The neurologist · 2011
Herpes simplex virus type 1 in saliva of patients with vestibular neuronitis: a preliminary study.
СтатьяНазвание и аннотация: Перевод в очереди
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Pollak Lea, Book Mazal, Smetana Zehava, Alkin Marina, Soupayev Zvia, Mendelson Ella
Аннотация
OBJECTIVES: Vestibular neuronitis (VN) is an inflammatory disease of the vestibular nerve, presumably caused by reactivation of the herpes simplex virus type l (HSV-1). We hypothesized that HSV-1 might be detected in saliva of patients with VN due to migration of the reactivated virus from the vestibular ganglia to the parotid gland.
METHODS: Twenty-one patients with VN and 15 healthy controls participated. HSV-1 DNA detection was performed using the real-time polymerase chain reaction method. Sera were collected and stored to be later analyzed for immunoglobulin (Ig) G and IgM antibody titers against HSV-1 by immunofluorescence and enzyme linked immunosorbent assay methods, respectively.
RESULTS: HSV-1 was detected in saliva of 14% of VN patients and in 6% of controls (P>0.05). Serological testing revealed borderline IgM (optical density±10% average of 2 cut off serums) antibodies to HSV-1 in 75% of patients versus 13% of controls (P=0.01). The IgG antibody test was positive in 17 of 20 patients and borderline (IgG ≤1:16) in 2 of 20 patients tested whereas 13 of 15 controls had positive IgG test results (P>0.05).
CONCLUSIONS: In this preliminary study we found serological evidence of higher exposure of patients with VN to HSV-1 in the past. We were not able to demonstrate that the virus can be detected in saliva of VN patients as evidence for herpetic infection or reactivation.
METHODS: Twenty-one patients with VN and 15 healthy controls participated. HSV-1 DNA detection was performed using the real-time polymerase chain reaction method. Sera were collected and stored to be later analyzed for immunoglobulin (Ig) G and IgM antibody titers against HSV-1 by immunofluorescence and enzyme linked immunosorbent assay methods, respectively.
RESULTS: HSV-1 was detected in saliva of 14% of VN patients and in 6% of controls (P>0.05). Serological testing revealed borderline IgM (optical density±10% average of 2 cut off serums) antibodies to HSV-1 in 75% of patients versus 13% of controls (P=0.01). The IgG antibody test was positive in 17 of 20 patients and borderline (IgG ≤1:16) in 2 of 20 patients tested whereas 13 of 15 controls had positive IgG test results (P>0.05).
CONCLUSIONS: In this preliminary study we found serological evidence of higher exposure of patients with VN to HSV-1 in the past. We were not able to demonstrate that the virus can be detected in saliva of VN patients as evidence for herpetic infection or reactivation.