Researchers from the University of Washington (UW) School of Medicine in Seattle discovered that the rate of shedding decreases during the first year.
Previously, herpes simplex virus type 1 (HSV-1) was predominantly responsible for cold sores and fever blisters on the lips, whereas herpes simplex virus type 2 (HSV-2) was mostly responsible for genital herpes. However, that has altered in recent decades, and HSV-1 is now the major cause of new genital herpes infections in many regions of the world.
Fewer people have been infected with HSV-1 as children in recent decades, making them susceptible to infection when they become sexually active.
The majority of genital herpes infections occur without symptoms. However, symptoms might include painful genital blisters and ulcers, fever, chills, weariness, muscular pains, and other flu-like symptoms. Infections can also induce mental anguish because patients may experience the social stigma associated with infection and be concerned about passing the virus to their sexual partners and, if pregnant, to their newborn.
Johnston and colleagues wanted to learn more about the progression of HSV-1 infections in the genital tract and how the immune system responds. Despite the fact that HSV-1 appears to cause fewer genital symptoms than HSV-2, this was the first study to look at both oral and genital HSV-1 shedding using the extremely sensitive polymerase chain reaction (PCR) assay.
They included 82 men and women who had been diagnosed with genital HSV-1 infection for the first time. There were 54 ladies (66%) and 28 guys (34%). Their ages ranged from 16 to 64, with a median of 26 years. Antibody testing revealed that almost half of the participants had previously been infected with HSV-1.
The participants swabbed their mouths and genitals daily for 30 days to identify shedding, two and 11 months after their first bout of genital HSV-1. The swabs were examined for HSV-1 presence. Blood samples were also taken at various stages throughout the trial to assess the individuals' immunological response to the illness. The participants used an antiviral medication to treat their initial episode but agreed not to take antiviral medications throughout the times when samples were obtained.
The length of time that participants shed virus varied. Some participants shed no virus at all, but at two months, shedding was rather prevalent, with patients shedding HSV-1 on 12% of days. However, after 11 months, the rate had dropped to 7% of days. Even though they were shedding virus, most individuals did not exhibit symptoms.
Participants who shed at least 10% of their days at 11 months underwent another 30 days of swabbing two years later. The rate of shedding had dropped even more in this group, to 1.3% of days. Despite the short sample size, the rates are significantly lower than those seen with HSV-2, where shedding occurs on around 34% of days in the first year and remains at 17% of days after 10 years. Recurrences occurred infrequently, with an average of one recurrence within the first year of illness.
The analysis of the virus samples and the individuals' immunological response to the infection did not explain why shedding rates varied among subjects. However, shedding was more likely in those who had just acquired the virus.
Patients who lack HSV-1 and -2 antibodies when diagnosed with their first incidence of genital herpes should be warned to expect more frequent shedding, according to Johnston, and they may be candidates for suppressive antiviral medication during the first year of infection.
Although neonatal herpes is uncommon, it can be fatal, she added. The discovery that shedding is widespread in the initial months after infection emphasizes the necessity of identifying pregnant women who are at high risk of getting HSV-1 and taking preventive measures to avoid infection.
