A viral aetiology has long been suspected for Alzheimer's disease (AD) but until now, techniques have not been sufficiently sensitive to provide clear evidence for or against the presence of any viral genome in AD brain. We have used the very highly sensitive method of polymerase chain reaction to look for herpes simplex virus type 1 (HSV1) DNA, specifically the viral thymidine kinase (TK) gene, in autopsy brain specimens. DNA-samples from HSV-infected and uninfected Vero cells have been examined concurrently to provide standard "HSV-positive" and "HSV-negative" samples, the latter guarding also against false positives caused by cross-contamination. To preclude false negatives, we have checked the presence of the human gene, hypoxanthine phosphoribosyl transferase. In all specimens from 8 AD patients and 6 normal individuals (temporal, frontal and hippocampal), we have found viral TK sequences. In contrast, in preliminary studies on lymphocytes from normals and AD patients, we did not find TK sequences. It is postulated that factors such as number or expression of viral genes and host susceptibility might be related to incidence of AD.

Acyclovir (ACV) has been used for more than 15 years in the management of herpes simplex virus (HSV) and varicella-zoster virus (VZV) disease. The present survey was undertaken to assess the level of ACV resistance in the population. More than 2,000 HSV isolates from both immunocompetent and immunocompromised patients in northwest England were collected over a 2-year period and tested for sensitivity to ACV. These studies suggested a prevalence of resistance of approximately 0.1 to 0.6% in immunocompetent individuals, with no apparent difference in prevalence between treated and untreated groups. In line with previous studies, the prevalence of resistance in treated immunocompromised individuals was approximately 6%.

Thirty patients who had not previously received treatment with factor VIII concentrate or who had been treated only infrequently with factor VIII concentrate were studied after a transfusion of factor VIII. Tests of liver function were performed frequently. Four patients had evidence of chronic liver disease before transfusion. In 17 of the remaining 26 patients serum transaminase activities became raised and 10 patients developed jaundice. All of the nine patients who had not previously received factor VIII transfusion developed non-A non-B hepatitis. Four out of 10 patients followed up for a year had persisting abnormalities of liver function.The pattern of illness suggests that more than one serotype of non-A non-B hepatitis virus may be transmitted by factor VIII concentrate prepared by the National Health Service from volunteer donors in the United Kingdom.

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