Herpesvirus latency and reactivation
Latency is the quiet, non-multiplying state in which every human herpesvirus lies dormant for life inside specific cells, able to reactivate (switch back to its active phase).
Remember
Every human herpesvirus stays dormant for life and can reactivate, so a later episode, such as a cold sore (small fluid-filled blisters on the lip), is the same virus returning, not a new infection.
Eight herpesviruses infect humans: herpes simplex virus types 1 and 2, varicella-zoster virus (which causes chickenpox and, on reactivation, shingles), Epstein-Barr virus, cytomegalovirus and human herpesviruses 6, 7 and 8. All are DNA viruses, so their genome is DNA rather than RNA.
These viruses alternate between two phases. In the lytic phase (the active phase) the virus produces new virus and may cause symptoms. In the latent phase (the dormant phase) the viral genome stays quiet inside particular host cells (the cells that harbour the virus), where few viral proteins are made and no new virus particles are produced. Latency begins after the first, or primary, infection, so the infection lasts for life.
Reactivation is the switch from latency back to the lytic phase. The virus then multiplies again and can cause recurrent disease such as cold sores (small fluid-filled blisters on the lip) or shingles. It can also be shed silently (given off without symptoms), so the virus can be passed on without the person knowing. Each episode is the same dormant virus waking up, not a new infection. For herpes simplex virus type 1, triggers such as physical or emotional stress, fever, sunlight, hormonal change and weakened immunity can cause reactivation.
Different members of the family hold the dormant virus in different cells. Herpes simplex virus lies in sensory neurons (nerve cells carrying touch and pain signals), within a ganglion (a cluster of nerve cell bodies) such as the trigeminal ganglion, which serves the face. Epstein-Barr virus lies in B lymphocytes (antibody-making white blood cells), and cytomegalovirus in bone marrow progenitor cells (immature blood cells) and monocytes.
Key facts
- Shared feature
- latency for life in specific cell types, with potential for reactivation.
- Phases
- an active lytic phase, which may cause symptoms, and a dormant latent phase.
- Latent sites
- cytomegalovirus in monocytes and bone marrow progenitor cells, Epstein-Barr virus in B lymphocytes, and herpes simplex virus in sensory neurons.
- Recurrence
- a later episode of cold sores or shingles is the same virus reactivating, not a new infection.
- Silent shedding
- reactivation without symptoms can still pass the virus on.
- Triggers
- for herpes simplex virus type 1, weakened immunity, hormonal change, sunlight, fever and stress can cause reactivation.
Exam traps
- Herpesviruses are not cleared by the immune system after the first infection, because the virus stays in the body for life, so a later episode of cold sores or shingles is the same virus reactivating, not a new infection.
- Lying dormant in sensory neurons is true of herpes simplex virus, but the site of latency differs across the family, so sensory neurons are not the shared site: Epstein-Barr virus lies in B lymphocytes and cytomegalovirus in monocytes and bone marrow progenitor cells.
- Reactivation is not restricted to people with weakened immunity: for herpes simplex virus type 1, stress, fever, sunlight and hormonal change can also trigger it, and cold sores are a common recurrent example.
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