encephalitis and genital herpes.
Genital HSV-1 infection has become an important cause of genital herpes, particularly following oral-genital sexual contact.
Compared with genital HSV-2 infection, genital HSV-1 generally produces fewer symptomatic recurrences and less frequent genital viral shedding.
However, recurrence patterns vary between individuals.
4. Herpes Simplex Virus Type 2 (HSV-2)
HSV-2 is predominantly associated with genital and anogenital infections.
It is transmitted mainly through sexual contact involving infected genital or perianal skin and mucous membranes.
HSV-2 commonly produces painful genital vesicles and ulcers.
Following primary infection, HSV-2 establishes latency within the sacral sensory ganglia.
Reactivation may produce recurrent genital lesions.
Genital HSV-2 infection generally causes more frequent recurrences and asymptomatic genital viral shedding than genital HSV-1 infection.
5. Transmission of Herpes Simplex Virus
HSV is transmitted through direct contact with infected skin, mucous membranes or secretions.
HSV-1 is commonly acquired through oral contact, including kissing, while HSV-2 is more commonly transmitted through sexual contact.
Both types can be transmitted during oral, vaginal or anal sexual activity.
Transmission is particularly likely when active vesicles or ulcers are present because these lesions contain infectious virus.
However, HSV can also be transmitted when no visible lesions are present.
This occurs because of asymptomatic viral shedding from infected epithelial surfaces.
Consequently, the absence of genital ulcers does not completely eliminate the possibility of HSV transmission.
6. Incubation Period
The incubation period for symptomatic HSV infection is generally approximately 2–12 days following exposure.
During this period, the virus replicates locally within epithelial cells.
The infected individual may subsequently develop vesicles, ulcers and regional lymphadenopathy.
However, many HSV infections are asymptomatic or produce symptoms so mild that they are not recognised.
Some individuals therefore remain unaware of their infection until a later symptomatic episode occurs.
Pathogenesis of HSV Infection
7. Entry into Epithelial Cells
HSV enters the body through mucous membranes or microscopic breaks in the skin.
The virus attaches to susceptible epithelial cells and introduces its genetic material into the host cell.
Viral replication occurs within the infected epithelial tissue.
This produces cellular injury and destruction, resulting in the formation of characteristic vesicular lesions.
The vesicles contain fluid and infectious viral particles.
When they rupture, they leave painful superficial ulcers.
8. Formation of Vesicles and Ulcers
HSV infection causes local epithelial cell destruction and inflammation.
Initially, small erythematous papules may appear at the affected site.
These subsequently develop into grouped, fluid-filled vesicles.
The vesicles are often fragile and rupture rapidly, especially on mucosal surfaces.
Their rupture produces shallow, painful ulcers with erythematous bases.
Several small ulcers may merge into larger irregular lesions.
The classical clinical association is multiple painful genital vesicles that rupture to form shallow ulcers.
9. Establishment of Viral Latency
One of the most important biological properties of HSV is its ability to establish lifelong latency.
Following initial epithelial infection, viral particles enter sensory nerve endings.
The virus travels through the sensory axons toward the neuronal cell bodies by retrograde axonal transport.
HSV then establishes latent infection within sensory ganglia.
During latency, the viral genome persists within neurons without producing the full cycle of infectious viral replication.
The immune system controls active viral replication but does not completely eliminate the latent viral genome.
This explains why HSV infection may persist for life.
10. Sites of HSV Latency
HSV-1 classically establishes latency within the trigeminal ganglion, particularly following oral or facial infection.
This explains why recurrent HSV-1 infection commonly produces cold sores around the lips.
HSV-2 classically establishes latency within the sacral sensory ganglia, particularly following genital infection.
This explains why recurrent HSV-2 infection commonly affects the genital and perianal regions.
However, the location of latency depends on the anatomical site of infection rather than the viral type alone.
Genital HSV-1 can also establish latency in sacral sensory ganglia.
11. Reactivation of Latent HSV
Latent HSV may reactivate after prolonged periods without symptoms.
Reactivation involves renewed viral replication within sensory neurons.
The virus travels from the ganglion toward the skin or mucous membrane through anterograde axonal transport.
It may then replicate within epithelial cells and produce recurrent vesicles or ulcers.
Reactivation can also result in asymptomatic viral shedding without visible lesions.
Therefore, recurrent infection may occur even after years of apparent dormancy.
12. Factors Associated with HSV Reactivation
Several physiological and environmental factors may be associated with HSV reactivation.
