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Relationship between antibodies to herpes simplex virus (HSV) and symptoms of HSV infection.
To determine the relationship between antibodies to herpes simplex virus (HSV) types 1 and 2 and diagnosis of orolabial and Genital Herpes, a cross-sectional survey was done among 869 sexually transmitted disease clinic attendees and 1594 blood donors in London. Among clinic attenders, the prevalence of HSV-1 infection was 59.5% and that of HSV-2 infection was 22.7%, and among blood donors the prevalence was 44.6% and 7.6%, respectively. The sensitivity and specificity of a diagnosis of oral herpes simplex for the presence of HSV-1 antibody was almost identical in the 2 groups (clinic attendees: sensitivity, 33.1%, and specificity, 91.4%; blood donors: sensitivity, 32.3%, and specificity, 94.3%). A diagnosis of genital herpes simplex was less sensitive for antibody for HSV-2 among donors than among clinic attenders (P < .001); however, the specificity was similar in the 2 populations (clinic attendees: sensitivity, 32.1%, and specificity, 96.6%; blood donors: sensitivity, 17.5%, and specificity, 99.5%). False-positive clinical histories were also relatively common (clinic attenders, 12%; donors, 6%). The sensitivity of the diagnosis of genital herpes simplex would be improved if accurate serologic assays for detection of HSV type-specific antibodies were more widely available.
An attenuated herpes simplex vaccine may protect Gyr hybrids from fatal inclusion body hepatitis. A preliminary report.
Four Gyr hybrids were used for this falcon herpes simplex vaccine experiment. Three falcons were given 1 ml of an attenuated falcon herpes simplex virus vaccine (DuFaHe) subcutaneously twice within 14 days, whereas the fourth falcon was used as a control. Eighteen days after the booster vaccination, all four Gyr hybrids were intranasally and ocularly challenged with a virulent low-passage falcon herpes simplex virus. The control falcon died 9 days after challenge with typical lesions of herpes simplex virus inclusion body hepatitis. The three vaccinated falcons seroconverted and did not show any symptoms. Following the challenge their antibody titres to falcon herpes simplex virus increased. No herpes simplex virus was isolated from any of the cloacal swabs taken during this experiment, indicating that there was no danger for any other birds from DuFaHe. This experiment shows that falcons can be protected from herpes simplex virus infection by an attenuated herpes simplex virus vaccine. However, it should be stressed that only four falcons were used for this experiment.
Herpesviruses in periodontal pocket and gingival tissue specimens.
Human cytomegalovirus (HCMV) and Epstein-Barr virus type 1 (EBV-1) are frequently detected in crevicular fluid of deep periodontal pockets, but little or no information is available on occurrence of herpes simplex viruses in gingival tissue. This investigation studied the presence of herpes simplex viruses in periodontal pockets and the corresponding gingival tissues from 11 periodontally healthy and 14 periodontitis sites. A nested-polymerase chain reaction was employed to identify the presence of HCMV, EBV-1, EBV-2, herpes simplex virus, human herpes simplex virus (HHV)-6, HHV-7 and HHV-8 in each test sample. In healthy periodontal sites, HCMV was detected in 1 (9%) and EBV-1 in 2 (18%) pocket samples, and HCMV was detected in 2 (18%) and EBV-1 in 3 (27%) gingival tissue samples. In periodontitis lesions, HCMV was detected in 9 (64%) pocket samples and in 12 (86%) gingival tissue samples, and EBV-1 was detected in 6 (43%) pocket samples and in 11 (79%) gingival tissue samples. HHV-6 and HHV-8 were detected exclusively in gingival tissue samples. The present findings confirm the frequent presence of HCMV and EBV-1 in periodontitis lesions and suggest using gingival tissue specimens for detecting periodontal HHV-6, HHV-7 and HHV-8.
Herpes virus infections occur frequently following treatment with fludarabine: results of a prospective natural history study.
We performed a prospective infectious natural history study of 21 patients with low-grade lymphoproliferative disorders receiving fludarabine as initial (n = 5) or salvage (n = 16) therapy. 12 (57%) of these patients developed herpes zoster (n = 9), herpes simplex I (n = 1) or herpes simplex II (n = 2) infections at a median of 8 (range 1-17) months following initiation of fludarabine, with 75% of these having completed therapy. All patients with herpes zoster developed severe post-herpetic neuralgia. Factors differentiating patients developing these infections included older age and low serum IgG or IgA. Based upon these prospective data, we conclude that herpes simplex virus infections frequently occur following fludarabine treatment, necessitating aggressive patient education and new prophylactic strategies.
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