Viral latency is a reversible state in which a virus persists within a host cell without producing infectious progeny, maintaining its genome for long periods until reactivation signals trigger a productive infection.
Explanation
Many DNA and retroviruses have evolved latency as a survival strategy to evade immune clearance and persist in the host. During latency the viral genome is either integrated into the host chromosome, as with retroviruses and some bacteriophages, or maintained as an episome within the nucleus, as in herpesviruses. Viral gene expression is highly restricted; only a few latency‑associated transcripts or proteins are produced to maintain the genome or modulate the host environment. Host factors such as chromatin modifications and transcriptional repressors keep the viral genome silent. For herpes simplex virus (HSV) and varicella‑zoster virus, latency is established in sensory neurons; the genomes exist as circular episomes and only latency‑associated transcripts are expressed. In Epstein‑Barr virus and Kaposi sarcoma‑associated herpesvirus, latency occurs in B cells with distinct latency programs expressing subsets of viral proteins. Retroviruses like HIV integrate their proviral DNA into the genome of resting CD4+ T cells, forming latent reservoirs that are transcriptionally silent but retain the capacity for replication. Reactivation from latency can be induced by cellular stress, immunosuppression, hormonal changes or co‑infections and involves chromatin remodeling and activation of lytic gene expression.
Illustrative examples
Cold sores recur because HSV 1 establishes latency in trigeminal ganglion neurons after primary infection; fever or sunlight can trigger reactivation and anterograde transport of virus to the mucosa. Varicella‑zoster virus causes chickenpox in childhood and then persists latently in dorsal root ganglia; decades later it may reactivate as shingles, producing a painful dermatomal rash. HIV infection is controlled by antiretroviral therapy, but latent proviruses in memory T cells remain unaffected and can reignite viremia if treatment stops. Epstein‑Barr virus persists in B lymphocytes and reactivation can cause infectious mononucleosis or contribute to malignancies such as Burkitt lymphoma. Phage λ alternates between lytic replication and lysogenic latency in E. coli, integrating into the bacterial chromosome until induction by DNA damage.
Viral latency allows pathogens to hide from immune surveillance and poses major obstacles to eradication. Understanding the molecular mechanisms that maintain latency and control reactivation is critical for developing curative therapies.
Related Terms: Lytic cycle, Provirus, Herpesvirus, Reactivation, Lysogeny