These include febrile illnesses, psychological stress, local trauma, ultraviolet light exposure and immunosuppression.
Menstruation may also be associated with recurrent episodes in some individuals.
However, many recurrences occur without an identifiable trigger.
The frequency of reactivation varies considerably between patients and generally decreases over time.
Clinical Features of Genital Herpes
13. Primary Genital Herpes
Primary genital herpes refers to the first episode of genital HSV infection in an individual without pre-existing antibodies to either HSV type.
It may produce a relatively severe clinical illness.
Patients can develop multiple painful vesicles and ulcers involving the genital or perianal region.
The lesions are often accompanied by local inflammation, tenderness and swelling.
Systemic symptoms may include fever, malaise, headache and muscle aches.
Primary infection may also produce tender inguinal lymphadenopathy.
However, many primary HSV infections are mild or asymptomatic.
14. Painful Genital Ulceration
Painful genital ulceration is the hallmark of symptomatic genital herpes.
The lesions commonly begin as clusters of small vesicles on an erythematous base.
These vesicles rupture and form shallow ulcers.
The ulcers may be particularly painful when they occur on sensitive genital mucosal surfaces.
Patients may experience burning, stinging or discomfort during movement and sexual intercourse.
The lesions usually heal without significant scarring in immunocompetent individuals.
15. Genital Herpes in Men
In men, genital herpes may involve the glans penis, foreskin, penile shaft, scrotum, perineum or perianal region.
The lesions may appear as grouped vesicles or painful superficial ulcers.
Patients may complain of genital pain, burning or irritation.
Tender inguinal lymphadenopathy may occur during the first episode.
Occasionally, extensive inflammation can make urination uncomfortable.
16. Genital Herpes in Women
In women, genital herpes may involve the vulva, labia, vaginal opening, vagina, cervix, perineum or perianal region.
Painful vesicles and ulcers may develop on external genital skin or mucosal surfaces.
Dysuria is common when urine contacts inflamed or ulcerated tissue.
Some patients experience significant vulval swelling and discomfort.
Cervical involvement may produce cervicitis or abnormal vaginal discharge.
Severe first episodes can occasionally cause urinary retention because of pain or sacral nerve involvement.
17. Systemic Symptoms
The first symptomatic episode of genital herpes may be accompanied by constitutional symptoms.
These include fever, malaise, fatigue, headache and generalised muscle aches.
Regional lymphadenopathy is also common.
Systemic symptoms are generally more pronounced during primary infection than during recurrent episodes.
However, the severity of the first recognised episode depends on the patient’s previous HSV exposure and immune response.
18. Prodromal Symptoms
Some patients experience prodromal symptoms shortly before recurrent lesions appear.
These may include tingling, itching, burning or localised pain in the genital or perianal region.
The prodrome reflects viral reactivation and early local nerve or epithelial involvement.
Lesions may develop within hours or a short period after the onset of these symptoms.
Recognition of the prodrome is clinically useful because episodic antiviral treatment is most effective when started early.
Recurrent Genital Herpes
19. Why Genital Herpes Recurs
Genital herpes recurs because HSV remains latent within sensory nerve ganglia.
The immune system suppresses viral replication but does not eliminate the latent viral genome.
When reactivation occurs, the virus travels along sensory nerves to the epithelial surface.
This may produce new vesicles or ulcers at or near the original site of infection.
The frequency of recurrence varies between individuals.
Some patients experience frequent episodes, whereas others have only occasional recurrences or none at all.
20. Clinical Features of Recurrent Genital Herpes
Recurrent genital herpes generally produces less severe symptoms than the initial symptomatic episode.
The lesions are usually fewer in number and more localised.
Systemic symptoms such as fever and malaise are less common.
Healing is typically faster than during primary infection.
Some patients experience only mild tingling, burning or a few small ulcers.
However, recurrent episodes can still be painful and distressing.
21. Differences Between HSV-1 and HSV-2 Recurrence
Genital HSV-2 infection generally causes more frequent symptomatic recurrences than genital HSV-1 infection.
HSV-2 is also associated with more frequent asymptomatic genital viral shedding.
Genital HSV-1 typically recurs less often, particularly after the first year of infection.
This difference is important when counselling patients about the expected natural history of genital herpes.
Nevertheless, individual recurrence patterns vary considerably.
22. Asymptomatic Viral Shedding
HSV can be released from infected genital skin or mucous membranes without producing visible ulcers or vesicles.
