Salam

The viruses are intelligent microorganism, upon body immunity is declined (pregnant women) or suppressed by cyclosporine (in the case of transplant patients). The viruses initiate replication and become recurrent.

Salam and Asghar,

I agree with you Asghar.  The HSV-2 is a DNA virus that definitely becomes more active during immuno-compromised states.  This virus has an affinity for sensory nerves in the genitals and stays in the dorsal root ganglion (DRG) in the lower back.  Because they remain latent in the DRG, any excess load on the immune system through infectious disease or drug-induced can cause reactivation.

During monthly period some women become stressed before the onset of menstruation. This stress can cause reactivation of HSV-2 virus that remain in dormant stage in respective dorsal root ganglia. Stress suppresses immunity. Not only among the women all people can develop reactivation of HSV-1 or II when they become stressed for a longer period.

All the above ideas, mostly focusing on the host, though broadly correct, yet, still leave some questions unanswered . In clinical practice, not every person diagnosed with primary HSV 2 infection subsequently presents with troublesome frequent relapses, be it linked to the phases in the menstrual cycle or not. Reactivation of HSV 2 from the dorsal nerve root ganglion could also be due to the virulence of the particular strain of the virus the person has been infected with. Mutations in the virus genome towards increased virulence could be a survival factor for the virus leading to its further spread and propagation. More frequent relapses statistically leading to more frequent exposure to virgin territory for the virus. For HSV 1 and 2, humans are the only known hosts, and, phylogenetically these viruses have evolved with mankind. Thus, the virus always has an eye 'on its own survival', so to speak. The decreased incidence of oro-labial herpes in the past few decades, mainly due to the loss of social promiscuity, at least in developed countries, had been offset by the causative HSV 1 virus by its steadily increasing tendency to cause genital infection. Genital infection, dominated by HSV 2 few decades ago, is now shared equally between the tow types. Although the reasons for this may be more complex than this, it is impossible to exclude some contributory adaptive change in the virus itself. Furthermore, stress leading to frequent recurrences of genital HSV 2 has been challenged, the suggestion being, stress when it is identified in association with HSV is very often due to the acquisition of the infection in an individual who had negative preconceived ideas about the infection, which have not been dislodged by timely, evidence based counseling and support that should ideally have been given with the culture or PCR test results. Having said that, stress, when it is operational, does increase the production of cortisol - a hormone known to be associated with depressed immunity.

According to personal observations, when estrogen and progesterone levels are low (first day of menses) and psychological stress is present (high cortisol), there is a oral herpetic reactivation; having trouble with herpes DNA detection with PCR assay. For these reason it is strictly necessary to use control negative samples.