Herpes is a systemic disease
When herpes infection occurs, the virus not only goes into the sensory neurons and dorsal root ganglia, but it also gets into epidermal cells, lymphatics, and blood. In primary herpes infections, viremia occurs, and the virus spreads to virtually all organs of the body. Viremia frequently occurs in neonatal herpes simplex infections, genital herpes, and herpes labialis in otherwise healthy individuals. By present testing, HSV viremia during attacks of primary and recurrent herpes infections is much more frequent than previously thought. Of note, the virus finds that the best location to avoid the host immune system is within nerves. The axon is sheathed in myelin layers that do not express major histocompatibility complex antibodies. The virus also produces substances to reduce the host’s immune response to its external coat.
PCR has revolutionized herpetic assessments because it detects HSV-specific DNA sequences in clinical samples that yield negative results by other testing procedures. Similar to viral cultures, PCR gives its most accurate results during the active phases of disease, as the bulk of the viruses hide from the host’s immune system within the nerve cells during periods of latency. Nevertheless, small numbers of HSV can be found by PCR in basically all organs of the body at all times.
On this point, any disease that causes pain in any organ for one to two weeks and later recurs in the same location might be herpetic in origin and may respond to antiherpetic oral medications. Examples of diseases that may be caused at least some of the time by herpes include recurrent lumbosacral herpes simplex, Bell’s palsy, erythema multiforme, middle ear infections, and proctitis. Oral antiherpetic therapy has also been beneficial in some cases of infertility.6
Asymptomatic shedding occurs sporadically in infected individuals who have no clinical evidence of disease, and transmission of the virus can occur in the absence of overt lesions. Genital herpetic disease is largely asymptomatic, and most transmission occurs during periods of asymptomatic shedding. As such, HSV can be isolated from the genital tract in the absence of genital lesions. In all the available studies in which seropositivity of HSV-2 has been assessed, only a minority of seropositive patients had a history of skin lesions.
All patients who are infected with HSV are potentially contagious regardless of whether clinical lesions are present. Approximately 70% of patients infected with HSV-2 are completely asymptomatic, with no history of overt clinical disease.
HSV-1 and genital herpes
HSV-1 causes 15%-25% of symptomatic genital herpes infections, and this percentage is increasing. Infection with HSV-2 is associated with a higher percentage of symptomatic recurrence and asymptomatic shedding than is infection with HSV-1. Only 50% of patients with symptomatic HSV-1 infections have clinical signs of recurrence. The increase in HSV-1 as a cause of genital herpes may be related to an increase in the practice of oral sex. Differentiating between HSV-1 and HSV-2 infection, however, may be clinically irrelevant because there are no practical clinical or treatment differences.