This is called asymptomatic viral shedding.
During these periods, infectious virus may be present even though the patient feels entirely well.
Asymptomatic shedding is an important mechanism of genital herpes transmission.
It explains why HSV can spread between sexual partners in the absence of recognised outbreaks.
Suppressive antiviral therapy can reduce viral shedding, although it does not eliminate transmission risk completely.
Other Clinical Manifestations of HSV
23. Herpes Labialis
Herpes labialis is a common manifestation of HSV-1 infection.
It typically produces recurrent clusters of painful vesicles around the lips or oral commissures.
Patients may experience tingling or burning before the lesions appear.
The vesicles rupture, crust and gradually heal.
Reactivation may be associated with febrile illness, ultraviolet exposure or other physiological stresses.
24. Herpetic Gingivostomatitis
Primary HSV-1 infection may cause acute gingivostomatitis, particularly in children.
The condition produces painful oral vesicles and ulcers, gingival inflammation and difficulty eating or drinking.
Fever, irritability and cervical lymphadenopathy may occur.
Severe oral discomfort can lead to dehydration.
Management focuses on adequate hydration, analgesia and antiviral treatment in selected cases.
25. Herpetic Keratitis
HSV may infect the cornea and produce herpetic keratitis.
A characteristic manifestation is dendritic corneal ulceration, which may be demonstrated using fluorescein staining.
Patients may experience eye pain, redness, photophobia, tearing and blurred vision.
Recurrent infection can produce corneal scarring and visual impairment.
Suspected herpetic keratitis requires prompt ophthalmological assessment.
Topical corticosteroids should not be used without specialist guidance because they can worsen active epithelial HSV keratitis.
26. Herpes Simplex Encephalitis
HSV-1 is an important cause of sporadic viral encephalitis.
The infection classically involves the temporal lobes and may produce haemorrhagic necrosis.
Patients may present with fever, headache, altered consciousness, behavioural changes, seizures or focal neurological deficits.
Diagnosis commonly involves cerebrospinal fluid HSV PCR and brain imaging.
Suspected HSV encephalitis is a medical emergency requiring prompt intravenous aciclovir, without waiting for confirmatory testing when clinical suspicion is high.
27. HSV Meningitis
HSV can also cause meningitis.
HSV-2 is particularly associated with aseptic meningitis and recurrent lymphocytic meningitis.
Patients may develop headache, fever, photophobia and neck stiffness.
Cerebrospinal fluid typically demonstrates a lymphocytic inflammatory response.
HSV PCR can help establish the diagnosis.
Management depends on disease severity, immune status and the clinical syndrome.
28. Neonatal Herpes
Neonatal herpes is a serious infection acquired most commonly during delivery through exposure to infected genital secretions or lesions.
The risk is particularly high when maternal genital HSV infection is newly acquired near the time of delivery.
Neonatal infection may present as skin, eye and mouth disease, central nervous system infection or disseminated infection.
Disseminated neonatal HSV may involve the liver, lungs and other organs.
Neonatal herpes requires urgent investigation and intravenous aciclovir because delayed treatment can result in severe neurological injury or death.
29. HSV Infection in Immunocompromised Patients
HSV infection may be more severe in patients with impaired immune function.
Individuals with advanced HIV infection, organ transplantation or significant immunosuppression may develop extensive or persistent lesions.
Ulcers may be unusually large, deep or slow to heal.
Disseminated infection or visceral involvement can occasionally occur.
These patients may require prolonged antiviral therapy and assessment for antiviral resistance when lesions fail to respond.
Diagnosis of Herpes Simplex Virus Infection
30. Clinical Diagnosis
Genital herpes may be suspected from the characteristic appearance of grouped vesicles and painful superficial ulcers.
A history of recurrent lesions at similar anatomical sites supports the diagnosis.
However, clinical examination alone is not sufficiently reliable because other infections and inflammatory conditions can produce similar lesions.
Some patients have atypical manifestations without obvious vesicles.
Therefore, laboratory confirmation is recommended when appropriate.
31. HSV Polymerase Chain Reaction (PCR)
HSV nucleic acid amplification testing, commonly performed by PCR, is the preferred laboratory test for active genital lesions.
A swab is collected from a fresh vesicle or ulcer.
PCR detects HSV genetic material and can distinguish HSV-1 from HSV-2.
This distinction is useful because the two types differ in their expected recurrence patterns.
PCR is generally more sensitive than viral culture.
However, a negative result does not completely exclude HSV infection, particularly when lesions are healing or viral shedding is intermittent.
