Epstein-Barr virus (EBV) encephalitis is rare and shows a wide range of clinical manifestations. We report an immunocompromised patient with EBV encephalitis diagnosed by EBV-specific PCR and antibody testing in the cerebrospinal fluid who presented with psychiatric symptoms and cognitive dysfunction in the absence of any neurological impairments or infectious signs. Clinical recovery and clearance of cerebrospinal fluid EBV DNA appeared following ganciclovir treatment within 6 weeks.

Many viral infections that cause minor illness in younger adults can lead to significant mortality and morbidity in older people, particularly as co-morbidities tend to accumulate with increased age. Respiratory and gastrointestinal viruses are ubiquitous and frequently cause outbreaks, with major impact on those in care homes or residential accommodation. Advances in medicine have opened the way for increased impact of the herpes viruses (varicella zoster virus, herpes simplex virus, Epstein–Barr virus and cytomegalovirus), as immune systems are manipulated. People are also leading more active lives in older age; human immunodeficiency virus (HIV) will be increasingly prevalent, as those living with HIV grow older in good health. In addition, new diagnoses of HIV, viral hepatitis and travel-related infections will present to those working in health care of older people. This review article of viral infections aims to highlight relevant pathology, with specific reference to management in older people.

Infectious mononucleosis is a clinical manifestation of primary Epstein–Barr virus infection. It is unknown whether genetic factors contribute to risk. To assess heritability, we compared disease concordance in monozygotic to dizygotic twin pairs from the population-based California Twin Program and assessed the risk to initially unaffected co-twins. One member of 611 and both members of 58 twin pairs reported a history of infectious mononucleosis. Pairwise concordance in monozygotic and dizygotic pairs was respectively 12·1% [standard error (s.e.)=1·9%] and 6·1% (s.e.=1·2%). The relative risk (hazard ratio) of monozygotic compared to dizygotic unaffected co-twins of cases was 1·9 [95% confidence interval (CI) 1·1–3·4, P=0·03], over the follow-up period. When the analysis was restricted to same-sex twin pairs, that estimate was 2·5 (95% CI 1·2–5·3, P=0·02). The results are compatible with a heritable contribution to the risk of infectious mononucleosis.

Infection with Epstein–Barr virus (EBV) followed by infectious mononucleosis (IM) is now considered to be a risk factor for Hodgkin's disease (HD). It is less clear whether EBV infection and IM are associated with an increased risk of cancer generally. We used a longstanding record-linkage dataset in Oxford (years 1963–1998), and a more recent record-linkage dataset covering England (1999–2005), to compare rate ratios for cancer between people admitted to hospital for IM and a reference cohort. In the Oxford cohort, there was an increased risk of subsequent HD [rate ratio (RR) 6·0, 95% confidence interval (CI) 2·4–12·5] but not of other cancers combined (RR 0·85, 95% CI 0·57–1·23). In the England cohort, there were increased risks of HD (RR 3·2, 95% CI 1·2–7·0), non-Hodgkin's lymphoma (RR 5·6, 95% CI 2·9–9·8), and oropharyngeal cancer (RR 5·4, 95% CI 1·1–16·2), but no significant overall risk of cancer when lymphomas were excluded (RR 1·01, 95% CI 0·71–1·41). We confirm an association between IM and lymphoma; but the risk, if any, of cancer more generally is likely to be small.

The Epstein–Barr virus (EBV) is a human herpesvirus that is usually carried lifelong as an asymptomatic infection. EBV is the causative agent of infectious mononucleosis and has been linked to the development of several malignant tumours, including B-cell neoplasms such as Burkitt's lymphoma and Hodgkin's disease, certain forms of T-cell lymphoma, and some epithelial tumours, such as undifferentiated nasopharyngeal carcinoma and a proportion of gastric cancers. All these tumours are characterised by the presence of multiple extrachromosomal copies of the circular viral genome in the tumour cells and the expression of EBV-encoded latent genes, which appear to contribute to the malignant phenotype. An increasing understanding of the function of EBV latent genes and of the nature of the immune response to the virus is providing exciting new possibilities for the treatment of EBV-associated malignancies. For example, adoptive transfer of virus-specific cytotoxic T lymphocytes has already been of value in the treatment of EBV-positive B-cell lymphomas arising in post-transplant patients, and this approach is currently being investigated in other EBV-associated tumours. In addition, gene therapy offers the opportunity to deliver agents that might directly interfere with the function of specific EBV genes. This review summarises the role of EBV in malignancy. In particular, it focuses on the latent proteins as a basis for understanding how EBV might contribute to the process of transformation. Strategies to target EBV in tumours, potentially providing alternative therapeutic approaches, are also discussed.