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Human Herpesviruses

Human Herpesviruses are eight enveloped, double-stranded DNA viruses that establish lifelong latency after infection. Reactivation is especially important in immunocompromised patients. They cause mucocutaneous disease, encephalitis, congenital infection, and malignancy

Also called

Herpesvirus infection

ICD-10

B00 - B01 - B02 - B25 - B27

Specialty

Infectious

Onset

Acute

Reviewed

August 2026
On This Page

Overview

-Human Herpesviruses include:

Virus Main Diseases
HHV-1 (HSV-1) Oral herpes, genital herpes, encephalitis
HHV-2 (HSV-2) Genital herpes, neonatal herpes, meningitis
HHV-3 (VZV) Varicella, herpes zoster
HHV-4 (EBV) Infectious Mononucleosis, malignancies
HHV-5 (CMV) Congenital and opportunistic disease
HHV-6 Roseola infantum
HHV-7 Roseola-like illness
HHV-8 (KSHV) Kaposi sarcoma

 

Etiology & Risk Factors

-Etiology

These viruses belong to the Herpesviridae family. Transmission varies and includes saliva, respiratory secretions, sexual contact, direct contact with lesions, blood, transplantation, and vertical transmission.

 

-Risk Factors

  • Close contact with infected individuals
  • Sexual exposure
  • Pregnancy or neonatal exposure
  • Immunosuppression
  • Organ transplantation

Pathophysiology

Viral exposureprimary replication → host immune responseestablishment of latencypersistence within host cells → periodic reactivation → recurrent infectionlocalized or disseminated disease

Clinical Presentation

-Symptoms:

Clinical findings depend on the virus:

  • Oral or genital vesicles and ulcers
  • Fever and malaise
  • Dermatomal painful rash
  • Pharyngitis and lymphadenopathy
  • Visual symptoms in CMV retinitis
  • Neurological symptoms in encephalitis or meningitis

 

-Signs:

  • Grouped vesicles
  • Painful mucocutaneous ulcers
  • Dermatomal vesicular eruption
  • Cervical lymphadenopathy
  • Hepatosplenomegaly
  • Retinal abnormalities

 

-Severe Disease

Severe infection may cause:

  • Encephalitis
  • Meningitis
  • Pneumonitis
  • Hepatitis
  • Retinitis
  • Disseminated infection
  • Severe neonatal disease
Human Herpesviruses Overview
Thromboangiitis Obliterans (TAO) Overview

The 8 Human Herpesviruses

Virology · The 8 Human Herpesviruses

1
HSV-1
2
HSV-2
3
VZV
4
EBV
5
CMV
6
HHV-6
7
HHV-7
8
KSHV
1
HSV-1
Herpes Simplex 1
DiseaseOral herpes — cold sores, gingivostomatitis, keratoconjunctivitis, encephalitis
LatencyTrigeminal ganglion
TxAciclovir — encephalitis: IV high dose
ExamMost common cause of viral encephalitis — temporal lobe involvement, HSV PCR on CSF
2
HSV-2
Herpes Simplex 2
DiseaseGenital herpes — painful ulcers; neonatal herpes (birth canal transmission)
LatencySacral ganglia (S2–S4)
TxAciclovir / Valaciclovir — suppression if recurrent
ExamNeonatal herpes — C-section if active lesions at labour; disseminated = fatal
3
VZV
Varicella-Zoster
DiseasePrimary: Chickenpox — vesicular rash all stages simultaneously. Reactivation: Shingles — dermatomal
LatencyDorsal root ganglia
TxAciclovir (severe) — Zoster: Valaciclovir within 72h
ExamRamsay Hunt syndrome — VZV in geniculate ganglion → facial palsy + ear vesicles
4
EBV
Epstein-Barr Virus
DiseaseInfectious mononucleosis — fever + posterior cervical LN + exudative pharyngitis + splenomegaly
LatencyMemory B-cells (CD21)
TxSupportive — no antivirals. Avoid amoxicillin (rash 90%)
ExamMalignancies: Burkitt's lymphoma, Hodgkin's, nasopharyngeal ca, PTLD
5
CMV
Cytomegalovirus
DiseaseCongenital CMV (blueberry muffin rash, sensorineural deafness), retinitis (CD4 <50), colitis, pneumonitis
LatencyMonocytes / myeloid progenitors
TxGanciclovir IV → Valganciclovir PO maintenance
ExamMost common cause of congenital viral infection. CMV retinitis = "pizza pie" fundoscopy
6
HHV-6
Roseolovirus
DiseaseRoseola infantum (Exanthem subitum) — high fever 3 days → fever breaks → rash appears
LatencyCD4+ T-cells, macrophages
TxSupportive (immunocompetent). Ganciclovir — immunocompromised reactivation
ExamAge 6 months–2 years. Febrile seizures common. Rash appears as fever breaks — opposite of measles
7
HHV-7
Roseolovirus 2
DiseaseRoseola-like illness (milder than HHV-6). Pityriasis rosea — possible association
LatencyCD4+ T-cells
TxSupportive — rarely clinically significant
ExamLeast clinically important HHV. Uses CD4 as receptor (same as HIV). Mainly exam-listed.
8
KSHV
Kaposi's Sarcoma HV
DiseaseKaposi's sarcoma — violaceous skin/mucosal lesions; pulmonary/GI involvement. Primary effusion lymphoma, Castleman's disease
LatencyB-cells, endothelial cells
TxART (HIV-related KS) → lesion regression. Chemotherapy for disseminated.
ExamAIDS-defining illness. Endemic form in elderly Mediterranean men — not HIV-related
High-Yield Exam Facts — Side by Side
HHVUnique hallmarkLatency siteAntiviralKey malignancy / complication
HSV-1 Temporal lobe encephalitis — PCR on CSF diagnostic Trigeminal ganglion Aciclovir IV (high dose) Encephalitis — 70% mortality without treatment
HSV-2 Neonatal herpes — C-section if active lesions at delivery Sacral ganglia S2–S4 Aciclovir / Valaciclovir Neonatal disseminated HSV — fatal if untreated
VZV All stages of rash simultaneously (macules + papules + vesicles + crusts) Dorsal root ganglia Valaciclovir within 72h (shingles) Ramsay Hunt — facial palsy + ear vesicles + vertigo
EBV Atypical lymphocytes (Downey cells) + monospot + amoxicillin rash Memory B-cells (CD21) None — supportive only Burkitt's t(8;14), Hodgkin's, nasopharyngeal ca, PTLD
CMV "Pizza pie" retinitis (CD4 <50). Congenital: blueberry muffin rash + periventricular calcification Monocytes / myeloid Ganciclovir IV → Valganciclovir PO Most common congenital viral infection. Blindness in AIDS.
HHV-6 Roseola — rash appears as fever BREAKS (distinguish from measles — rash with fever) CD4+ T-cells Supportive (Ganciclovir if immunocompromised) Febrile seizures — most common age <2 years
HHV-7 Clinically similar to HHV-6. Uses CD4 receptor (like HIV). Rarely tested. CD4+ T-cells Supportive Pityriasis rosea (association — not confirmed)
KSHV Violaceous lesions — skin, oral mucosa, GI, lung. Any CD4 count in HIV. B-cells, endothelial ART → regression. Chemo if disseminated. Kaposi's sarcoma + Primary effusion lymphoma + Castleman's disease
Memory hook — antiviral coverage: HSV-1, HSV-2, VZV → Aciclovir (Valaciclovir PO). CMV, HHV-6 → Ganciclovir / Valganciclovir. EBV → no antiviral. HHV-8 → ART (if HIV-related). All 8 share: dsDNA genome, nuclear replication, lifelong latency.