32. Viral Culture
HSV can be isolated from clinical lesions using viral culture.
However, culture is less sensitive than PCR, especially when lesions are older or beginning to heal.
Its sensitivity also decreases during recurrent episodes.
For this reason, PCR-based testing is generally preferred when available.
Viral culture may still be useful in selected circumstances, including specialised investigations.
33. HSV Serological Testing
Type-specific HSV serology detects antibodies against HSV-1 or HSV-2.
It may be useful in selected situations, such as recurrent symptoms with negative lesion testing or assessment of a partner’s infection status.
However, HSV antibodies may take weeks to develop after acquisition.
HSV-1 seropositivity does not establish whether infection is oral or genital.
Low-positive HSV-2 antibody results may also require confirmatory testing because false-positive reactions occur.
HSV IgM testing is not recommended for routine diagnosis because it is unreliable and cannot reliably distinguish new from recurrent infection.
Treatment of Herpes Simplex Virus
34. Principles of Treatment
The treatment of genital herpes aims to reduce the duration and severity of symptoms, accelerate lesion healing and decrease the frequency of recurrences.
Antiviral therapy can also reduce viral shedding and, in selected circumstances, the risk of transmission.
However, currently available antiviral drugs do not eradicate latent HSV from sensory ganglia.
Therefore, treatment controls viral replication rather than permanently curing the infection.
The main antiviral medications used are aciclovir, valaciclovir and famciclovir.
35. Aciclovir
Aciclovir is a nucleoside analogue with activity against HSV-1 and HSV-2.
It is activated initially by viral thymidine kinase within infected cells.
Subsequent phosphorylation by host enzymes produces aciclovir triphosphate, the active form.
This compound inhibits viral DNA polymerase and interferes with viral DNA synthesis.
As a result, viral replication is suppressed.
Aciclovir is particularly useful because its activation preferentially occurs in infected cells, providing selective antiviral activity.
36. Effect of Aciclovir on Genital Herpes
The original notes state that aciclovir reduces the time during which lesions are present.
This is correct.
Aciclovir can shorten the duration of symptoms, reduce viral shedding and accelerate lesion healing.
It is most effective when started early during an outbreak.
For recurrent herpes, treatment ideally begins during the prodromal period or within approximately one day of lesion onset.
Aciclovir does not remove the latent virus from sensory ganglia and therefore cannot prevent every future recurrence.
37. Treatment of the First Clinical Episode
A first clinical episode of genital herpes is generally treated with oral antiviral therapy.
One commonly recommended adult regimen is aciclovir 400 mg orally three times daily for 7–10 days.
Alternative regimens include valaciclovir or famciclovir.
Treatment may be extended when lesions have not healed adequately.
Supportive care includes analgesia, hydration and measures to reduce local discomfort.
Patients with severe complications, such as disseminated infection or significant neurological involvement, may require hospitalisation and intravenous aciclovir.
38. Episodic Treatment of Recurrent Herpes
Episodic antiviral therapy is used to treat individual recurrent outbreaks.
Patients begin treatment when prodromal symptoms or early lesions appear.
Short courses of aciclovir, valaciclovir or famciclovir may be prescribed.
Early initiation can reduce the duration and severity of the episode.
This approach is particularly suitable for patients who experience infrequent recurrences.
39. Suppressive Antiviral Therapy
Suppressive therapy involves taking antiviral medication regularly to reduce the frequency of recurrent outbreaks.
It may be considered for patients with frequent or distressing recurrences.
Common options include daily aciclovir or valaciclovir.
Suppressive treatment can substantially reduce recurrent genital herpes episodes.
In patients with genital HSV-2 infection, daily valaciclovir has also been shown to reduce transmission risk in certain discordant heterosexual couples.
However, transmission remains possible because antiviral treatment does not completely eliminate viral shedding.
40. Valaciclovir
Valaciclovir is a prodrug of aciclovir.
After oral administration, it is converted into aciclovir within the body.
It has improved oral bioavailability compared with aciclovir.
This allows less frequent dosing in many treatment regimens.
Valaciclovir is used for first episodes, recurrent outbreaks and suppressive treatment of genital herpes.
41. Famciclovir
Famciclovir is an oral prodrug that is converted into penciclovir.
Penciclovir inhibits viral DNA polymerase after activation within infected cells.
Famciclovir is an alternative treatment for genital HSV infection.
It can be used for episodic or suppressive therapy.
