The possible relationship of herpes simplex virus infection to cause of retardation in severe mental handicap

1980 ◽  
Vol 10 (3) ◽  
pp. 555-557
Author(s):  
A. H. Reid ◽  
K. W. Martin ◽  
B. R. Ballinger ◽  
B. B. Heather

SYNOPSISThe relationship between herpes simplex virus type 1 and mental retardation is explored by studying the antibody levels to this virus in a group of 86 severely and profoundly retarded adults. A tendency towards higher antibody levels is found in patients whose retardation is of unknown aetiology. The relationship of these observations to previous research findings and the possible significance of herpes simplex virus in the aetiology of mental retardation are discussed

2002 ◽  
Vol 96 (5) ◽  
pp. 1168-1174 ◽  
Author(s):  
Ichiro Takasaki ◽  
Atsushi Sasaki ◽  
Tsugunobu Andoh ◽  
Hiroshi Nojima ◽  
Kimiyasu Shiraki ◽  
...  

Background Postherpetic neuralgia is pain that persists long after the disappearance of the cutaneous lesions of herpes zoster. However, the mechanisms of this delayed pain are unclear. Herpes simplex virus infection induces cutaneous lesions and pain-related responses in mice. The authors examined whether such responses would persist after the disappearance of the cutaneous lesions and whether some analgesics would be effective against them. Methods Female BALB/c mice were inoculated with herpes simplex virus type 1 on the unilateral hind paw. Pain-related responses of hind paw were determined using von Frey filaments. Beginning 5 days after inoculation, mice were given perorally the antiherpes agent acyclovir five times a day for 7 days. Effects of morphine (3-5 mg/kg subcutaneously), gabapentin (30-100 mg/kg perorally), mexiletine (10-30 mg/kg intraperitoneally), and diclofenac (30 mg/kg intraperitoneally) on pain-related responses were examined on days 25-35 after inoculation. Results Viral inoculation induced cutaneous lesions and pain-related responses beginning on day 5 after inoculation. Acyclovir treatment healed all skin lesions by day 15 after inoculation. Approximately half of the mice given acyclovir showed pain-related responses at least until day 40 after inoculation. Morphine, gabapentin, and mexiletine dose-dependently inhibited pain-related responses, but diclofenac had no effects. Conclusions The authors show a mouse model of delayed postherpetic pain. This may be useful for manifesting the mechanisms of postherpetic neuralgia and the factors contributing to the transition from acute herpetic pain to delayed postherpetic pain. This may also be useful for the development of new analgesics against postherpetic neuralgia.


1999 ◽  
Vol 13 (3) ◽  
pp. 201-211 ◽  
Author(s):  
Marc Baker ◽  
Sansanee Noisakran ◽  
Bryan M. Gebhardt ◽  
John D. Kriesel ◽  
Daniel J.J. Carr

1987 ◽  
Vol 104 (sup446) ◽  
pp. 157-164 ◽  
Author(s):  
Kosuke Ishii ◽  
Takeshi Kurata ◽  
Tetsutaro Sata ◽  
Mai Van Hao ◽  
Yasuya Nomura

1998 ◽  
Vol 72 (8) ◽  
pp. 6888-6892 ◽  
Author(s):  
N. M. Sawtell

ABSTRACT The purpose of this study was to define the relationship between herpes simplex virus (HSV) latency and in vivo ganglionic reactivation. Groups of mice with numbers of latently infected neurons ranging from 1.9 to 24% were generated by varying the input titer of wild-type HSV type 1 strain 17syn+. Reactivation of the virus in mice from each group was induced by hyperthermic stress. The number of animals that exhibited virus reactivation was positively correlated with the number of latently infected neurons in the ganglia over the entire range examined (r = 0.9852, P< 0.0001 [Pearson correlation]).


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