Incidence of herpes zoster in pediatricians and history of reexposure to varicella-zoster virus in patients with herpes zoster

We found that pediatricians have enhanced specific cellular immunity to varicella-zoster virus (VZV) compared with the general population, which may be due to reexposure to VZV from children with chickenpox. There have been some reported that the varicella vaccine enhance the specific cellular immunity. To estimate the efficacy of varicella vaccine for protection against herpes zoster in the elderly, we investigated the incidence of herpes zoster in 500 pediatricians and family practitioners with their fifties and sixties, and history of reexposure to VZV in 61 patients with herpes zoster by questionnaires retrospectively. Thirty-four of 352 pediatricians had a past history of herpes zoster. The incidence per 100,000 person-years of herpes zoster was 65.2 in those in their fifties and 158.2 in those in their sixties, which are 1/2 to 1/8 of other reports regarding the general population. Among 61 immunocompetent patients with herpes zoster, only 4 patients (6.6%) had the chance for reexpose to VZV before their herpes zoster. Only 7 (17.5%) of the 40 patients older than 50 years of age lived with their children less than 14 years of age. Twenty-three (57.5%) of them lived without their children and grandchildren. They are thought to be less chance to reexpose to VZV through children. We may think that the booster effect by reexposure to VZV plays an important role to prevent herpes zoster. Therefore, we can speculate that the varicella vaccine may protect against herpes zoster in the elderly by the enhanced specific cellular immunity due to the booster effect.

Coagulation initiated on herpes simplex viruses.

Herpesviruses have been previously correlated to vascular disease and shown to cause thrombogenic and atherogenic changes to host cells. Herein we show that even in the absence of cells, purified cytomegalovirus (CMV) and herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) can initiate thrombin production. Functional assays demonstrated that purified HSV-1 and HSV-2 provide the necessary phospholipid (proPL) for assembling the coagulation factors Xa and Va into prothrombinase, which is responsible for generating thrombin. These observations are consistent with our earlier studies involving CMV. The presence of proPL on all three herpes simplex viruses was confirmed directly by flow cytometry and electron microscopy by using annexin V and factor Va, respectively, as proPL-specific probes. Of equal importance, we found that CMV, HSV-1, and HSV-2 were also able to facilitate factor Xa generation from the inactive precursor factor X, but only when factor VII/VIIa and Ca2+ were present. Monoclonal antibodies specific for tissue factor (TF), the coagulation initiator, inhibited this factor X activation and, furthermore, enabled identification of TF antigen on each virus type by flow cytometry and electron microscopy. Collectively, these data show that CMV, HSV-1, and HSV-2 can initiate the generation of thrombin by having essential proPL and TF activities on their surface. Unlike the normal cellular source, the viral activity is constitutive and, therefore, not restricted to sites of vascular injury. Thus cell-independent thrombin production may be the earliest event in vascular pathology mediated by herpes simplex viruses.

Are human herpes simplex viruses or measles virus associated with esophageal achalasia?

In order to test the hypothesis that esophageal achalasia may be due to neurotropic viral damage to the esophageal myenteric plexus, esophageal tissue with or without achalasia was analyzed by polymerase chain reaction for the presence of human herpes simplex virus DNA or measles virus RNA. The DNA and RNA were extracted from the esophageal muscle of 12 patients with achalasia and six patients with upper esophageal carcinoma. Peripheral blood mononuclear cells from eight adult volunteers and two samples of umbilical blood mononuclear cells were also used as controls. PCR amplification with a pair of primers specific for herpes simplex type 1 and 2 viruses identified 92-bp fragments in nearly all specimens, including those without achalasia. Each 92-bp fragment was confirmed to be identical to a single herpes simplex virus sequence by automated DNA sequence analysis. No amplification for five other herpes simplex viruses or measles virus was detected. Therefore, a specific viral etiology for achalasia was not identified in this study.

Reactivation of genital herpes simplex virus type 2 infection in asymptomatic seropositive persons.

BACKGROUND: Most persons who have serologic evidence of infection with herpes simplex virus (HSV) type 2 (HSV-2) are asymptomatic. Historically, it has been assumed that these persons have less frequent viral reactivation than those with symptomatic infection. METHODS: We conducted a prospective study to investigate genital shedding of HSV among 53 subjects who had antibodies to HSV-2 but who reported having no history of Genital Herpes, and we compared their patterns of viral shedding with those in a similar cohort of 90 subjects with symptomatic HSV-2 infection. Genital secretions of the subjects in both groups were sampled daily and cultured for HSV for a median of 94 days. RESULTS: HSV was isolated from the genital mucosa in 38 of the 53 HSV-2-seropositive subjects (72 percent) who reported no history of Genital Herpes, and HSV DNA was detected by the polymerase-chain-reaction assay in cultures prepared from genital mucosal swabs in 6 additional subjects. The rate of subclinical shedding of HSV in the subjects with no reported history of genital herpes simplex was similar to that in the subjects with such a history (3.0 percent vs. 2.7 percent). Of the 53 subjects who had no reported history of Genital Herpes, 33 (62 percent) subsequently reported having typical herpetic lesions; the duration of their recurrences in these subjects was shorter (median, three days vs. five days; P<0.001) and the frequency lower (median, 3.0 per year vs. 8.2 per year; P<0.001) than in the 90 subjects with previously diagnosed symptomatic infection. Only 1 of these 53 subjects had no clinical or virologic evidence of HSV infection. CONCLUSIONS: Seropositivity for HSV-2 is associated with viral shedding in the genital tract, even in subjects with no reported history of Genital Herpes.