The choice between aciclovir, valaciclovir and famciclovir depends on clinical circumstances, dosing convenience, availability and patient preference.
42. Adverse Effects and Precautions
Aciclovir and related antiviral medications are generally well tolerated.
Possible adverse effects include nausea, headache and gastrointestinal discomfort.
Aciclovir is eliminated primarily through the kidneys, so dosage adjustment may be necessary in patients with impaired renal function.
Intravenous aciclovir can occasionally cause crystal-associated kidney injury, particularly when hydration is inadequate or infusion is too rapid.
Rare neurological adverse effects may occur, especially when drug accumulation develops in renal impairment.
Appropriate dosing and renal monitoring are important in susceptible patients.
Prevention of Genital Herpes
43. Reducing Sexual Transmission
HSV transmission can be reduced through several preventive measures.
Avoiding sexual contact during active genital lesions or prodromal symptoms is particularly important because viral shedding is often increased.
Condoms reduce the risk of transmission but do not provide complete protection because infected skin may remain uncovered.
Daily suppressive antiviral therapy may reduce transmission risk in selected patients with genital HSV-2 infection.
Patients should understand that asymptomatic shedding can still occur.
44. Partner Counselling
Patients diagnosed with genital herpes should receive clear information about the lifelong nature of HSV infection.
A diagnosis does not establish when the infection was acquired because HSV may remain asymptomatic for prolonged periods.
Partners may already have HSV infection without recognised symptoms.
Type-specific testing may be considered in selected situations after appropriate counselling.
Open communication and an understanding of asymptomatic transmission are important aspects of management.
45. Genital Herpes During Pregnancy
Genital HSV infection during pregnancy is clinically important because of the risk of neonatal herpes.
The greatest risk of neonatal transmission occurs when a pregnant patient acquires genital HSV near the time of delivery.
Patients with recurrent genital herpes generally have a lower transmission risk because pre-existing maternal antibodies provide some protection.
Suppressive antiviral therapy may be offered near the end of pregnancy to reduce genital recurrences at delivery.
Caesarean delivery is generally recommended when active genital lesions or prodromal symptoms are present at the onset of labour.
Management should follow obstetric guidelines and consider the timing and type of maternal infection.
HSV and Other Causes of Genital Ulceration
46. Herpes Simplex Virus
Genital herpes typically produces multiple painful vesicles that rupture into shallow ulcers.
Patients may experience burning, tingling, dysuria and tender inguinal lymphadenopathy.
Recurrent episodes are common, particularly with genital HSV-2.
HSV PCR from a lesion is the preferred diagnostic test.
Treatment involves antiviral medication such as aciclovir.
47. Primary Syphilis
Primary syphilis is caused by Treponema pallidum.
It classically produces a solitary, painless, indurated genital ulcer called a chancre.
Regional lymphadenopathy is usually non-tender.
Diagnosis relies on serological testing and direct detection methods where available.
Treatment is penicillin G.
48. Chancroid
Chancroid is caused by Haemophilus ducreyi.
It classically produces painful genital ulcers with soft, irregular edges.
Tender inguinal lymphadenopathy may occur, sometimes progressing to suppurative buboes.
Chancroid is less common than genital herpes in many regions.
The diagnosis and treatment differ from those of HSV infection.
49. Important Examination Distinction
The classical clinical distinction between genital herpes and primary syphilis is based on ulcer characteristics.
Genital herpes → Multiple painful vesicles and shallow ulcers.
Primary syphilis → Usually a painless, indurated chancre.
Chancroid → Painful, soft genital ulcer with tender lymphadenopathy.
However, these findings are not absolute, and laboratory testing is important because clinical presentations may overlap.
Important Corrections and Clarifications
50. HSV-1 and HSV-2 Distribution
The original notes state that HSV-1 mainly affects the oral region and HSV-2 mainly affects the genital region.
This remains a useful traditional association.
However, HSV-1 is also an important cause of genital herpes, and HSV-2 can occasionally cause oral infection.
Therefore, viral type does not exclusively determine anatomical location.
51. Lifelong Dormancy
The original notes correctly state that HSV can remain dormant for very long periods.
HSV establishes lifelong latency within sensory nerve ganglia.
Reactivation may occur after months or years, even in patients who have remained asymptomatic for prolonged periods.
52. Painful Genital Ulceration
The original notes correctly identify painful genital ulceration as a major feature of HSV infection.
The classical lesion begins as a vesicle that ruptures to form a shallow, painful ulcer.
