Step by Step
HSV
HSV-1/2 — sensory ganglia, cold sores and genital lesions
HSV-1/2 establishes latency in the trigeminal or sacral sensory ganglia, reactivating as cold sores or genital lesions specifically triggered by stress, UV light exposure, or immunosuppression.
Example: a person under significant stress experiencing a cold sore outbreak, reflecting HSV-1 reactivating from its latent site in the trigeminal ganglion.
VZV
VZV — dorsal root ganglia, chickenpox then shingles
VZV's primary infection causes chickenpox, after which it establishes latency in the dorsal root ganglia; reactivation later in life causes shingles, characteristically appearing in a dermatomal (single nerve root) distribution.
Example: an older adult developing a painful, band-like rash confined to one side of their torso, following a single dermatome — a classic presentation of shingles from reactivated VZV.
EBV
EBV — B lymphocytes, mononucleosis and lymphoma risk
EBV establishes latency within B lymphocytes, with primary infection typically causing mononucleosis; reactivation in immunocompromised individuals is specifically associated with lymphoma risk.
Example: a young adult presenting with the classic mononucleosis triad (fever, pharyngitis, lymphadenopathy), reflecting primary EBV infection.
CMV
CMV — myeloid cells, dangerous in transplant recipients
CMV establishes latency within myeloid cells, and while often mild or asymptomatic in healthy individuals, it poses a particularly dangerous reactivation risk in transplant recipients due to their immunosuppressed state.
Example: a transplant recipient on immunosuppressive therapy being closely monitored for CMV reactivation, given how dangerous this reactivation can be specifically in that immunocompromised population.
Applied Walkthrough
1
An older adult presents with a painful, band-like rash confined to one side of their body, following a single dermatome.
2
Ask: which herpesvirus and which latency site is most likely responsible? VZV, reactivating from its latent site in the dorsal root ganglia — this dermatomal presentation is the classic pattern for shingles.
3
Contrast: if the patient instead presented with a cold sore following a stressful period, HSV-1 reactivating from the trigeminal ganglion would be the more likely culprit.
4
Knowing each herpesvirus's specific latency site (sensory ganglia for HSV, dorsal root ganglia for VZV, B lymphocytes for EBV, myeloid cells for CMV) helps predict both the reactivation trigger and the resulting clinical presentation.
Exam Application
Exams test whether you can match each herpesvirus (HSV, VZV, EBV, CMV) to its specific latency site and characteristic reactivation presentation, and whether you understand why immunocompromised states (transplant, HIV) specifically increase reactivation risk across this whole family of viruses.
⚠ Common Trap
The most common trap is confusing VZV's two distinct clinical presentations — chickenpox (primary infection) versus shingles (reactivation) — as if they were caused by different viruses. They're the same virus at two different stages: primary infection causes chickenpox, and later reactivation from the same latent infection causes shingles.
✓ Quick Self-Check
1. Where does HSV-1/2 establish latency?
Trigeminal or sacral sensory ganglia.
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2. Where does VZV establish latency, and what does its reactivation cause?
Dorsal root ganglia; reactivation causes shingles, in a dermatomal distribution.
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3. Where does EBV establish latency, and what is a key reactivation risk?
B lymphocytes; reactivation in immunocompromised individuals is associated with lymphoma risk.
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4. Where does CMV establish latency, and in what population is reactivation especially dangerous?
Myeloid cells; especially dangerous in transplant recipients.
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5. Name three common triggers for herpesvirus reactivation.
Stress, UV light exposure, or immunosuppression (any of these, depending on the specific virus).
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