17.2
Herpes is a contagious viral disease caused by the herpes simplex virus type 1. It is marked by painful skin lesions, most commonly around the mouth.
Transmission occurs through direct contact with infected secretions or mucosal surfaces, allowing the virus to infect epithelial cells.
HSV-1 first binds to heparan sulfate on the cell surface and then to a secondary receptor such as nectin.
The viral envelope fuses with the host plasma membrane, releasing the capsid and proteins into the cytoplasm.
The viral DNA enters the nucleus, circularizes, and hijacks the host machinery to replicate its genome and produce viral mRNA. These mRNAs are translated into viral proteins, which assemble to form nucleocapsids.
These nucleocapsids exit the nucleus, acquire an envelope from host cell membranes, and are released by exocytosis.
After replication, HSV-1 enters sensory nerve cells and travels to the trigeminal ganglia, where it remains latent.
Stress, fever, or immune suppression can trigger reactivation of the virus. It then travels back to the skin or mucosa, replicates, and causes recurrent lesions.
Herpes simplex type 1 (HSV‑1) is a widespread pathogen responsible for orolabial lesions. It is an enveloped, double-stranded DNA (dsDNA) virus belonging to the family Herpesviridae. Once the virus infects a host cell, its double‑stranded DNA genome is delivered into the nucleus, where a coordinated cascade of immediate‑early, early, and late gene expression directs viral DNA replication, structural protein synthesis, and virion assembly. After primary infection of epithelial cells, HSV-1 establishes latency in sensory neurons of the trigeminal ganglion. Reactivation, prompted by triggers such as stress or immunosuppression, results in recurrent mucocutaneous lesions.
Diagnosis
HSV‑1 infection is often recognized through characteristic lesions. Laboratory confirmation may involve polymerase chain reaction (PCR) testing, viral culture, or direct fluorescent antibody assays from lesion samples. Serologic testing for HSV‑1 antibodies has limitations—particularly for differentiating oral from genital infection—and is generally not used as the sole diagnostic approach. Clinical evaluation remains central, especially when lab tests are inconclusive.
Treatment
HSV‑1 is incurable, but antiviral agents such as acyclovir, valacyclovir, and famciclovir effectively reduce symptom severity and shorten outbreaks by targeting viral DNA polymerase. For recurrent episodes—such as herpes labialis—topical agents (e.g., penciclovir, docosanol) may be used, although oral therapy is generally more effective. Suppressive antiviral therapy may be considered in individuals with frequent recurrences.
Prevention
Transmission is likely during active lesions, though asymptomatic viral shedding can also transmit infection. Preventive measures include avoiding direct contact with active lesions, practicing good hygiene (e.g., handwashing), and avoiding sharing personal items like lip balm or utensils. During oral‑genital contact, using barrier methods (e.g., dental dams) may reduce the risk of transmission. There is currently no licensed vaccine for HSV‑1, although vaccine candidates are under investigation.
Herpes is a contagious viral disease caused by the herpes simplex virus type 1. It is marked by painful skin lesions, most commonly around the mouth.
Transmission occurs through direct contact with infected secretions or mucosal surfaces, allowing the virus to infect epithelial cells.
HSV-1 first binds to heparan sulfate on the cell surface and then to a secondary receptor such as nectin.
The viral envelope fuses with the host plasma membrane, releasing the capsid and proteins into the cytoplasm.
The viral DNA enters the nucleus, circularizes, and hijacks the host machinery to replicate its genome and produce viral mRNA. These mRNAs are translated into viral proteins, which assemble to form nucleocapsids.
These nucleocapsids exit the nucleus, acquire an envelope from host cell membranes, and are released by exocytosis.
After replication, HSV-1 enters sensory nerve cells and travels to the trigeminal ganglia, where it remains latent.
Stress, fever, or immune suppression can trigger reactivation of the virus. It then travels back to the skin or mucosa, replicates, and causes recurrent lesions.
From Chapter 17:
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