However, many HSV infections are asymptomatic or produce atypical symptoms.
Therefore, the absence of painful ulcers does not exclude HSV infection.
53. Role of Aciclovir
Aciclovir inhibits viral DNA synthesis and reduces the duration and severity of symptomatic outbreaks.
It can also be used as daily suppressive therapy.
However, it does not eliminate latent HSV from sensory ganglia.
Therefore, HSV infection may recur despite previous successful treatment.
54. Severity of Recurrent Infection
The original notes state that recurrent episodes are normally less aggressive than the initial infection.
This is generally correct.
Recurrent episodes usually involve fewer lesions, milder symptoms and shorter healing times.
Systemic symptoms are also less common.
However, recurrence severity varies, and immunocompromised individuals may experience severe or persistent disease.
Important Clinical Associations – Note Form
55. HSV-1
HSV-1 is predominantly associated with oral herpes, herpes labialis and primary gingivostomatitis.
It is also an important cause of genital herpes, herpetic keratitis and herpes simplex encephalitis.
Following oral infection, latency classically occurs in the trigeminal ganglion.
56. HSV-2
HSV-2 is predominantly associated with genital herpes.
It commonly establishes latency within sacral sensory ganglia.
Genital HSV-2 infection generally produces more frequent recurrences and asymptomatic genital shedding than genital HSV-1 infection.
HSV-2 is also associated with aseptic meningitis.
57. Primary Genital Herpes
Primary genital herpes may cause multiple painful vesicles and ulcers accompanied by fever, malaise, dysuria and tender inguinal lymphadenopathy.
The first clinical episode may be more severe and prolonged than later recurrences.
Oral antiviral therapy is recommended for symptomatic first episodes.
58. Recurrent Genital Herpes
Recurrent genital herpes results from reactivation of latent HSV.
Patients may experience tingling, itching or burning before lesions develop.
Recurrent outbreaks are generally shorter and less severe than the initial symptomatic episode.
59. Aciclovir
Aciclovir is a nucleoside analogue activated initially by viral thymidine kinase.
Its active metabolite inhibits viral DNA polymerase.
It reduces viral replication, accelerates lesion healing and decreases symptom duration.
It does not eradicate latent HSV.
60. HSV Encephalitis
HSV-1 encephalitis classically affects the temporal lobes.
Patients may develop fever, altered mental status, seizures and focal neurological abnormalities.
Prompt intravenous aciclovir is essential.
61. HSV Keratitis
HSV keratitis may produce dendritic corneal ulcers.
Patients may develop eye pain, photophobia and blurred vision.
Recurrent disease can cause corneal scarring and visual impairment.
62. Neonatal HSV
Neonatal HSV may cause skin, eye and mouth disease, encephalitis or disseminated infection.
Transmission commonly occurs during delivery.
Neonatal HSV is a serious infection requiring urgent intravenous aciclovir.
Key Clinical Pattern
The defining characteristic of herpes simplex virus is its ability to cause recurrent painful mucocutaneous lesions through reactivation of lifelong latent infection within sensory nerve ganglia.
HSV-1 → Mainly oral herpes, but can also cause genital herpes.
HSV-2 → Mainly genital herpes, with more frequent genital recurrences.
Primary genital herpes → Multiple painful vesicles and shallow ulcers, sometimes with fever and tender lymphadenopathy.
Viral latency → HSV persists within sensory nerve ganglia for life.
Trigeminal ganglion → Classical site of latency following oral HSV infection.
Sacral ganglia → Classical site of latency following genital HSV infection.
Reactivation → Virus travels along sensory nerves and may produce recurrent lesions.
Recurrent herpes → Usually milder, shorter and less extensive than the initial symptomatic episode.
Asymptomatic viral shedding → HSV transmission can occur without visible lesions.
HSV PCR → Preferred diagnostic test for active genital lesions.
Aciclovir → Inhibits viral DNA polymerase and reduces lesion duration.
Suppressive antiviral therapy → Reduces recurrence frequency and viral shedding.
HSV-1 encephalitis → Temporal lobe involvement requiring urgent intravenous aciclovir.
HSV keratitis → Dendritic corneal ulceration.
Neonatal herpes → Potentially severe infection acquired around delivery.
For examinations, remember the classical association: HSV causes painful genital vesicles and ulcers, remains latent within sensory ganglia, and can reactivate repeatedly. Aciclovir shortens outbreaks and suppresses viral replication but does not provide a permanent cure.
