Herpes simplex virus (HSV) is a highly common infection caused by a virus that exists in two main types: HSV-1 and HSV-2. HSV-1 is traditionally associated with oral sores, often called cold sores, while HSV-2 is most frequently linked to genital lesions. Both types can infect either area of the body. Herpes is a viral infection and is absolutely not a genetic or inherited condition. This distinction is foundational to understanding how the virus is acquired and persists in the human body.
Infection Versus Inherited Conditions
The fundamental difference between an infection and an inherited condition lies in the source of the biological agent that causes the disease. Inherited conditions, or genetic disorders, are the result of specific variations or mutations in a person’s DNA. These DNA instructions are passed directly from biological parents to their offspring through reproductive cells, such as sperm and egg. A classic example of a genetic disorder is cystic fibrosis, which results from inheriting two copies of a faulty gene.
In contrast, an infection is an acquired condition, meaning it results from an external biological agent entering the body during a person’s lifetime. These external agents, known as pathogens, include viruses, bacteria, or fungi, and they must be transmitted from one source to the host. Herpes simplex virus is a neurotropic virus that must be transmitted through contact, demonstrating that it is an acquired infectious disease, not a trait coded into the inherited genome.
Viral Transmission and Acquisition
Since herpes is not genetic, acquisition occurs through direct physical contact with an infected person. Both HSV-1 and HSV-2 are transmitted through skin-to-skin contact, which allows the virus to enter the body through mucosal surfaces or abraded skin. This contact can be oral-to-oral, genital-to-genital, or oral-to-genital, with the risk of transmission being highest when active sores or blisters are present.
Transmission is also common during periods of asymptomatic viral shedding, which is when the virus is active on the skin surface without causing any visible lesions. A significant number of HSV transmissions occur when the infected partner has no noticeable symptoms. After initial exposure, the virus travels along nerve pathways and establishes a permanent, latent infection in the sensory ganglia, where it can periodically reactivate and travel back to the skin surface. A unique route of acquisition is vertical transmission, where an infant can acquire the virus from the mother during passage through the birth canal, which can lead to serious neonatal herpes.
Host Genetic Factors and Disease Severity
While the virus is acquired and not inherited, an individual’s genetic makeup can influence the outcome and severity of the infection after it has been established. These “host genetic factors” relate primarily to the genes that govern the immune system’s response to the pathogen. Specific alleles of the Human Leukocyte Antigen (HLA) system, which helps the immune system recognize foreign invaders, have been studied for their association with HSV.
Certain HLA class I allotypes, such as B\18, C\15, and the group of alleles encoding A19, have been shown to modify the risk of suffering a clinical HSV-1 infection. These genes impact how effectively the immune system’s cytotoxic cells, like T-cells and Natural Killer (NK) cells, can control the virus and prevent it from reactivating. Polymorphisms in other immune-related genes, such as the killer cell immunoglobulin-like receptors (KIR), have also been linked to differences in viral shedding rates and the frequency of outbreaks. These variations do not determine whether a person gets herpes, but rather how often they experience symptomatic recurrences or how severe those outbreaks might be.