Viral causes of the acute retinal necrosis syndrome.

PURPOSE: The primary goal of this study was to determine the viral cause of the acute retinal necrosis syndrome in 28 patients (30 eyes). A secondary goal was to investigate possible associations between viral cause and patient age, and viral cause and central nervous system disease. METHODS: A retrospective case series in which we reviewed the laboratory results and clinical histories of 28 patients (30 eyes) diagnosed with acute retinal necrosis syndrome, from whom vitreous or aqueous specimens were received, for diagnostic evaluation using previously described polymerase chain reaction-based assays. RESULTS: Varicella-zoster virus, herpes simplex virus, and cytomegalovirus (CMV) DNA were detected in aqueous and/or vitreous specimens from 27 of 28 patients (29 of 30 eyes with a clinical history of acute retinal necrosis syndrome). No sample was positive for DNA from more than one virus. Varicella-zoster virus DNA was detected in 13 patients (15 eyes). Median age was 57 years. Herpes Simplex virus type 1 DNA was detected in seven patients (seven eyes). Median age was 47 years. Six of these patients had a history of herpes simplex virus encephalitis. Herpes Simplex virus type 2 DNA was detected in six patients (six eyes). Median age was 20 years. Three of these patients had a likely history of meningitis. Cytomegalovirus DNA was detected in one patient who was immunosuppressed iatrogenically. No viral DNA was detected in one patient from whom a sample was taken after 6 weeks of Acyclovir therapy. CONCLUSIONS: The data suggest that varicella-zoster virus or herpes simplex virus type 1 cause acute retinal necrosis syndrome in patients older than 25 years, whereas herpes simplex virus type 2 causes acute retinal necrosis in patients younger than 25 years. A history of central nervous system infection in a patient with acute retinal necrosis syndrome suggests that herpes simplex virus is likely to be the viral cause.

Nosocomial Kikuchi's disease--a search for herpes simplex virus sequences in lymph node tissues using PCR.

BACKGROUND: Histiocytic necrotizing lymphadenitis, also known as Kikuchi's disease (KD), is a rare disease. Fever and lymphadenopathies with characteristic pathologic features are present. The etiology of this disease remains undetermined. Since the disorder is self-limiting, different viruses have been implicated as the causative agent. PATIENTS AND METHODS: Seven cases of KD were studied. Three patients acquired the disease nosocomially, three had community-acquired KD and one case was associated with systemic lupus erythematosus. PCR was performed on DNA extracted from lymph node tissues in order to detect herpes simplex virus-specific DNA sequences: herpes simplex virus type 1 and 2 (HSV1-2), varicella zoster virus (VZV), human cytomegalovirus (HCMV), human herpes simplex virus 6 (HHV6), Epstein-Barr virus (EBV) and human herpes simplex virus 8 (HHV8). RESULTS: Viral DNA was not detected in any of the lymph node tissues from the seven cases of KD. CONCLUSION: We conclude that these herpes simplex viruses were not involved in the etiology of the three cases of nosocomial KD, nor in the other four cases of KD investigated in this study.

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.

DNA sequence of the UL6 to UL20 genes of infectious laryngotracheitis virus and characterization of the UL10 gene product as a nonglycosylated and nonessential virion protein.

The 24 kbp KpnI restriction fragment A from the unique long genome region of infectious laryngotracheitis virus (ILTV, gallid herpes simplex virus-1) has been sequenced. The analysed region contains 14 open reading frames sharing homology with conserved alphaherpes virus genes. Arrangement of the UL6 to UL20 homologues of ILTV is almost identical to that found in the herpes simplex virus type 1 genome. As in other herpes simplex viruses the UL15 gene consists of two exons and is expressed from a spliced mRNA. However, the UL16 gene, which is usually localized within the intron sequence of UL15, is not conserved at this position of the ILTV genome. Another unique feature is the absence of any putative N-glycosylation motifs within the deduced ILTV UL10 gene product, which is the homologue of the conserved herpes simplex virus glycoprotein M. After preparation of a monospecific antiserum, two distinct UL10 proteins with apparent molecular masses of 36 and 31 kDa were identified in ILTV-infected cells as well as in purified virions. None of these UL10 gene products is modified by N- or O-linked glycosylation. Isolation of a green fluorescent protein-expressing UL10 deletion mutant of ILTV revealed that this gene is not required for virus replication in cell culture.