History Taking

-Ask about:

  • Fever and mucocutaneous lesions
  • Neurological or visual symptoms
  • Previous similar episodes
  • Sexual exposure when relevant
  • Pregnancy or neonatal exposure
  • Immunosuppression
  • Organ transplantation

Physical Examination

-General Examination

  • Temperature
  • General condition
  • Hydration
  • Lymphadenopathy
  • Signs of systemic illness

 

-System-Specific Examination:

  • Inspect skin and mucous membranes
  • Examine oral and genital lesions
  • Assess dermatomal rash
  • Neurological examination when indicated
  • Eye examination when retinitis is suspected

Investigations

-Biochemistry / Specific Tests

  • Viral Polymerase Chain Reaction (PCR)

  • Virus-specific serology

  • Liver function tests when EBV or CMV disease is suspected

  • Cerebrospinal Fluid analysis for suspected Central Nervous System infection

 

-Special / Confirmatory Tests

PCR can detect viral DNA in cerebrospinal fluid, blood, or lesion specimens. Serology is useful in selected infections, especially EBV and CMV.

 

Important Investigation Note

Testing should be selected according to the suspected virus and site of infection.

Diagnosis

-Human Herpesviruses are diagnosed clinically and with targeted laboratory testing when required.

Diagnosis is based on:

Characteristic clinical syndrome → identify likely virus → targeted PCR or serology → assess organ involvement

Management

1 Definitive Treatment

Treatment of Human Herpesviruses depends on the virus:

  • HSV: antiviral therapy when indicated

  • VZV: antiviral therapy for selected or severe disease

  • CMV: specific antiviral therapy for significant disease

  • EBV, HHV-6, HHV-7: mainly supportive treatment

  • HHV-8: treatment directed at associated malignancy

 

2. Medical Treatment

Important antivirals include:

  • Acyclovir

  • Valacyclovir

  • Ganciclovir

  • Valganciclovir

Choice depends on the virus, severity, immune status, and kidney function.

 

3. Supportive Management

  • Adequate hydration

  • Analgesia and fever control

  • Nutritional support

Complications

  • Encephalitis
  • Meningitis
  • Pneumonitis
  • Hepatitis
  • Retinitis
  • Neonatal infection
  • Disseminated infection
  • Malignancy

Prognosis

The prognosis of Human Herpesviruses infection varies with the virus, affected organ, and immune status. Most uncomplicated infections are self-limited or manageable. Severe disease in neonates and immunocompromised patients may cause permanent organ damage or death.

Key Points / Clinical Pearls

  • Human Herpesviruses are enveloped double-stranded DNA viruses.
  • There are eight recognized human herpesviruses.
  • HSV-1 commonly causes oral herpes and encephalitis.
  • HSV-2 commonly causes genital and neonatal herpes.
  • VZV causes varicella and herpes zoster.
  • EBV causes Infectious Mononucleosis and is associated with malignancy.
  • CMV causes congenital and opportunistic disease.
  • HHV-6 is associated with roseola infantum.
  • HHV-7 causes less specific disease.
  • HHV-8 is associated with Kaposi sarcoma.
  • Herpesviruses establish lifelong latency.
  • Reactivation is more common with impaired immunity.
  • PCR is important for serious disease.
  • Acyclovir is important for HSV and VZV.
  • Ganciclovir and valganciclovir are important for significant CMV disease.